Your browser doesn't support javascript.
loading
Mostrar: 20 | 50 | 100
Resultados 1 - 20 de 76
Filtrar
1.
Ecotoxicol Environ Saf ; 269: 115742, 2024 Jan 01.
Artículo en Inglés | MEDLINE | ID: mdl-38039849

RESUMEN

The purpose of this study was to explore the protective effect of SeMet on renal injury induced by AFB1 in rabbits and its molecular mechanism. Forty rabbits of 35 days old were randomly divided into control group, AFB1 group (0.3 mg AFB1/kg b.w), 0.2 mg/kg Se + AFB1 group (0.3 mg AFB1/kg b.w + 0.2 mg SeMet/kg feed) and 0.4 mg/kg Se + AFB1 group (0.3 mg AFB1/kg b.w + 0.4 mg SeMet/kg feed). The SeMet treatment group was fed different doses of SeMet diets every day for 21 days. On the 17-21 day, the AFB1 treatment group, the 0.2 mg/kg Se + AFB1 group and the 0.4 mg/kg Se + AFB1 group were administered 0.3 mg AFB1 /kg b.w by gavage (dissolved in 0.5 ml olive oil) respectively. The results showed that AFB1 poisoning resulted in the changes of renal structure, the increase of renal coefficient and serum biochemical indexes, the ascent of ROS and MDA levels, the descent of antioxidant enzyme activity, and the significant down-regulation of Nrf2, HO-1 and NQO1. Besides, AFB1 poisoning increased the number of renal apoptotic cells, rised the levels of PTEN, Bax, Caspase-3 and Caspase-9, and decreased the levels of PI3K, AKT, p-AKT and Bcl-2. In summary, SeMet was added to alleviate the oxidative stress injury and apoptosis of kidney induced by AFB1, and the effect of 0.2 mg/kg Se + AFB1 is better than 0.4 mg/kg Se + AFB1.


Asunto(s)
Riñón , Estrés Oxidativo , Selenometionina , Animales , Conejos , Antioxidantes/farmacología , Antioxidantes/metabolismo , Apoptosis/efectos de los fármacos , Proteína 1 Asociada A ECH Tipo Kelch/metabolismo , Riñón/patología , Factor 2 Relacionado con NF-E2/metabolismo , Estrés Oxidativo/efectos de los fármacos , Fosfatidilinositol 3-Quinasas/metabolismo , Proteínas Proto-Oncogénicas c-akt/metabolismo , Transducción de Señal , Selenometionina/farmacología , Aflatoxina B1/toxicidad , NAD(P)H Deshidrogenasa (Quinona)/efectos de los fármacos , NAD(P)H Deshidrogenasa (Quinona)/metabolismo
2.
Anticancer Res ; 43(11): 4879-4885, 2023 Nov.
Artículo en Inglés | MEDLINE | ID: mdl-37910001

RESUMEN

BACKGROUND/AIM: Current NPC treatment methods have improved the 5-year survival rates of patients; however, some patients do not benefit from the treatments. Therefore, the existing treatment methods or new drugs must be developed to improve the patient's prognosis. NAD (P)H:quinone oxidoreductase 1 (NQO1), an electron reductase highly expressed in various cancers, can convert aziridinyl-substituted quinone-derived compound into an alkylating agent, resulting in cell apoptosis. Therefore, a di-aziridinyl-substituted quinone-derived compound, AZ-1, was designed previously. The present study investigated whether AZ-1 has anticancer activities in NPC cells and explored the underlying mechanism. MATERIALS AND METHODS: NPC-TW01 cells were used in the study, and 3-(4,5-dimethylthiazol- 2-yl)-2,5-diphenyltetrazolium bromide, colony formation, terminal deoxynucleotidyl transferase dUTP nick end labeling, and immunoblotting assays were performed to assess the cell viability, cell survival, DNA fragmentation, and protein expression, respectively. RESULTS: The results show that AZ-1 significantly inhibited the viability and survival of NPC-TW01 cells. AZ-1 also induced the expression of cleaved PARP, cleaved caspase-8, cleaved caspase-9, and cleaved caspase-3, and triggered DNA fragmentation in NPC-TW01 cells. In addition, AZ-1 induced γH2AX expression, a DNA damage marker, in NPC-TW01 cells. Treatment with dicoumarol, an NQO1 activity inhibitor, not only reversed AZ-1-induced cell viability inhibition but also decreased AZ-1-induced expression of γH2AX, cleaved caspase-8, cleaved caspase-9, and cleaved caspase-3. CONCLUSION: NQO1 reverses AZ-1-triggered cell viability inhibition, DNA damage, and apoptosis. The findings of this study may provide a basis for the possible clinical application of AZ-1 in the treatment of NPC to improve the prognosis of patients with NPC.


Asunto(s)
NAD(P)H Deshidrogenasa (Quinona) , NAD , Neoplasias Nasofaríngeas , Humanos , Caspasa 3 , Caspasa 8 , Caspasa 9 , Carcinoma Nasofaríngeo/tratamiento farmacológico , Neoplasias Nasofaríngeas/tratamiento farmacológico , Quinonas , NAD(P)H Deshidrogenasa (Quinona)/efectos de los fármacos , NAD(P)H Deshidrogenasa (Quinona)/metabolismo
3.
Acta Pharmacol Sin ; 43(3): 692-702, 2022 Mar.
Artículo en Inglés | MEDLINE | ID: mdl-34035487

RESUMEN

The tumor suppressor p53 is usually inactivated by somatic mutations in malignant neoplasms, and its reactivation represents an attractive therapeutic strategy for cancers. Here, we reported that a new quinolone compound RYL-687 significantly inhibited non-small cell lung cancer (NSCLC) cells which express wild type (wt) p53, in contract to its much weaker cytotoxicity on cells with mutant p53. RYL-687 upregulated p53 in cells with wt but not mutant p53, and ectopic expression of wt p53 significantly enhanced the anti-NSCLC activity of this compound. RYL-687 induced production of reactive oxygen species (ROS) and upregulation of Nrf2, leading to an elevation of the NAD(P)H:quinoneoxidoreductase-1 (NQO1) that can protect p53 by inhibiting its degradation by 20S proteasome. RYL-687 bound NQO1, facilitating the physical interaction between NQO1 and p53. NQO1 was required for RYL-687-induced p53 accumulation, because silencing of NQO1 by specific siRNA or an NQO1 inhibitor uridine, drastically suppressed RYL-687-induced p53 upregulation. Moreover, a RYL-687-related prodrug significantly inhibited tumor growth in NOD-SCID mice inoculated with NSCLC cells and in a wt p53-NSCLC patient-derived xenograft mouse model. These data indicate that targeting NQO1 is a rational strategy to reactivate p53, and RYL-687 as a p53 stabilizer bears therapeutic potentials in NSCLCs with wt p53.


Asunto(s)
Carcinoma de Pulmón de Células no Pequeñas/patología , Neoplasias Pulmonares/patología , NAD(P)H Deshidrogenasa (Quinona)/efectos de los fármacos , Quinolonas/farmacología , Proteína p53 Supresora de Tumor/efectos de los fármacos , Apoptosis/efectos de los fármacos , Línea Celular Tumoral , Proliferación Celular/efectos de los fármacos , Supervivencia Celular/efectos de los fármacos , Humanos , Factor 2 Relacionado con NF-E2/efectos de los fármacos , ARN Interferente Pequeño/farmacología , Especies Reactivas de Oxígeno/metabolismo , Proteína p53 Supresora de Tumor/genética , Regulación hacia Arriba
4.
Neuroreport ; 32(17): 1370-1378, 2021 12 08.
Artículo en Inglés | MEDLINE | ID: mdl-34718249

RESUMEN

Ketamine is clinically used as a narcotic. However, ketamine has certain deficits and produces toxicity to neurons. As a member of the NR4A receptor subfamily, Nur77 decreases neurodegenerative disorders. The study aims to investigate the effects of upregulated Nur77 on ketamine-induced rat hippocampal neurons damage and the active mechanism. Neurons were obtained from rat hippocampal and identified by immunofluorescence assays. The treatment groups contained ketamine group, Nur77 group, ketamine + Nur77 group and ketamine + L-cam group. Neurons apoptosis and reactive oxygen species (ROS) were determined by a related kit using flow cytometry. Enzyme NAD(P)H quinone oxidoreductase 1 (NQO1), enzyme heme oxygenase 1 (HO1), Nur77, the expression of Bax, Bcl-2 and cleaved-caspase-3 and inflammatory cytokines were measured using western blot assays and reverse transcription-quantitative PCR (RT-qPCR) assays. Ketamine-induced neurons apoptosis; however, Nur77 decreased ketamine-induced neurons apoptosis. A low level of ROS was observed in two combination groups. Neurons treated by ketamine only had the lowest levels of Nur77, NQO1 and HO1, compared with other treatment groups. The levels of Bax and cleaved-caspase-3 in two combination groups were lower than those in the ketamine group. Furthermore, the ketamine group had higher levels of tumor necrosis factor alpha, IL-1ß and IL-6 but the lowest level of IL-4. Upregulated Nur77 reduced the ketamine-induced toxicity in neurons. The mechanism of Nur77 involved antioxidation, apoptosis signaling pathway and inflammation signaling pathway. Our study provides a novel therapy that could attenuate ketamine-induced toxicity.


Asunto(s)
Apoptosis/efectos de los fármacos , Hipocampo/citología , Ketamina/toxicidad , Neuronas/efectos de los fármacos , Síndromes de Neurotoxicidad/genética , Miembro 1 del Grupo A de la Subfamilia 4 de Receptores Nucleares/genética , Animales , Apoptosis/genética , Citocinas/efectos de los fármacos , Citocinas/genética , Citocinas/metabolismo , Hemo Oxigenasa (Desciclizante)/efectos de los fármacos , Hemo Oxigenasa (Desciclizante)/genética , Hemo Oxigenasa (Desciclizante)/metabolismo , Inflamación/genética , Inflamación/metabolismo , NAD(P)H Deshidrogenasa (Quinona)/efectos de los fármacos , NAD(P)H Deshidrogenasa (Quinona)/genética , NAD(P)H Deshidrogenasa (Quinona)/metabolismo , Síndromes de Neurotoxicidad/etiología , Estrés Oxidativo/efectos de los fármacos , Estrés Oxidativo/genética , Proteínas Proto-Oncogénicas c-bcl-2/efectos de los fármacos , Proteínas Proto-Oncogénicas c-bcl-2/genética , Proteínas Proto-Oncogénicas c-bcl-2/metabolismo , Ratas , Especies Reactivas de Oxígeno/metabolismo , Regulación hacia Arriba , Proteína X Asociada a bcl-2/efectos de los fármacos , Proteína X Asociada a bcl-2/genética , Proteína X Asociada a bcl-2/metabolismo
5.
PLoS Genet ; 17(8): e1009732, 2021 08.
Artículo en Inglés | MEDLINE | ID: mdl-34437536

RESUMEN

Cancer patients exhibit a broad range of inter-individual variability in response and toxicity to widely used anticancer drugs, and genetic variation is a major contributor to this variability. To identify new genes that influence the response of 44 FDA-approved anticancer drug treatments widely used to treat various types of cancer, we conducted high-throughput screening and genome-wide association mapping using 680 lymphoblastoid cell lines from the 1000 Genomes Project. The drug treatments considered in this study represent nine drug classes widely used in the treatment of cancer in addition to the paclitaxel + epirubicin combination therapy commonly used for breast cancer patients. Our genome-wide association study (GWAS) found several significant and suggestive associations. We prioritized consistent associations for functional follow-up using gene-expression analyses. The NAD(P)H quinone dehydrogenase 1 (NQO1) gene was found to be associated with the dose-response of arsenic trioxide, erlotinib, trametinib, and a combination treatment of paclitaxel + epirubicin. NQO1 has previously been shown as a biomarker of epirubicin response, but our results reveal novel associations with these additional treatments. Baseline gene expression of NQO1 was positively correlated with response for 43 of the 44 treatments surveyed. By interrogating the functional mechanisms of this association, the results demonstrate differences in both baseline and drug-exposed induction.


Asunto(s)
Antineoplásicos/farmacología , Biomarcadores Farmacológicos/análisis , NAD(P)H Deshidrogenasa (Quinona)/genética , Línea Celular Tumoral , Estudio de Asociación del Genoma Completo/métodos , Ensayos Analíticos de Alto Rendimiento/métodos , Humanos , NAD(P)H Deshidrogenasa (Quinona)/efectos de los fármacos , NAD(P)H Deshidrogenasa (Quinona)/metabolismo
6.
Neurotox Res ; 38(2): 421-433, 2020 Aug.
Artículo en Inglés | MEDLINE | ID: mdl-32378055

RESUMEN

Excessive alcohol intake affects hippocampal function and neuronal communication through oxidative stress and mitochondrial impairment. Previous studies have suggested that the melanocortin system (MCS) plays an essential role in alcohol consumption and addiction. The MCS is a hypothalamic region involved in regulating inflammatory processes in the brain, and its pharmacological activation through the melanocortin-4 receptor (MC4R) reduces both alcohol consumption and the neuroinflammatory responses in the brain. However, the cellular mechanisms involved in the beneficial actions of MCS against ethanol toxicity are not entirely understood. The objective of this study was to investigate the protective role of the MC4R pharmacological activator RO27-3225 on oxidative damage and mitochondrial impairment present in hippocampal neuronal cultures acutely exposed to ethanol (50, 75 mM, 24 h). Pre-treatment with RO27-3225 (250 nM, 1 h) prevented reactive oxygen species (ROS) increase, dysregulation of cytosolic calcium homeostasis, and mitochondrial potential loss induced by ethanol. Improvement of mitochondrial failure produced by RO27-3225 was accompanied by a significant increase in ATP production in ethanol-treated neurons. More importantly, RO27-3225 promoted the activation of the antioxidant pathway Nrf-2, demonstrated by an increase in the expression and nuclear translocation of Nrf-2, and upregulation of mRNA levels of NAD(P)H quinone oxidoreductase 1 (NQO1), an antioxidant enzyme which expression is activated by this pathway. These results suggest that the stimulation of MC4R prevents oxidative damage and mitochondrial stress induced by ethanol through the activation of the Nrf-2 pathway in cultured hippocampal neurons. These results are novel and demonstrate the critical function of MC4R in promoting antioxidant defense and reducing mitochondrial damage produced by ethanol in the brain.


Asunto(s)
Calcio/metabolismo , Potencial de la Membrana Mitocondrial/fisiología , Mitocondrias/metabolismo , Neuronas/metabolismo , Fármacos Neuroprotectores/farmacología , Estrés Oxidativo/fisiología , Péptidos/farmacología , Receptor de Melanocortina Tipo 4/metabolismo , Animales , Antioxidantes , Células Cultivadas , Depresores del Sistema Nervioso Central/toxicidad , Etanol/toxicidad , Hipocampo/citología , Inflamación/metabolismo , Potencial de la Membrana Mitocondrial/efectos de los fármacos , Mitocondrias/efectos de los fármacos , NAD(P)H Deshidrogenasa (Quinona)/efectos de los fármacos , NAD(P)H Deshidrogenasa (Quinona)/genética , Factor 2 Relacionado con NF-E2/efectos de los fármacos , Factor 2 Relacionado con NF-E2/metabolismo , Neuronas/efectos de los fármacos , Estrés Oxidativo/efectos de los fármacos , ARN Mensajero/efectos de los fármacos , ARN Mensajero/metabolismo , Ratas , Especies Reactivas de Oxígeno/metabolismo , Receptor de Melanocortina Tipo 4/agonistas
7.
Planta Med ; 85(5): 379-384, 2019 Mar.
Artículo en Inglés | MEDLINE | ID: mdl-30466132

RESUMEN

Previous studies on the therapeutic potential of plant species found in the diet of chimpanzees living in Taï National Park have shown that they could be potential candidates for the search of new molecules useful for humans. Based on the screening of some of these plants, the fruits of Beilschmiedia mannii, whose dichloromethane extract showed cancer chemopreventive properties, were selected. Bioactivity-guided fractionation of the extract resulted in the isolation and identification of two γ-pyrones, including desmethoxydihydromethysticin (1: ), found in a natural source for the first time, and a new congener, beilschmiediapyrone (2: ), as well as five known alkamides (3:  - 7: ). Their structures were established by using nuclear magnetic resonance spectroscopy and mass spectrometry methods. The isolated compounds were evaluated for their cancer chemopreventive potential by using quinone reductase induction and nuclear factor-kappa B inhibition tests in Hepa 1c1c7 and HEK-293/NF-κB-Luc cells, respectively. Among them, compounds 1: and 2: were the most active. The concentrations to double the quinone reductase activity were 7.5 µM for compound 1: and 6.1 µM for compound 2: . Compounds 1: and 2: inhibited nuclear factor-kappa B with IC50 values of 2.1 and 3.4 µM, respectively. These results are promising with regard to cancer chemoprevention, especially because this plant is also used for cooking by the local population around the Taï forest.


Asunto(s)
Antiinflamatorios/farmacología , Lauraceae/química , NAD(P)H Deshidrogenasa (Quinona)/efectos de los fármacos , Extractos Vegetales/farmacología , Pironas/farmacología , Antiinflamatorios/química , Antiinflamatorios/aislamiento & purificación , Frutas/química , Células HEK293 , Humanos , Espectroscopía de Resonancia Magnética , Cloruro de Metileno , NAD(P)H Deshidrogenasa (Quinona)/genética , NAD(P)H Deshidrogenasa (Quinona)/metabolismo , FN-kappa B/efectos de los fármacos , FN-kappa B/genética , FN-kappa B/metabolismo , Extractos Vegetales/química , Extractos Vegetales/aislamiento & purificación , Pironas/química , Pironas/aislamiento & purificación
8.
ACS Chem Neurosci ; 9(12): 3108-3116, 2018 12 19.
Artículo en Inglés | MEDLINE | ID: mdl-29989791

RESUMEN

Honokiol (Hon), a polyphenol and main active ingredient from the bark of Magnolia officinalis, has been documented as having multiple pharmacological functions, including neuroprotection. However, the mechanisms underlying its neuroprotective effects are not well-defined. In this study, we reported that Hon attenuates the H2O2- or 6-hydroxydopamine (6-OHDA)-induced apoptosis of PC12 cells by increasing the glutathione level and upregulating a multitude of cytoprotective proteins, including heme oxygenase 1, NAD(P)H:quinone oxidoreductase 1, thioredoxin 1, and thioredoxin reductase 1. Further studies reveal that Hon promotes transcription factor Nrf2 nuclear translocation and activation. Moreover, the cytoprotection of Hon was antagonized by silence of Nrf2 expression, highlighting the fact that Nrf2 is critically engaged in the cellular functions of Hon. Taken together, our study identified that Hon is an effective agonist of Nrf2 in the neuronal system and displays potent neuroprotection against oxidative stress-mediated PC12 cell damage. These findings indicate that Hon is promising for further development as a therapeutic drug against oxidative stress-related neurodegenerative disorders.


Asunto(s)
Compuestos de Bifenilo/farmacología , Lignanos/farmacología , Factor 2 Relacionado con NF-E2/efectos de los fármacos , Neuronas/efectos de los fármacos , Fármacos Neuroprotectores/farmacología , Estrés Oxidativo/efectos de los fármacos , Adrenérgicos/farmacología , Animales , Apoptosis/efectos de los fármacos , Glutatión/efectos de los fármacos , Glutatión/metabolismo , Hemo Oxigenasa (Desciclizante)/efectos de los fármacos , Hemo Oxigenasa (Desciclizante)/metabolismo , Peróxido de Hidrógeno/farmacología , NAD(P)H Deshidrogenasa (Quinona)/efectos de los fármacos , NAD(P)H Deshidrogenasa (Quinona)/metabolismo , Factor 2 Relacionado con NF-E2/metabolismo , Neuronas/metabolismo , Oxidantes/farmacología , Oxidopamina/farmacología , Células PC12 , Ratas , Tiorredoxina Reductasa 1/efectos de los fármacos , Tiorredoxina Reductasa 1/metabolismo , Tiorredoxinas/efectos de los fármacos , Tiorredoxinas/metabolismo
9.
BMC Complement Altern Med ; 18(1): 163, 2018 May 22.
Artículo en Inglés | MEDLINE | ID: mdl-29788962

RESUMEN

BACKGROUND: There are increasing interests in natural compounds for cancer chemoprevention. Blocking agents represent an important class of chemopreventive compounds. They prevent carcinogens from undergoing metabolic activation and thereby suppressing their interaction with cellular macromolecular targets. METHODS: The effect of phenolic compounds isolated from Barleria cristata var. alba as chemopreventive agent was evaluated. The ethyl acetate fraction of B. cristata was subjected to different chromatographic techniques for isolation of its major phenolic compounds. The isolated compounds were evaluated for their potential to induce the cancer chemopreventive enzyme marker NAD(P)H quinonereductase 1 (NQO1) in murine Hepa-1c1c7 cell model. RESULTS: The ethyl acetate fraction of B. cristata var. alba yielded five known compounds identified as verbascoside (1), isoverbascoside (2), dimethoxyverbascoside (3), p-hydroxy benzoic acid (4), and apigenin-7-O-glucoside (5). Among the tested compounds, isoverbascoside (2) was shown to potently induce the activity of the enzyme in a dose -dependent manner. As a functional assay for detoxification, compound 2 was the strongest to protect Hepa-1c1c7 against the toxicity of menadione, a quinone substrate for NQO1. CONCLUSION: This effect seemed to be attributed to the compound's potential to induce both the catalytic activity and protein expression of NQO1 as revealed by enzyme assay and Western blotting, respectively.


Asunto(s)
Acanthaceae , Anticarcinógenos/farmacología , NAD(P)H Deshidrogenasa (Quinona) , Fenoles/farmacología , Extractos Vegetales/farmacología , Animales , Línea Celular Tumoral , Ratones , NAD(P)H Deshidrogenasa (Quinona)/efectos de los fármacos , NAD(P)H Deshidrogenasa (Quinona)/metabolismo
10.
Mol Biol Rep ; 45(3): 379-387, 2018 Jun.
Artículo en Inglés | MEDLINE | ID: mdl-29611025

RESUMEN

ß-Lapachone (ß-Lap), morphine (Mor), and electromagnetic field (EMF) generate reactive oxygen species. The goal of the present study was to examine the effects of Mor and EMF, in combination with ß-Lap on the cell growth inhibition and expression of several antioxidant genes. The 0.50 mT intensity of 50 Hz EMF and two exposure conditions ("15 min field-on/15 min field-off" and "30 min field-on continuously") on SH-SY5Y cells were used. The effects of Mor and EMF, in combination with ß-Lap on cell growth inhibition and the expression levels of several antioxidant genes (NQO1, NQO2, SOD1, SOD2, CAT, GSTO1, GSTM2, GSTM3, GSTP1, MGST1, MGST3) in SH-SY5Y cells were measured. The relative mRNA levels were calculated according to the [Formula: see text]. Whereas NQO1 mRNA level decreased in the "15 min field-on/15 min field-off" condition, the expression level of NQO2 was increased. Both NQO1 and NQO2 expressions increased in Mor treated cells. IC50 values of ß-Lap in combination with Mor, EMF, and "Mor + EMF" were higher than cells treated only with ß-Lap. The NQO1 expression level in the cells treated with ß-Lap was higher than the other treatments, indicating that ß-Lap induces the expression of NQO1. Moreover, multiple linear regression analysis indicated that NQO1 mRNA levels were associated positively with ß-Lap and negatively with EMF. At least in part, the mRNA levels of NQO1 were associated with IC50 values of ß-Lap in designed treatments. There is a negative association between mRNA levels of NQO1 and IC50 values of ß-Lap but not NQO2.


Asunto(s)
Línea Celular Tumoral/efectos de los fármacos , NAD(P)H Deshidrogenasa (Quinona)/efectos de los fármacos , Naftoquinonas/farmacología , Antioxidantes/metabolismo , Campos Electromagnéticos , Perfilación de la Expresión Génica/métodos , Regulación Neoplásica de la Expresión Génica/efectos de los fármacos , Humanos , Magnetoterapia , Morfina/metabolismo , Morfina/farmacología , NAD(P)H Deshidrogenasa (Quinona)/genética , Naftoquinonas/metabolismo , Naftoquinonas/toxicidad , ARN Mensajero/genética , Especies Reactivas de Oxígeno/metabolismo , Regulación hacia Arriba/efectos de los fármacos
11.
Behav Pharmacol ; 29(1): 28-40, 2018 02.
Artículo en Inglés | MEDLINE | ID: mdl-28763303

RESUMEN

Ample evidence has pointed to a close link between oxidative stress, mitochondrial dysfunction, and depression. Nuclear factor-erythroid 2-related factor-2 (Nrf2) is a master regulator of cellular redox homeostasis and affects mitochondrial function. Nrf2 holds promise for depression prevention and treatment. This study aimed to investigate the potential prophylactic antidepressant effect of cilostazol and the contribution of the Nrf2 pathway toward the putative neuroprotection. The behavioral and neurochemical effects of concomitant treatment of oral cilostazol at doses of 7.5, 15, and 30 mg/kg/day in Wistar rats exposed to chronic restraint stress (CRS) for 4 weeks were assayed. Cilostazol prevented CRS-induced depressive-like behavior shown in sucrose-preference, forced-swimming, and open-field tests, and hypothalamus-pituitary-adrenal axis hyperactivity (adrenal gland weight and serum corticosterone). Cilostazol prevented CRS-induced increase in hippocampal lipid peroxidation and 8-hydroxy-2'-deoxyguanosine, and a decrease in antioxidant activities (glutathione level, superoxide dismutase, and catalase). Western blot and PCR showed that cilostazol favorably modulated the Nrf2 protein and heme oxygenase-1 and NAD(P)H: quinone oxidoreductase-1 gene expression in the hippocampus of CRS rats. Cilostazol also prevented the decrease in the hippocampal activities of mitochondrial respiratory enzyme complexes I-IV. These behavioral and biochemical findings indicated the potential prophylactic antidepressant effect and mechanism of cilostazol by preventing oxidative stress by activation of redox defense mechanisms mediated through the Nrf2 pathway and restoring mitochondrial dysfunction.


Asunto(s)
Cilostazol/farmacología , Factor 2 Relacionado con NF-E2/efectos de los fármacos , Animales , Antidepresivos/farmacología , Antioxidantes/farmacología , Corticosterona/metabolismo , Depresión/tratamiento farmacológico , Trastorno Depresivo/tratamiento farmacológico , Glutatión/metabolismo , Hemo-Oxigenasa 1/efectos de los fármacos , Sistema Hipotálamo-Hipofisario/metabolismo , Peroxidación de Lípido/efectos de los fármacos , Masculino , Mitocondrias/efectos de los fármacos , Mitocondrias/metabolismo , NAD(P)H Deshidrogenasa (Quinona)/efectos de los fármacos , Factor 2 Relacionado con NF-E2/fisiología , Oxidación-Reducción/efectos de los fármacos , Estrés Oxidativo/efectos de los fármacos , Sistema Hipófiso-Suprarrenal/metabolismo , Ratas , Ratas Wistar , Estrés Psicológico/fisiopatología , Superóxido Dismutasa/metabolismo
12.
J Exp Ther Oncol ; 11(2): 139-416, 2017 Sep.
Artículo en Inglés | MEDLINE | ID: mdl-28976137

RESUMEN

OBJECTIVE: Urothelial carcinoma of the bladder is a common malignancy ranked 9th with an estimated 356,600 new cases diagnosed annually worldwide. The study showed the protective effects of Lupeol in N-Butyl-N-(4-hydroxybutyl) nitrosamine induced bladder carcinogenesis in in vivo experimental model. Forty male healthy wistar rats were selected randomly divided into four groups. Group I rats served as healthy control. Group II rats were treated with BBN (150 mg/gavage/twice a week) for 8 weeks. Group III rats were treated with BBN + Lupeol [ Lupeol (50 mg/kg bw/day) treatment was started 1 week prior to the BBN treatment, and it was orally administered for 8 weeks]. Group IV rats were treated with Lupeol alone (50 mg/kg bw/day) for 8 weeks. All the experimental rats were maintained and euthanized at 32nd week. Serum and bladder tissues were collected and examined for biochemical parameters, serum markers and histopathological evaluation. Preventive (BBN + Lupeol) group modulates the activity of antioxidant enzymes such as Superoxide dismutase, Catalase, Reduced glutathione, Glutathione Peroxidase, Thiobarbituric acid reactive substances (TBARS) and drug metabolizing enzymes such as Cytochrome P450, Cytochrome b5, NADPH Cytochrome c reductase, NADPH- Quinone Oxidoreductase 1 and Glutathione-S-transferase when compared to BBN treated rats. Serological markers such as Aspartate aminotransferase (AST) and Alanine aminotransferase (ALT) were significantly (P<0.05) decreased in preventive lupeol treated groups. Lupeol supplementation protects BBN induced bladder carcinogenesis in experimental rats by its antioxidant, anti-inflammatory and antiproliferative properties.


Asunto(s)
Antiinflamatorios/farmacología , Butilhidroxibutilnitrosamina/toxicidad , Carcinogénesis/efectos de los fármacos , Carcinoma de Células Transicionales/enzimología , Triterpenos Pentacíclicos/farmacología , Neoplasias de la Vejiga Urinaria/enzimología , Vejiga Urinaria/efectos de los fármacos , Animales , Antioxidantes , Carcinoma de Células Transicionales/inducido químicamente , Carcinoma de Células Transicionales/metabolismo , Carcinoma de Células Transicionales/patología , Catalasa/efectos de los fármacos , Catalasa/metabolismo , Sistema Enzimático del Citocromo P-450/efectos de los fármacos , Sistema Enzimático del Citocromo P-450/metabolismo , Citocromos b5/efectos de los fármacos , Citocromos b5/metabolismo , Glutatión/efectos de los fármacos , Glutatión/metabolismo , Glutatión Peroxidasa/efectos de los fármacos , Glutatión Peroxidasa/metabolismo , Glutatión Transferasa/efectos de los fármacos , Glutatión Transferasa/metabolismo , Masculino , NAD(P)H Deshidrogenasa (Quinona)/efectos de los fármacos , NAD(P)H Deshidrogenasa (Quinona)/metabolismo , NADPH-Ferrihemoproteína Reductasa/efectos de los fármacos , NADPH-Ferrihemoproteína Reductasa/metabolismo , Ratas , Ratas Wistar , Superóxido Dismutasa/efectos de los fármacos , Superóxido Dismutasa/metabolismo , Sustancias Reactivas al Ácido Tiobarbitúrico/metabolismo , Vejiga Urinaria/enzimología , Vejiga Urinaria/metabolismo , Vejiga Urinaria/patología , Neoplasias de la Vejiga Urinaria/inducido químicamente , Neoplasias de la Vejiga Urinaria/metabolismo , Neoplasias de la Vejiga Urinaria/patología
13.
Int J Pediatr Otorhinolaryngol ; 92: 61-66, 2017 Jan.
Artículo en Inglés | MEDLINE | ID: mdl-28012535

RESUMEN

OBJECTIVE: Cisplatin is commonly used to treat solid tumors. However, permanent hearing loss is a major side effect of cisplatin chemotherapy and often results in dose reduction of the cisplatin chemotherapy. Peanut sprouts show cytoprotective properties owing to their antioxidant activities. This study was designed to investigate the effect of peanut sprout extract (PSE) on cisplatin-induced ototoxicity in an auditory cell line, HEI-OC1 cells. METHODS: Cells were exposed to cisplatin for 24 h, with or without pre-treatment with PSE, cell viability was examined using the MTT assay. Apoptotic cells were identified by double staining with Hoechst 33258 and propidium iodide. Western blot analysis was performed to examine apoptotic proteins including C-PARP and C-caspase, anti-apoptotic protein Bcl-2, and Nrf2 redox system activation. Mitochondrial reactive oxygen species (ROS) were investigated to examine whether PSE could scavenge cisplatin-induced ROS. Real-time PCR analyses were performed to investigate the mRNA levels of antioxidant enzymes including NQO1, HO-1, GPx2, Gclc, and catalase. RESULTS: The cisplatin-treated group showed reduced cell viability, increased apoptotic properties and markers, and increased ROS levels. PSE pre-treatment before cisplatin exposure significantly increased cell viability and reduced apoptotic properties and ROS production. These effects resulted from the up-regulation of antioxidant genes, including NQO1, HO-1, GPx2, Gclc, and catalase through Akt phosphorylation and Nrf2 activation. CONCLUSION: Our results demonstrate that PSE protects from cisplatin-induced cytotoxicity by activating the antioxidant effects via the Akt/Nrf-2 pathway in this auditory cell line, and indicate that PSE may provide novel treatment to prevent cisplatin-induced ototoxicity.


Asunto(s)
Antineoplásicos/toxicidad , Apoptosis/efectos de los fármacos , Arachis , Cisplatino/toxicidad , Células Ciliadas Auditivas/efectos de los fármacos , Células Laberínticas de Soporte/efectos de los fármacos , Extractos Vegetales/farmacología , Plantones , Animales , Western Blotting , Caspasas/efectos de los fármacos , Caspasas/metabolismo , Catalasa/efectos de los fármacos , Catalasa/genética , Línea Celular , Supervivencia Celular/efectos de los fármacos , Glutamato-Cisteína Ligasa/efectos de los fármacos , Glutamato-Cisteína Ligasa/genética , Glutatión Peroxidasa/efectos de los fármacos , Glutatión Peroxidasa/genética , Hemo-Oxigenasa 1/efectos de los fármacos , Hemo-Oxigenasa 1/genética , Técnicas In Vitro , Proteínas de la Membrana/efectos de los fármacos , Proteínas de la Membrana/genética , Ratones , Mitocondrias/efectos de los fármacos , Mitocondrias/metabolismo , NAD(P)H Deshidrogenasa (Quinona)/efectos de los fármacos , NAD(P)H Deshidrogenasa (Quinona)/genética , Factor 2 Relacionado con NF-E2/efectos de los fármacos , Factor 2 Relacionado con NF-E2/metabolismo , Oxidación-Reducción/efectos de los fármacos , Poli(ADP-Ribosa) Polimerasas/efectos de los fármacos , Poli(ADP-Ribosa) Polimerasas/metabolismo , Proteínas Proto-Oncogénicas c-bcl-2/efectos de los fármacos , Proteínas Proto-Oncogénicas c-bcl-2/metabolismo , Especies Reactivas de Oxígeno/metabolismo , Reacción en Cadena en Tiempo Real de la Polimerasa , Regulación hacia Arriba
14.
J Headache Pain ; 17(1): 99, 2016 Dec.
Artículo en Inglés | MEDLINE | ID: mdl-27778243

RESUMEN

BACKGROUND: Antioxidants have been proven to weaken hyperalgesia in neuropathic pain. Endogenous antioxidant defense system may have a role in the prevention of hyperalgesia in migraine. In this study, we aimed to evaluate the role of nuclear factor E2-related factor 2/antioxidant response element (Nrf2/ARE) pathway in regulating the activation of the trigeminovascular system (TGVS) and hypersensitivity in nitroglycerin (NTG)-induced hyperalgesia rats. METHODS: The expression levels of Nrf2, HO, HO1, and NQO1 in the trigeminal nucleus caudalis (TNC) were detected by western blot. Immunofluorescence was used to demonstrate the cell-specific localization of Nrf2 in TNC. Sulforaphane, a Nrf2 activator, was administered to NTG-induced rats. Then, the number of c-Fos- and nNOS-immunoreactive neurons in TNC was evaluated using immunofluorescence, and c-Fos and nNOS protein levels were quantified using western blot. Von Frey hair testing was used to evaluate the tactile thresholds of rats at different time points in different groups. RESULTS: Total cellular and nuclear levels of the proteins Nrf2, HO1, and NQO1 were elevated in TNC after NTG injection, and Nrf2 was found to be located in the nucleus and cytoplasm of the neurons. Sulforaphane pretreatment significantly increased the nuclear Nrf2, HO1, and NQO1 levels in TNC. In addition, sulforaphane exposure effectively inhibited the expression of nNOS and c-Fos, reduced the number of nNOS and c-Fos immunoreactive neurons in TNC, and attenuated the tactile thresholds induced by NTG injection. CONCLUSION: Oxidative stress was involved in nitroglycerin-induced hyperalgesia. Activation of the Nrf2/ARE pathway inhibited the activation of TGVS and prevented the induction of hyperalgesia. Sulforaphane might therefore be an effective agent for hyperalgesia. Further studies are needed to discover the underlying mechanisms of the process.


Asunto(s)
Elementos de Respuesta Antioxidante/efectos de los fármacos , Hiperalgesia/metabolismo , Factor 2 Relacionado con NF-E2/efectos de los fármacos , Neuronas/efectos de los fármacos , Proteínas Proto-Oncogénicas c-fos/efectos de los fármacos , Núcleo Caudal del Trigémino/efectos de los fármacos , Animales , Anticarcinógenos/farmacología , Hemo Oxigenasa (Desciclizante)/efectos de los fármacos , Hemo Oxigenasa (Desciclizante)/metabolismo , Hiperalgesia/inducido químicamente , Isotiocianatos/farmacología , Masculino , Trastornos Migrañosos/metabolismo , NAD(P)H Deshidrogenasa (Quinona)/efectos de los fármacos , NAD(P)H Deshidrogenasa (Quinona)/metabolismo , Factor 2 Relacionado con NF-E2/metabolismo , Neuronas/metabolismo , Óxido Nítrico Sintasa de Tipo I/efectos de los fármacos , Óxido Nítrico Sintasa de Tipo I/metabolismo , Nitroglicerina/farmacología , Estrés Oxidativo/efectos de los fármacos , Proteínas Proto-Oncogénicas c-fos/metabolismo , Ratas , Sulfóxidos , Núcleo Caudal del Trigémino/metabolismo , Vasodilatadores/farmacología
15.
J Nat Prod ; 79(6): 1508-13, 2016 06 24.
Artículo en Inglés | MEDLINE | ID: mdl-27196335

RESUMEN

A new fatty acid ester disaccharide, 2-O-(ß-d-glucopyranosyl)-1-O-(2E,4Z,7Z)-deca-2,4,7-trienoyl-ß-d-glucopyranose (1), a new ascorbic acid derivative, 2-caffeoyl-3-ketohexulofuranosonic acid γ-lactone (2), and a new iridoid glycoside, 10-dimethoxyfermiloside (3), were isolated along with 13 known compounds (4-16) from fermented noni fruit juice (Morinda citrifolia). The structures of the new compounds, together with 4 and 5, were determined by 1D and 2D NMR experiments, as well as comparison with published values. Compounds 2 and 7 showed moderate inhibitory activities in a TNF-α-induced NF-κB assay, and compounds 4 and 6 exhibited considerable quinone reductase-1 (QR1) inducing effects.


Asunto(s)
Antiinflamatorios/aislamiento & purificación , Antiinflamatorios/farmacología , Disacaridasas/aislamiento & purificación , Disacaridasas/farmacología , Morinda/química , NAD(P)H Deshidrogenasa (Quinona)/efectos de los fármacos , Antiinflamatorios/análisis , Antiinflamatorios/química , Disacaridasas/química , Ácidos Grasos/química , Fermentación , Frutas/química , Iridoides/análisis , Iridoides/química , Iridoides/aislamiento & purificación , Iridoides/farmacología , Estructura Molecular , NAD(P)H Deshidrogenasa (Quinona)/metabolismo , FN-kappa B/metabolismo , Factor de Necrosis Tumoral alfa/análisis
16.
Phytochemistry ; 126: 4-10, 2016 Jun.
Artículo en Inglés | MEDLINE | ID: mdl-27048854

RESUMEN

Four meroterpenoids [talarolutins A-D] and one known compound [purpurquinone A] were characterized from an endophytic fungal isolate of Talaromyces minioluteus (G413), which was obtained from the leaves of the medicinal plant milk thistle [Silybum marianum (L.) Gaertn. (Asteraceae)]. The structures of talarolutins A-D were determined by the analysis of various NMR and MS techniques. The relative and absolute configuration of talarolutin A was determined by X-ray diffraction analysis. A combination of NOESY data and comparisons of ECD spectra were employed to assign the relative and absolute configuration of the other analogs. Talarolutins B-D were tested for cytotoxicity against human prostate carcinoma (PC-3) cell line, antimicrobial activity, and induction of quinone reductase; no notable bioactivity was observed in any assay.


Asunto(s)
Talaromyces/química , Terpenos/aislamiento & purificación , Cristalografía por Rayos X , Humanos , Masculino , Pruebas de Sensibilidad Microbiana , Silybum marianum/microbiología , Conformación Molecular , Estructura Molecular , NAD(P)H Deshidrogenasa (Quinona)/efectos de los fármacos , Resonancia Magnética Nuclear Biomolecular , Hojas de la Planta/microbiología , Neoplasias de la Próstata/tratamiento farmacológico , Terpenos/química , Terpenos/farmacología
17.
Int J Clin Exp Pathol ; 8(4): 3441-50, 2015.
Artículo en Inglés | MEDLINE | ID: mdl-26097528

RESUMEN

The present study demonstrates the effect of DHPEA on suppression of irradiation-induced pulmonary fibrosis. A (60)Co irradiator was used to induce pulmonary fibrosis in a rat model at a dose of 22 Gy. The rats of the treatment and positive control group were intraperitoneally injected DHPEA (10 mg/kg) or dexamethasone (DEX; 5 mg/kg) daily for 30 days. Hydroxyproline assay was used to evaluate the fibrosis of pulmonary and lung tissue sections after irradiation. Hematoxylin and eosin (H&E) and Masson's trichrome stained lung section were used for alveolitis and fibrosis score analyses, respectively. Immunohistochemistry was used for surfactant protein-B (SPB) and α-SMA expression analysis. Western blot analysis was employed for analysis of nuclear transcription factor NF-E2-related factor 2 (Nrf-2) and its associated antioxidant enzymes like heme oxygenase-1 (HO-1) and NAD (P) H: quinone oxidoreductase-1 (NQO-1). Results revealed a significant decrease in mortality rates and lung index scores, decreased collagen deposition, reduced MDA content and enhanced superoxide dismutase (SOD) activity in DHPEA treated rats compared to DEX-treated rats. DHPEA treatment also inhibited (myo) fibroblast proliferation, and regulated serum levels of TGF-ß1, IL-6, IL-10, and TNF-α. In addition, DHPEA-treatment activated Nrf-2 and its downstream antioxidant enzymes HO-1 and NQO-1. Thus DHPEA can be a promising agent for the suppression of irradiation-induced pulmonary fibrosis.


Asunto(s)
Antioxidantes/uso terapéutico , Alcohol Feniletílico/análogos & derivados , Fibrosis Pulmonar/prevención & control , Traumatismos Experimentales por Radiación/prevención & control , Animales , Antiinflamatorios/metabolismo , Antioxidantes/química , Antioxidantes/farmacología , Citocinas/sangre , Dexametasona/farmacología , Modelos Animales de Enfermedad , Hemo-Oxigenasa 1/efectos de los fármacos , Hemo-Oxigenasa 1/metabolismo , Humanos , Pulmón/efectos de los fármacos , Pulmón/patología , Masculino , NAD(P)H Deshidrogenasa (Quinona)/efectos de los fármacos , NAD(P)H Deshidrogenasa (Quinona)/metabolismo , Factor 2 Relacionado con NF-E2/efectos de los fármacos , Factor 2 Relacionado con NF-E2/metabolismo , Alcohol Feniletílico/química , Alcohol Feniletílico/farmacología , Alcohol Feniletílico/uso terapéutico , Fibrosis Pulmonar/tratamiento farmacológico , Fibrosis Pulmonar/metabolismo , Fibrosis Pulmonar/patología , Traumatismos Experimentales por Radiación/tratamiento farmacológico , Traumatismos Experimentales por Radiación/metabolismo , Traumatismos Experimentales por Radiación/patología , Ratas , Ratas Sprague-Dawley
18.
J Med Food ; 18(2): 182-9, 2015 Feb.
Artículo en Inglés | MEDLINE | ID: mdl-25602788

RESUMEN

In this study, we investigated the hepatoprotective effects of ethanol extracts from Chlorella vulgaris (CH) on animals. We measured its effect on the quinone reductase (QR) activity in Hepa1c1c7 cells, finding that CH induced a significantly higher QR activity in these cells. We isolated the active fraction (CH F4-2) from CH using chromatography methods. CH F4-2 may activate cellular antioxidant enzymes through upregulation of the Nrf2 pathway in hepatocarcinoma cells with CH F4-2 (25.0-200 µg/mL) for 48 h. Furthermore, CH F4-2 increased the expression of NQO1 [ NAD(P)H: quinone oxidoreductase, also known as QR], heme oxygenase-1, and glutathione-S-transferase P. Moreover, we found that ethanol-induced hepatic pathological changes-elevations in glutamic oxaloacetic transaminase, glutamic pyruvic transaminase, γ-glutamyltransferase, and lactate dehydrogenase-were significantly decreased. The inhibitory effect of CH on alcohol-induced liver injury was associated with the suppression of alcohol-induced increases in intestinal permeability. The ethanol extract from CH was found to induce QR activation, making it a potentially good candidate for a hepatoprotection agent.


Asunto(s)
Enfermedad Hepática Inducida por Sustancias y Drogas , Chlorella vulgaris , Etanol , Factor 2 Relacionado con NF-E2 , Fitoterapia , Extractos Vegetales , Animales , Masculino , Ratas , Alanina Transaminasa/sangre , Aspartato Aminotransferasas/sangre , Enfermedad Hepática Inducida por Sustancias y Drogas/tratamiento farmacológico , Enfermedad Hepática Inducida por Sustancias y Drogas/enzimología , Chlorella vulgaris/química , Etanol/toxicidad , gamma-Glutamiltransferasa/sangre , L-Lactato Deshidrogenasa/sangre , Hígado/citología , Hígado/metabolismo , Hígado/patología , Neoplasias Hepáticas Experimentales/tratamiento farmacológico , Neoplasias Hepáticas Experimentales/metabolismo , NAD(P)H Deshidrogenasa (Quinona)/efectos de los fármacos , NAD(P)H Deshidrogenasa (Quinona)/metabolismo , Factor 2 Relacionado con NF-E2/efectos de los fármacos , Factor 2 Relacionado con NF-E2/metabolismo , Extractos Vegetales/farmacología , Quinona Reductasas/efectos de los fármacos , Quinona Reductasas/metabolismo , Ratas Sprague-Dawley , Regulación hacia Arriba/efectos de los fármacos
19.
J Nat Prod ; 77(7): 1644-9, 2014 Jul 25.
Artículo en Inglés | MEDLINE | ID: mdl-24992702

RESUMEN

New compounds 18-nor-3,17-dihydroxyspongia-3,13(16),14-trien-2-one (1), 18-nor-3,5,17-trihydroxyspongia-3,13(16),14-trien-2-one (2), and spongiapyridine (3) and the known compound 17-hydroxy-4-epi-spongialactone A (4) were isolated from an Indonesian sponge of the genus Spongia. The structures of 1-3 were deduced by analyses of physical and spectroscopic data. Diterpene 3 is unusual, as the D-ring is a pyridyl ring system rather than the standard δ-lactone. The structure elucidation of this compound was complicated by facile exchange of the axial proton at the C-11 methylene with deuterium from methanol-d4. The isolated compounds were tested for biological activity in a battery of in vitro assays (TNF-α-induced NFκB, LPS-induced iNOS, RXR stimulation, quinone reductase 1 induction, aromatase inhibition, TRPM7 ion channels, and aspartic protease BACE1 inhibition). Norditerpene 2 modestly inhibited aromatase with an IC50 of 34 µM and induced quinone reductase 1 activity with a CD (the concentration needed to double the enzymatic response) of 11.2 µM. The remaining isolates were inactive.


Asunto(s)
Diterpenos/aislamiento & purificación , Poríferos/química , Animales , Diterpenos/química , Diterpenos/farmacología , Lactonas/química , Lipopolisacáridos/farmacología , Estructura Molecular , NAD(P)H Deshidrogenasa (Quinona)/efectos de los fármacos , FN-kappa B/antagonistas & inhibidores , Factor de Necrosis Tumoral alfa/farmacología
20.
J Ethnopharmacol ; 152(3): 508-21, 2014 Mar 28.
Artículo en Inglés | MEDLINE | ID: mdl-24509154

RESUMEN

ETHNOPHARMACOLOGICAL RELEVANCE: Dragon's blood has been used as a famous traditional medicine since ancient times by many cultures. It is a deep red resin, obtained from more than 20 different species of four distinct genera. Red resin of Dracaena cochinchinensis S.C. Chen, known as Chinese dragon's blood or Yunnan dragon's blood, has been shown to promote blood circulation, alleviate inflammation, and to treat stomach ulcers, diarrhea, diabetes, and bleeding. This study investigated an effective approach to identify natural therapeutic agents for neurodegeneration from herbal medicine. The dichloride extract and isolated effective constituents of Chinese dragon's blood showed quinone oxidoreductase 1 (NQO1) inducing activity and anti-inflammatory effect significantly, which are therapy targets of various neurodegenerative diseases. MATERIALS AND METHODS: Multiple chromatography and spectra analysis were utilized to afford effective constituents. Then Hepa 1c1c7 and BV-2 cells were employed to assay their NQO1 inducing and anti-inflammatory activities, respectively. RESULTS: Bioactivities guided isolation afforded 21 effective constituents, including two new polymers cochinchinenene E (1), cochinchinenene F (2) and a new steroid dracaenol C (16). The main constituent 3 (weight percent 0.2%), 5 (weight percent 0.017%), 4 (weight percent 0.009%), 9 (weight percent 0.094%), 10 (weight percent 0.017%) and 8 (weight percent 0.006%) are responsible for the anti-inflammatory activities of Chinese dragon's blood. While, new compounds 1, 2 and known compounds 5, 11 showed good NQO1 inducing activities. The brief feature of the activities and structures was discussed accordingly. CONCLUSION: Overviewing the bioactivities and phytochemical study result, 4'-hydroxy-2,4-dimethoxydihydrochalcone (3) and pterostilbene (5) as effective constituents of Chinese dragon's blood, were found to be potential candidate therapeutic agents for neurodegenerative diseases.


Asunto(s)
Dracaena/química , Medicina Tradicional China , Enfermedades Neurodegenerativas/tratamiento farmacológico , Extractos Vegetales/farmacología , Animales , Antiinflamatorios/farmacología , Línea Celular , Línea Celular Tumoral , Inflamación/tratamiento farmacológico , Inflamación/patología , Ratones , NAD(P)H Deshidrogenasa (Quinona)/efectos de los fármacos , NAD(P)H Deshidrogenasa (Quinona)/metabolismo , Enfermedades Neurodegenerativas/fisiopatología , Extractos Vegetales/química , Resinas de Plantas
SELECCIÓN DE REFERENCIAS
DETALLE DE LA BÚSQUEDA