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OBJECTIVES: Rheumatoid arthritis (RA) seriously affects the daily life of people. The whole plant of Artemisia ordosica Krasch. (AOK) has been used in folk medicine. This study aimed to investigate the in vivo anti-RA effects of AOK extract (AOKE) on collagen-induced arthritis in rats. METHODS: AOKE (400, 200, or 100 mg/kg) was administered orally to animals for 30 days. Body weight, paw swelling, arthritis index, thymus, and spleen indices, and pathological changes were assessed for effects of AOKE on RA. Furthermore, the inflammatory cytokines in rat serum were detected. In addition, the expressions of STAT3, Caspase-3, Galectin-3, and S100A9 in synovial tissue were researched using immunohistochemistry. KEY FINDINGS: The AOKE significantly reduced the arthritis indices, paw swelling, spleen, and thymus indices. Meanwhile, AOKE (400 mg/kg) decreased the levels of tumor necrosis factor (TNF)-α, interleukin (IL)-1ß, IL-6, IL-17A, and increased the level of IL-10 in rat serum. Histopathological examination showed that AOKE reduced inflammatory cell infiltration and cartilage erosion. Then, AOKE decreased the expressions of STAT3, Galectin-3, S100A9, and increased the expression of Caspase-3. CONCLUSION: AOKE had interesting anti-RA activity in rats, which deserved further research for the development and clinical use of this medicinal resource.
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With the increasing prevalence of metabolic disorders, hyperglycemia has become a common risk factor that endangers people's lives and the need for new drug solutions is burgeoning. Trans-2, 4-dimethoxystilbene (TDMS), a synthetic stilbene, has been found as a novel hypoglycemic small molecule from glucose consumption test. Normal C57BL/6â¯J mice, mouse models of type 1 diabetes mellitus and diet-induced obesity subjected to TDMS gavage were found with lower glycemic levels and better glycemic control. TDMS significantly improved the symptoms of polydipsia and wasting in type 1 diabetic mice, and could rise their body temperature at the same time. It was found that TDMS could promote the expression of key genes of glucose metabolism in HepG2, as do in TDMS-treated liver, while it could improve the intestinal flora and relieve intestinal metabolic dysbiosis in hyperglycemic models, which in turn affected its function in the liver, forming the gut-liver axis. We further fished PPARγ by virtual screening that could be promoted by TDMS both in-vitro and in-vivo, which was regulated by upstream signaling of AMPKα phosphorylation. As a novel hypoglycemic small molecule, TDMS was proven to be promising with its glycemic improvements and amelioration of diabetes symptoms. It promoted glucose absorption and utilization by the liver and improved the intestinal flora of diabetic mice. Therefore, TDMS is expected to become a new hypoglycemic drug that acts through gut-liver axis via AMPKα-PPARγ signaling pathway in improving glycemic metabolism, bringing new hope to patients with diabetes and glucose metabolism disorders.
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Proteínas Quinasas Activadas por AMP , Microbioma Gastrointestinal , Hipoglucemiantes , Hígado , Ratones Endogámicos C57BL , PPAR gamma , Transducción de Señal , Estilbenos , Animales , Microbioma Gastrointestinal/efectos de los fármacos , Hipoglucemiantes/farmacología , Hígado/efectos de los fármacos , Hígado/metabolismo , Humanos , PPAR gamma/metabolismo , Proteínas Quinasas Activadas por AMP/metabolismo , Ratones , Masculino , Estilbenos/farmacología , Transducción de Señal/efectos de los fármacos , Células Hep G2 , Diabetes Mellitus Experimental/tratamiento farmacológico , Glucemia/efectos de los fármacos , Glucemia/metabolismoRESUMEN
Glioblastoma (GBM) is the most common, malignant, and lethal primary brain tumor in adults. Up to now, the chemotherapy approaches for GBM are limited. Therefore, more studies on identifying and exploring new chemotherapy drugs or strategies overcome the GBM are essential. Natural products are an important source of drugs against various human diseases including cancers. With the better understanding of the molecular etiology of GBM, the development of new anti-GBM drugs has been increasing. Here, we summarized recent researches of natural products for the GBM therapy and their potential mechanisms in details, which will provide new ideas for the research on natural products and promote developing drugs from nature products for GBM therapy.
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Productos Biológicos , Neoplasias Encefálicas , Glioblastoma , Humanos , Glioblastoma/tratamiento farmacológico , Glioblastoma/patología , Productos Biológicos/farmacología , Productos Biológicos/uso terapéutico , Neoplasias Encefálicas/tratamiento farmacológico , Neoplasias Encefálicas/patologíaRESUMEN
Glioblastoma (GBM) is the most common malignant tumor in the brain with temozolomide (TMZ) as the only approved chemotherapy agent. GBM is characterized by susceptibility to radiation and chemotherapy resistance and recurrence as well as low immunological response. There is an urgent need for new therapy to improve the outcome of GBM patients. We previously reported that 3-O-acetyl-11-keto-ß-boswellic acid (AKBA) inhibited the growth of GBM. In this study we characterized the anti-GBM effect of S670, a synthesized amide derivative of AKBA, and investigated the underlying mechanisms. We showed that S670 dose-dependently inhibited the proliferation of human GBM cell lines U87 and U251 with IC50 values of around 6 µM. Furthermore, we found that S670 (6 µM) markedly stimulated mitochondrial ROS generation and induced ferroptosis in the GBM cells. Moreover, S670 treatment induced ROS-mediated Nrf2 activation and TFEB nuclear translocation, promoting protective autophagosome and lysosome biogenesis in the GBM cells. On the other hand, S670 treatment significantly inhibited the expression of SXT17, thus impairing autophagosome-lysosome fusion and blocking autophagy flux, which exacerbated ROS accumulation and enhanced ferroptosis in the GBM cells. Administration of S670 (50 mg·kg-1·d-1, i.g.) for 12 days in a U87 mouse xenograft model significantly inhibited tumor growth with reduced Ki67 expression and increased LC3 and LAMP2 expression in the tumor tissues. Taken together, S670 induces ferroptosis by generating ROS and inhibiting STX17-mediated fusion of autophagosome and lysosome in GBM cells. S670 could serve as a drug candidate for the treatment of GBM.
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Neoplasias Encefálicas , Ferroptosis , Glioblastoma , Humanos , Animales , Ratones , Glioblastoma/tratamiento farmacológico , Glioblastoma/metabolismo , Especies Reactivas de Oxígeno/metabolismo , Autofagosomas/metabolismo , Amidas/farmacología , Transducción de Señal , Lisosomas/metabolismo , Línea Celular Tumoral , Neoplasias Encefálicas/tratamiento farmacológico , Neoplasias Encefálicas/metabolismo , Proteínas Qa-SNARERESUMEN
Dopaminergic neurons in the substantia nigra (SN) expressing SUR1/Kir6.2 type ATP-sensitive potassium channels (K-ATP) are more vulnerable to rotenone or metabolic stress, which may be an important reason for the selective degeneration of neurons in Parkinson's disease (PD). Baicalein has shown neuroprotective effects in PD animal models. In this study, we investigated the effect of baicalein on K-ATP channels and the underlying mechanisms in rotenone-induced apoptosis of SH-SY5Y cells. K-ATP currents were recorded from SH-SY5Y cells using whole-cell voltage-clamp recording. Drugs dissolved in the external solution at the final concentration were directly pipetted onto the cells. We showed that rotenone and baicalein opened K-ATP channels and increased the current amplitudes with EC50 values of 0.438 µM and 6.159 µM, respectively. K-ATP channel blockers glibenclamide (50 µM) or 5-hydroxydecanoate (5-HD, 250 µM) attenuated the protective effects of baicalein in reducing reactive oxygen species (ROS) content and increasing mitochondrial membrane potential and ATP levels in rotenone-injured SH-SY5Y cells, suggesting that baicalein protected against the apoptosis of SH-SY5Y cells by regulating the effect of rotenone on opening K-ATP channels. Administration of baicalein (150, 300 mg·kg-1·d-1, i.g.) significantly inhibited rotenone-induced overexpression of SUR1 in SN and striatum of rats. We conducted surface plasmon resonance assay and molecular docking, and found that baicalein had a higher affinity with SUR1 protein (KD = 10.39 µM) than glibenclamide (KD = 24.32 µM), thus reducing the sensitivity of K-ATP channels to rotenone. Knockdown of SUR1 subunit reduced rotenone-induced apoptosis and damage of SH-SY5Y cells, confirming that SUR1 was an important target for slowing dopaminergic neuronal degeneration in PD. Taken together, we demonstrate for the first time that baicalein attenuates rotenone-induced SH-SY5Y cell apoptosis through binding to SUR1 and activating K-ATP channels.
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Flavanonas , Neuroblastoma , Canales de Potasio de Rectificación Interna , Humanos , Ratas , Animales , Canales KATP , Rotenona/farmacología , Receptores de Sulfonilureas , Canales de Potasio de Rectificación Interna/metabolismo , Gliburida/farmacología , Simulación del Acoplamiento Molecular , Apoptosis , Neuronas Dopaminérgicas/metabolismo , Adenosina Trifosfato/farmacologíaRESUMEN
Glioblastoma (GBM) is a major type of primary brain tumor without ideal prognosis and it is therefore necessary to develop a novel compound possessing therapeutic effects. Chrysomycin A (Chr-A) has been reported to inhibit the proliferation, migration and invasion of U251 and U87-MG cells through the Akt/GSK-3ß signaling pathway, but the mechanism of Chr-A against glioblastoma in vivo and whether Chr-A modulates the apoptosis of neuroglioma cells is unclear. The present study aims to elucidate the potential of Chr-A against glioblastoma in vivo and how Chr-A modulates the apoptosis of neuroglioma cells. Briefly, the anti-glioblastoma activity was assessed in human glioma U87 xenografted hairless mice. Chr-A-related targets were identified via RNA-sequencing. Apoptotic ratio and caspase 3/7 activity of U251 and U87-MG cells were assayed via flow cytometry. Apoptosis-related proteins and possible molecular mechanisms were validated via Western blotting. The results showed that Chr-A treatment significantly inhibits glioblastoma progression in xenografted hairless mice, and enrichment analysis suggested that apoptosis, PI3K-Akt and Wnt signaling pathways were involved in the possible mechanisms. Chr-A increased the apoptotic ratio and the activity of caspase 3/7 in U251 and U87-MG cells. Western blotting revealed that Chr-A disturbed the balance between Bax and Bcl-2, activating a caspase cascade reaction and downregulating the expression of p-Akt and p-GSK-3ß, suggesting that Chr-A may contribute to glioblastoma regression modulating in the Akt/GSK-3ß signaling pathway to promote apoptosis of neuroglioma cells in vivo and in vitro. Therefore, Chr-A may hold therapeutic promise for glioblastoma.
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Glioblastoma , Proteínas Proto-Oncogénicas c-akt , Ratones , Animales , Humanos , Proteínas Proto-Oncogénicas c-akt/metabolismo , Glucógeno Sintasa Quinasa 3 beta/metabolismo , Caspasa 3/metabolismo , Fosfatidilinositol 3-Quinasas/metabolismo , Ratones Pelados , Proliferación Celular , Transducción de Señal , Apoptosis , Glioblastoma/patología , Línea Celular TumoralRESUMEN
Alzheimer's Disease (AD) is an irreversible neurodegenerative disease, which urgently needs more effective treatment strategies. Arctium lappa L. leaf (burdock leaf) performs wide pharmacological activities, increasing evidence hinted that burdock leaves can ameliorate AD. This research aims to explore the bioactive ingredients and mechanisms of burdock leaves against AD by performing chemical profiles, network pharmacology, and molecular docking. 61 components are identified by liquid chromatography equipped with mass spectrometry. 792 targets of ingredients and 1661 AD-related genes are retrieved from public databases. Ten critical ingredients are identified from the topology analysis of the compound-target network. CytoNCA, AlzData database, and Aging Atlas database contribute to the foundation of 36 potential targets and four clinically significant targets (STAT3, RELA, MAPK8, and AR). The gene ontology (GO) analysis manifests that the included processes are close to the pathogenesis of AD. PI3K-Akt signaling pathway and AGE-RAGE signaling pathway may be important therapeutic mechanisms. Molecular docking results imply that network pharmacology results are reliable. Furthermore, the clinical meanings of core targets are also evaluated with the Gene Expression Omnibus (GEO) database. This research will provide research direction for the application of burdock leaves in the treatment of AD.
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Enfermedad de Alzheimer , Arctium , Enfermedades Neurodegenerativas , Enfermedad de Alzheimer/tratamiento farmacológico , Enfermedad de Alzheimer/genética , Simulación del Acoplamiento Molecular , Farmacología en Red , Vehículos Farmacéuticos , Fosfatidilinositol 3-Quinasas , Hojas de la Planta , HumanosRESUMEN
Alzheimer's disease (AD) is a common chronic neurodegenerative disease. Some studies have suggested that dysregulation of microglia activation and the resulting neuroinflammation play an important role in the development of AD pathology. Activated microglia have both M1 and M2 phenotypes and inhibition of M1 phenotype while stimulating M2 phenotype has been considered as a potential treatment for neuroinflammation-related diseases. Baicalein is a class of flavonoids with anti-inflammatory, antioxidant and other biological activities, but its role in AD and the regulation of microglia are limited. The purpose of this study was to investigate the effect of baicalein on the activation of microglia in AD model mice and the related molecular mechanism. Our results showed that baicalein significantly improved the learning and memory ability and AD-related pathology of 3 × Tg-AD mice, inhibited the level of pro-inflammatory factors TNF-α, IL-1ß and IL-6, promoted the production of anti-inflammatory factors IL-4 and IL-10, and regulated the microglia phenotype through CX3CR1/NF-κB signaling pathway. In conclusion, baicalein can regulate the phenotypic transformation of activated microglia and reduce neuroinflammation through CX3CR1/NF-κB pathway, thereby improving the learning and memory ability of 3 × Tg-AD mice.
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Enfermedad de Alzheimer , Enfermedades Neurodegenerativas , Ratones , Animales , FN-kappa B/metabolismo , Ratones Transgénicos , Enfermedad de Alzheimer/metabolismo , Enfermedades Neurodegenerativas/metabolismo , Enfermedades Neuroinflamatorias , Microglía , Antiinflamatorios/farmacología , Receptor 1 de Quimiocinas CX3C/metabolismoRESUMEN
Eight undescribed ß-bergamotene-type sesquiterpene oliganins A-H (1-8) and one known α-bergamotene-type sesquiterpene (9) were isolated from the leaves and twigs of Illicium oligandrum Merr. & Chun. The structures of compounds 1-8 were elucidated by extensive spectroscopic data, and the absolute configurations were determined by using a modified Mosher's method and electronic circular dichroism calculations. The isolates were further evaluated in terms of their anti-inflammatory potential on nitric oxide (NO) generation in lipopolysaccharide-stimulated RAW264.7 and BV2 cells. Compounds 2 and 8 exhibited potent inhibitory effects on the production of NO with IC50 values ranging from 21.65 to 49.28 µM, which were greater than or comparable to those of dexamethasone (positive control).
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Illicium , Sesquiterpenos , Illicium/química , Estructura Molecular , Sesquiterpenos/farmacología , Sesquiterpenos/química , Antiinflamatorios/farmacología , Antiinflamatorios/química , Dicroismo Circular , Óxido NítricoRESUMEN
Salvianolic acid A (SAA) is a traditional Chinese medicine that has a good therapeutic effect on cardiovascular disease. However, the underlying mechanisms by which SAA improves mitochondrial respiration and cardiac function in diabetic cardiomyopathy (DCM) remain unknown. This study aims to elucidate whether SAA had any cardiovascular protection on the pathophysiology of DCM and explored the potential mechanisms. Diabetes was induced in rats by 30 mg/kg of streptozotocin (STZ) treatment. After a week of stability, 5 mg/kg isoprenaline (ISO) was injected into the rats subcutaneously. 3 mg/kg SAA was orally administered for six weeks and 150 mg/kg Metformin was selected as a positive group. At the end of this period, cardiac function was assessed by ultrasound, electrocardiogram, and relevant cardiac injury biomarkers testing. Treatment with SAA improved cardiac function, glucose, and lipid levels, mitochondrial respiration, and suppressed myocardial inflammation and apoptosis. Furthermore, SAA treatment inhibits the apoptosis pathway through CRYAB in diabetic cardiomyopathy rats. As a result, this study not only provides new insights into the mechanism of SAA against DCM but also provides new therapeutic ideas for the discovery of anti-DCM compounds in the clinic.
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Diabetes Mellitus , Cardiomiopatías Diabéticas , Animales , Ratas , Apoptosis , Cardiomiopatías Diabéticas/metabolismo , Ratas Sprague-Dawley , Respiración , CorazónRESUMEN
BACKGROUND: Fibroblast growth factors (FGFs) are key factors affecting diabetic wound healing. However, the FGF family's expression patterns in skin and wounds influenced by both diabetes and sex are still unknown. METHODS AND RESULTS: In this study, normal and Streptozotocin (STZ)-induced type 1 diabetic C57BL/6J male and female mice were used to study the FGF family's expression in non-wound skin and wounds. We found that the expression patterns of Fgfs were affected by sex in both normal and diabetic animals during wound healing. In normal control mice, sex difference had a limited effect on basal skin Fgf expressions. However, it significantly influenced Fgf expressions in wounds. Type 1 diabetes reduced basal and wound-induced skin Fgf expressions. Female mice had far lower wound-induced skin Fgf expressions in diabetic mice. In addition, sex differently influenced Fibroblast growth factors receptor (Fgfr) expression patterns of non-wound skin and wounds in both normal and diabetic mice. Moreover, female mice had a lower relative level of Fibronectin leucine-rich repeat transmembrane protein 2 (FLRT2) - a FGFR activation marker gene - in wound and blood plasma. Correspondingly, the wound areas of female animals were larger than that of male animals in the early stage of wound healing (less than 3-day injury). CONCLUSION: Our research shows that the FGF family have different expression patterns in normal and diabetic wound healing in mice of different sex. Additionally, we also provide the signatures of individual FGFs in diabetic wound healing, which deserve further investigation.
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Diabetes Mellitus Experimental , Diabetes Mellitus Tipo 1 , Ratones , Femenino , Masculino , Animales , Factores de Crecimiento de Fibroblastos/genética , Factores de Crecimiento de Fibroblastos/metabolismo , Estreptozocina/metabolismo , Diabetes Mellitus Experimental/metabolismo , Diabetes Mellitus Tipo 1/genética , Diabetes Mellitus Tipo 1/metabolismo , Caracteres Sexuales , Ratones Endogámicos C57BL , Piel/metabolismo , Receptores de Factores de Crecimiento de Fibroblastos/genética , Receptores de Factores de Crecimiento de Fibroblastos/metabolismo , Glicoproteínas de Membrana/metabolismoRESUMEN
Chrysomycin A (Chr-A), an antibiotic from Streptomyces, is reported to have anti-tumor and anti-tuberculous activities, but its anti-glioblastoma activity and possible mechanism are not clear. Therefore, the current study was to investigate the mechanism of Chr-A against glioblastoma using U251 and U87-MG human cells. CCK8 assays, EdU-DNA synthesis assays and LDH assays were carried out to detect cell viability, proliferation and cytotoxicity of U251 and U87-MG cells, respectively. Transwell assays were performed to detect the invasion and migration abilities of glioblastoma cells. Western blot was used to validate the potential proteins. Chr-A treatment significantly inhibited the growth of glioblastoma cells and weakened the ability of cell migration and invasion by down regulating the expression of slug, MMP2 and MMP9. Furthermore, Chr-A also down regulated Akt, p-Akt, GSK-3ß, p-GSK-3ß and their downstream proteins, such as ß-catenin and c-Myc in human glioblastoma cells. In conclusion, Chr-A may inhibit the proliferation, migration and invasion of glioblastoma cells through the Akt/GSK-3ß/ß-catenin signaling pathway.
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Glioblastoma , beta Catenina , Aminoglicósidos , Antibacterianos/farmacología , Línea Celular Tumoral , Movimiento Celular , Proliferación Celular , ADN/farmacología , Glioblastoma/metabolismo , Glucógeno Sintasa Quinasa 3 beta , Humanos , Metaloproteinasa 2 de la Matriz/metabolismo , Metaloproteinasa 9 de la Matriz/genética , Metaloproteinasa 9 de la Matriz/metabolismo , Invasividad Neoplásica , Proteínas Proto-Oncogénicas c-akt/metabolismo , beta Catenina/metabolismoRESUMEN
Kaempferol, a natural plant flavonoid compound, has a neuroprotective effect on ischemic stroke, while the specific mechanism remains unclear. In the current study, we applied the comprehensive strategy that combines network pharmacology and experimental evaluation to explore the potential mechanism of kaempferol in the treatment of cerebral ischemia. First, network pharmacology analysis identified the biological process of kaempferol, suggesting that kaempferol may partly help in treating ischemic stroke by regulating apoptosis and inflammatory response. Then, we evaluated the efficacy of kaempferol in the acute stage of ischemic stroke and elucidated its effects and possible mechanisms on cell apoptosis and neuroinflammation involved by neutrophils. The results showed that kaempferol could significantly reduce the modified neurological severity score (mNSS), and reduce the volume of cerebral infarction and the degree of cerebral edema. In terms of anti-apoptosis, kaempferol could significantly reduce the number of TUNEL-positive cells, inhibit the expression of pro-apoptotic proteins and promote the expression of anti-apoptotic proteins. Kaempferol may play an anti-apoptotic role by up-regulating the expression level of the BDNF-TrkB-PI3K/AKT signaling pathway. In addition, we found that kaempferol inhibited neuron loss and the activation of glial cells, as well as the expression level of the inflammatory protein COX-2 and the classic pro-inflammatory signaling pathway TLR4/MyD88/NF-κB in the ischemic brain, reduced MPO activity and neutrophil counts in peripheral blood, and down-regulated neutrophil aggregation and infiltration in the ischemic brain. Western blot revealed that kaempferol down-regulated the activation of the JAK1/STAT3 signaling pathway in neutrophils and ischemic brains. Our study showed that kaempferol inhibited the activation and number of neutrophils in the rat peripheral blood and brain, which may be related to the down-regulation of the JAK1/STAT3 pathway.
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Isquemia Encefálica , Accidente Cerebrovascular Isquémico , Fármacos Neuroprotectores , Animales , Ratas , Quempferoles/farmacología , Quempferoles/uso terapéutico , Fármacos Neuroprotectores/farmacología , Fármacos Neuroprotectores/uso terapéutico , Neutrófilos/metabolismo , FN-kappa B/metabolismo , Proteínas Proto-Oncogénicas c-akt/metabolismo , Fosfatidilinositol 3-Quinasas/metabolismo , Receptor Toll-Like 4/metabolismo , Ciclooxigenasa 2/metabolismo , Factor 88 de Diferenciación Mieloide/metabolismo , Factor Neurotrófico Derivado del Encéfalo/metabolismo , Enfermedades Neuroinflamatorias , Farmacología en Red , Isquemia Encefálica/tratamiento farmacológico , Isquemia Encefálica/metabolismo , Proteínas Reguladoras de la Apoptosis/metabolismoRESUMEN
This study investigated anti-viral, antioxidant activity and anti-pyretic of crude extract from Artemisia afra, Artemisia absinthium and Pittiosporum viridflorum leaves. The crude extracts were prepared by maceration using aqueous, methanol and dichloromethane respectively. Antiviral studies were evaluated with influenza virus using Fluorescence based - Neuraminidase inhibitors. Antioxidant activities determined with DPPH, Nitric oxide, hydroxyl and super oxide anion radicals' Anti-pyretic activities were evaluated using rats with yeast induced pyrexia. Total phenol, flavonoids, and pro-anthocyanin contents of the plants samples were evaluated using standard protocols. The crude extracts exhibited neuraminidase inhibitory activity against the influenza virus at different thresholds. Artemisia absinthiumaqueous extract showed the best activity against A/Sydney/5/97. Whereas Artemisia afra methanol crude extract displayed highest antioxidant potential against the tested antioxidant parameters. All the crude extracts significantly reversed yeast induced pyrexia in rats, similar to paracetamol. Thus, they could serve as natural remedy for respiratory diseases such as Influenza.
Este estudio investigó la actividad antiviral, antioxidante y antipirética del extracto crudo de hojas de Artemisia afra, Artemisia absinthium y Pittiosporum viridflorum. Los extractos crudos se prepararon mediante maceración utilizando metanol acuoso y diclorometano respectivamente. Los estudios antivirales se evaluaron con el virus de la influenza utilizando inhibidores de neuraminidasa basados en fluorescencia. Actividades antioxidantes determinadas con DPPH, radicales aniónicos de óxido nítrico, hidroxilo y superóxido. Las actividades antipiréticas se evaluaron utilizando ratas con pirexia inducida por levaduras. El contenido total de fenol, flavonoides y proantocianina de las muestras de plantas se evaluó utilizando protocolos estándar. Los extractos crudos mostraron actividad inhibidora de neuraminidasa contra el virus de la influenza en diferentes umbrales. El extracto acuoso de Artemisia absinthium mostró la mejor actividad contra A/Sydney/5/97. Mientras que el extracto crudo de Artemisia aframetanol mostró el mayor potencial antioxidante contra los parámetros antioxidantes probados. Todos los extractos crudos revirtieron significativamente la pirexia inducida por levaduras en ratas, similar al paracetamol. Por tanto, podrían servir como remedio natural para enfermedades respiratorias como la Influenza.