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1.
Clin Sci (Lond) ; 2020 Feb 17.
Artigo em Inglês | MEDLINE | ID: mdl-32065214

RESUMO

Cancer-derived exosomal miRNAs play an important role in the development of metastasis, but the effects and underlying mechanisms remain unclear. In the present study, we investigated the miRNA expression profiles of 5 paired serum exosomal samples from metastatic colorectal cancer (mCRC) and non-mCRC patients via RNA sequencing. After we evaluated the differentially expressed miRNAs in 80 CRC patients, miR-106b-3p was selected as a metastasis-associated miRNA of CRC. We showed that the expression level of serum exosomal miR-106b-3p was significantly higher in CRC patients with metastasis than those without metastasis. Additionally, high serum exosomal miR-106b-3p expression in patients was correlated with a poor prognosis. Coculture of low-metastatic CRC cells with high-metastatic CRC cell-derived exosomes promoted cell migration, invasion, and epithelial to mesenchymal transition (EMT), which was caused by the transport and transduction of miR-106b-3p in vitro. Moreover, exosomal miR-106b-3p promoted lung metastasis of CRC cells in vivo. In addition, we demonstrated that miR-106b-3p regulated metastasis by targeting deleted in liver cancer-1 (DLC-1). A negative correlation was also identified between miR-106b-3p and DLC-1 expression in human CRC tumour tissues and in mouse lung metastatic lesions. Collectively, our study indicated that metastasis-associated miR-106b-3p from serum exosomes could be used as a potential prognostic biomarker and therapeutic target for CRC patients.

2.
Aging (Albany NY) ; 12(1): 156-177, 2020 Jan 02.
Artigo em Inglês | MEDLINE | ID: mdl-31896739

RESUMO

A promising new strategy for cancer therapy is to target the autophagic pathway. However, comprehensive characterization of autophagy genes and their clinical relevance in cancer is still lacking. Here, we systematically characterized alterations of autophagy genes in multiple cancer lines by analyzing data from The Cancer Genome Atlas and CellMiner database. Interactions between autophagy genes and clinically actionable genes (CAGs) were identified by analyzing co-expression, protein-protein interactions (PPIs) and transcription factor (TF) data. A key subnetwork was identified that included 18 autophagy genes and 22 CAGs linked by 28 PPI pairs and 1 TF-target pair, which was EGFR targeted by RARA. Alterations in the expression of autophagy genes were associated with patient survival in multiple cancer types. RARA and EGFR were associated with worse survival in colorectal cancer patients. The regulatory role of EGFR in 5-FU resistance was validated in colon cancer cells in vivo and in vitro. EGFR contributed to 5-FU resistance in colon cancer cells through autophagy induction, and EGFR overexpression in 5-FU resistant colon cancer was regulated by RARA. The present study provides a comprehensive analysis of autophagy in different cancer cell lines and highlights the potential clinical utility of targeting autophagy genes.

4.
Aging Dis ; 10(6): 1233-1245, 2019 Dec.
Artigo em Inglês | MEDLINE | ID: mdl-31788335

RESUMO

Autophagy is a lysosome-dependent cellular catabolic mechanism that mediates the turnover of dysfunctional organelles and aggregated proteins. It has a neuroprotective role on neurodegenerative diseases. Here, we hypothesized that autophagy may also have a neuroprotective role in diabetes-associated cognitive decline (DACD). In current study, we found that db/db mice display cognitive decline with inferior learning and memory function. The accumulation of ß-amyloid1-42 (Aß1-42), which is a characteristic of Alzheimer's disease (AD), was markedly higher in the prefrontal cortex (PFC), cornu ammon1 (CA1), and dentate gyrus (DG) areas of the hippocampus in db/db mice. Moreover, BDNF and microtubule associated protein 2 (MAP2) levels were lower in the hippocampus of db/db mice. However, there was no noticeable differences in the level of apoptosis in the hippocampus between control (CON) mice and db/db mice. Markers of autophagy in the hippocampus were elevated in db/db mice. The expression levels of ATG5, ATG7, and LC3B were higher, and the level of P62 was lower. An autophagy inhibitor, 3-MA, and ATG7 siRNA significantly reversed the activation of autophagy in vitro, which was accompanied with a higher level of apoptosis. Taken together, our current study suggests that diabetes is associated with cognitive decline, and activation of autophagy has a neuroprotective role in DACD.

5.
Oxid Med Cell Longev ; 2019: 8783197, 2019.
Artigo em Inglês | MEDLINE | ID: mdl-31885823

RESUMO

Osteoarthritis (OA) is an age-related degenerative disease with complicated pathology involving chondrocyte apoptosis and extracellular matrix (ECM) degradation. Previous studies have shown that moderate autophagy has a protective effect against apoptosis in chondrocyte. Mangiferin is a natural polyphenol and exerts multiple pharmacological effects on different diseases in various preclinical studies. In this study, we investigated the effects of mangiferin on OA and delineated a potential molecular mechanism. In vitro, mangiferin treatment inhibited the expression of proapoptotic proteins induced by tert-butyl hydroperoxide (TBHP), increased the expression of antiapoptotic Bcl-2, and prevented ECM degradation by inhibiting the production of matrix-degrading enzyme. Mechanistically, mangiferin enhanced autophagy by activating the AMP-activated protein kinase (AMPK) signaling pathway. On the contrary, inhibition of autophagy partly abolished the protective effects of mangiferin on antiapoptosis and ECM synthesis in TBHP-treated chondrocyte. Correspondingly, the protective effect of mangiferin was also found in a mouse OA model. In conclusion, our results suggested that mangiferin serves as a potentially applicable candidate for treating OA.

6.
J Neurochem ; 2019 Oct 11.
Artigo em Inglês | MEDLINE | ID: mdl-31602651

RESUMO

In recent years, many studies have focused on autophagy, an evolutionarily conserved mechanism that relies on lysosomes to achieve cellular metabolic requirements and organelle turnover, and revealed its important role in animal models of traumatic injury. Autophagy is a double-edged sword. Appropriate levels of autophagy can promote the removal of abnormal proteins or damaged organelles, while hyperactivated autophagy can induce autophagic apoptosis. However, recent studies suggest that autophagic flux seems to be blocked after traumatic brain injury (TBI), which contributes to the apoptosis of brain cells. In this study, valproic acid (VPA), which was clinically used for epilepsy treatment, was used to treat TBI. The Morris water maze test, hematoxylin & eosin staining and Nissl staining were first conducted to confirm that VPA treatment had a therapeutic effect on mice after TBI. Western blotting, enzyme-linked immunosorbent assay and immunofluorescence staining were then performed to reveal that VPA treatment reversed TBI-induced blockade of autophagic flux, which was accompanied by a reduced inflammatory response. In addition, the variations in activation and phenotypic polarization of microglia were observed after VPA treatment. Nevertheless, the use of the autophagy inhibitor 3-methyladenine partially abolished VPA-induced neuroprotection and the regulation of microglial function after TBI, resulting in the deterioration of the central nervous system microenvironment and neurological function. Collectively, VPA treatment reversed the TBI-induced blockade of autophagic flux in the mouse brain cortex, subsequently inhibiting brain cell apoptosis and affecting microglial function to achieve the promotion of functional recovery in mice after TBI.

7.
Gastroenterol Res Pract ; 2019: 9097276, 2019.
Artigo em Inglês | MEDLINE | ID: mdl-31263495

RESUMO

Many animal experiments and clinical trials showed that probiotics are effective for the treatment of alcoholic liver disease. Alcohol disrupts the composition of intestinal flora; probiotics modulate the gut microbiota and reverse alcohol-associated intestinal barrier dysfunction by decreasing intestinal mucosal permeability and preventing intestinal bacteria from translocating. Probiotics enhance immune responses and reduce the levels of alcohol-induced inflammatory cytokines and reactive oxygen species (ROS) production in the liver and intestine. Probiotics also increase fatty acid ß-oxidation and reduce lipogenesis, combating alcohol-induced hepatic steatosis. In this review, we summarize the current knowledge regarding the mechanism of action of probiotics for reducing the effects of alcoholic liver disease.

8.
Oncol Lett ; 17(6): 5662-5668, 2019 Jun.
Artigo em Inglês | MEDLINE | ID: mdl-31186789

RESUMO

Application value of epidural anesthesia combined with epidural analgesia and general anesthesia combined with intravenous analgesia in ovarian cancer surgery was explored. In total 298 ASA I-III grade patients with ovarian cancer, undergoing extensive total hysterectomy and pelvic lymphotomy, were retrospectively analyzed. Patients were divided into two groups: the epidural anesthesia combined with epidural analgesia group (group A, 158 cases), and the general anesthesia combined with intravenous analgesia group (group B, 140 cases). The first exhaust time, incidence of adverse reactions, Aldrete score, and recovery were observed, and the visual analogue scale (VAS) scores during resting, exercise and cough at 24 h after surgery were recorded. Fasting venous blood (2 ml) was drawn at the same time before anesthesia and at 24 h after anesthesia in both groups to determinate cortisol (COR) and C-reactive protein (CRP) levels. The first exhaust time and incidence of adverse reactions in group A were significantly lower than those in group B (P<0.05). The Aldrete score and extubation time (ET) in group A were significantly higher than that in group B. Eye opening time (EOT), recovery orientation time (ROT) and post-anesthesia care unit (PACU) time in group A were significantly lower than those in group B (P<0.05). The VAS scores in group A during resting, exercise and cough were lower than those in group B (P<0.05). Compared with before anesthesia, the levels of COR and CRP increased significantly in both groups at 24 h after anesthesia (P<0.05), while the level of COR and CRP in group A was significantly lower than that in group B, at 24 h after surgery (P<0.05). Epidural anesthesia combined with epidural analgesia has better analgesic effect, higher safety, lower incidence of adverse reactions, and is beneficial to the recovery of patients with ovarian cancer after radical operation when compared with general anesthesia combined with intravenous analgesia.

9.
J Neurotrauma ; 36(24): 3394-3409, 2019 Dec 15.
Artigo em Inglês | MEDLINE | ID: mdl-31232175

RESUMO

Spinal cord injury (SCI) is a devastating neurological disorder that usually leads to a loss of motor and sensory function in patients. The expression of hypoxia inducible factor-1α (HIF-1α) is increased, and exerts a protective role after traumatic SCI. However, the endogenous activity of HIF-1α is insufficient for promoting functional recovery. The present study tested the potential effect of the sustained activation of HIF-1α by the prolylhydroxylase (PHD) inhibitor dimethyloxalylglycine (DMOG) on anti-apoptotic process and the regulation of axonal regeneration after SCI. Here, we found that treatment with DMOG significantly increased the expression of HIF-1α and that the stabilization of HIF-1α induced by DMOG not only decreased the expression of apoptotic proteins to promote neural survival, but also enhanced axonal regeneration by regulating microtubule stabilization in vivo and in vitro. In addition, we found that DMOG promoted neural survival and axonal regeneration by activating autophagy, which is induced by the HIF-1α/BNIP3 signaling pathway, and that the inhibition of HIF-1α or autophagy abrogated the protective effect of DMOG, as expected. Taken together, our results demonstrate that treatment with DMOG improves functional recovery after SCI and that DMOG may serve as a potential candidate for treating SCI.

10.
Clin Exp Pharmacol Physiol ; 46(9): 861-871, 2019 Sep.
Artigo em Inglês | MEDLINE | ID: mdl-31206801

RESUMO

Colorectal cancer (CRC) is a prevalent malignant tumour that causes considerable cancer-related deaths globally. The sphingolipid transporter 2 (SPNS2), a sphingosine-1-phosphate (S1P) transporter, modulates multiple biological events including malignancy of cancer cells. In this study, the effects of SPNS2 on CRC progression were studied. We found that SPNS2 expression was significantly upregulated in CRC tissues compared to that in adjacent non-tumour tissues. To assess the role of SPNS2 in CRC cells, we performed loss- and gain-of-function experiments in SW480 and HCT116 cells, respectively. The results demonstrated that SPNS2 promoted proliferation, migration and invasion, and inhibited apoptosis in CRC cells. Additionally, SPNS2 enhanced the release of intracellular S1P, and increased S1P receptor 1 (S1PR1) and S1PR3 expression. Moreover, SPNS2 activated the Akt and ERK pathways, and the biological behaviours of SPNS2 were attenuated by Akt or ERK inhibitor in HCT116 cells. In conclusion, our results demonstrated that SPNS2 promoted proliferation, migration and invasion, and inhibited apoptosis by regulating S1P/S1PR1/3 axis and activating Akt and ERK pathway in CRC cells.

11.
Artigo em Inglês | MEDLINE | ID: mdl-31106843

RESUMO

To investigate the changes of blood flow signal in residual cancer after ultrasound-guided radiofrequency ablation(RFA) treatment of rabbit liver cancer over time , and to analyze the correlation between changes in blood flow signal and changes in HIF-1α, VEGF, and MMP-9 in residual cancer tissue after RFA. One hundred and ten rabits were randomly selected ,VX2 tumor cells were implanted subcutaneously, tumor cells were implanted in liver. 90 rabits were divided into 2 groups. Group 1(untreated controls). Group 2 was surgical resection group ,tumor size, blood flow signal, Microvessel density (MVD) in liver cancer were counted, Correlation of HIF-1α, VEGF, MMP-9 mRNA and protein expressions with blood flow signal in residual cancer were observed.liver tumor was 2.3 ± 0.32 cm, significant differences in the grade of blood flow signal were noted among different time points (days 0, 3, 7, and 14) (P < 0.05). Significant differences were also observed between the surgical resection and RFA groups at the same time points (P < 0.05),The MVD in the RFA group was lower than that in the control group, but higher than that in the surgical resection group. The immunohistochemical scores for VEGF and MMP-9 in the RFA group were lower than those in the control group, but higher than those in the surgical resection group .The grade of ultrasound blood flow signal was positively correlated with the expression of two angiogenesis-related factors, VEGF and MMP-9, and the MVD in the control, RFA, and surgical resection groups. There is a higher risk of tumor recurrence with RFA than with surgical resection.

12.
Polymers (Basel) ; 11(5)2019 May 10.
Artigo em Inglês | MEDLINE | ID: mdl-31083356

RESUMO

The conjugates of black bean protein isolate (BBPI) and glucose (G) were prepared via the wet heating Maillard reaction with ultrasound pretreatment. The physicochemical properties of UBBPI-G conjugates prepared by ultrasound pretreatment Maillard reaction had been compared with classical Maillard reaction (BBPI-G). The reaction rate between BBPI and glucose was speeded up by ultrasound pretreatment. A degree of glycation (DG) of 20.49 was achieved by 2 h treatment for UBBPI-G, whereas 5 h was required using the classical heating. SDS-PAGE patterns revealed that the BBPI-G conjugates with higher molecular weight were formed after glycosylation. The results of secondary structure analysis suggested that the α-helix and ß-sheet content of UBBPI-G were lower than that of BBPI-G. In addition, UBBPI-G conjugates had exhibited bathochromic shift compared with BBPI by fluorescence spectroscopy analysis. Finally, UBBPI-G achieved higher level of surface hydrophobicity, solubility, emulsification property and antioxidant activity than BBPI and BBPI-G (classical Maillard reaction).

13.
Clin Res Hepatol Gastroenterol ; 43(6): 707-714, 2019 Nov.
Artigo em Inglês | MEDLINE | ID: mdl-31029643

RESUMO

Acetaminophen (APAP) overdose/abuse is the leading cause of acute liver failure in many countries. Fibroblast growth factor 1 (FGF 1) is a metabolic regulator with several physiological functions. Previous studies suggested that FGF1 promotes differentiation and maturation of liver-derived stem cells. In this study, we investigated the protective effects of FGF1 against APAP-induced hepatotoxicity in mice. APAP markedly increased circulating levels of ALT and AST, while FGF1 significantly inhibited increases in the serum levels of ALT and AST, as compared to littermates. In addition, histopathological evaluation of the livers revealed that FGF1 prevented APAP-induced centrilobular necrosis. Livers exhibited severe inflammation, apoptosis, oxidative stress and endoplasmic reticulum stress in response to APAP toxicity, whereas these changes were reversed by a single injection of FGF1. In conclusion, our findings suggest that FGF1 protects mice from APAP-induced hepatotoxicity through suppression of inflammation, apoptosis, and oxidative and endoplasmic reticulum stress. Therefore, FGF1 may represent a promising therapeutic agent for APAP-induced acute liver injury.

14.
J Gastroenterol Hepatol ; 34(5): 880-889, 2019 May.
Artigo em Inglês | MEDLINE | ID: mdl-30395690

RESUMO

BACKGROUND AND AIM: Differentially expressed (DE) genes detected at the population-level through case-control comparison provide no information on the dysregulation frequencies of DE genes in a cancer. In this work, we aimed to identify the genes with universally upregulated or downregulated expressions in colorectal cancer (CRC). METHODS: We firstly clarified that DE genes in an individual cancer tissue should be the disease-relevant genes, which are dysregulated in the cancer tissue in comparison with its own previously normal state. Then, we identified DE genes at the individual level for 2233 CRC samples collected from multiple data sources using the RankComp algorithm. RESULTS: We found 26 genes that were upregulated or downregulated in almost all the 2233 CRC samples and validated the results using 124 CRC tissues with paired adjacent normal tissues. Especially, we found that two genes (AJUBA and EGFL6), upregulated universally in CRC tissues, were extremely lowly expressed in normal colorectal tissues, which were considered to be oncogenes in CRC oncogenesis and development. Oppositely, we found that one gene (LPAR1), downregulated universally in CRC tissues, was silenced in CRC tissues but highly expressed in normal colorectal tissues, which were considered to be tumor suppressor genes in CRC. Functional evidences revealed that these three genes may induce CRC through deregulating pathways for ribosome biogenesis, cell proliferation, and cell cycle. CONCLUSIONS: In conclusion, the individual-level DE genes analysis can help us find genes dysregulated universally in CRC tissues, which may be important diagnostic biomarkers and therapy targets.


Assuntos
Neoplasias Colorretais/diagnóstico , Neoplasias Colorretais/genética , Regulação para Baixo/genética , Regulação Neoplásica da Expressão Gênica/genética , Proteínas com Domínio LIM/genética , Glicoproteínas de Membrana/genética , Receptores de Ácidos Lisofosfatídicos/genética , Regulação para Cima/genética , Idoso , Neoplasias Colorretais/terapia , Feminino , Expressão Gênica , Humanos , Masculino , Pessoa de Meia-Idade , Terapia de Alvo Molecular
15.
J Neurotrauma ; 36(12): 1949-1964, 2019 Jun 15.
Artigo em Inglês | MEDLINE | ID: mdl-30543130

RESUMO

Axon retraction greatly limits functional recovery after spinal cord injury (SCI) and neuron polarization, which affects processes including axon formation and development, is a promising target for promoting axon regeneration. Increasing microtubule stability has been demonstrated to improve intrinsic axon regeneration processes and is critically related to endoplasmic reticulum (ER)-mitochondria interactions. We used real-time polymerase chain reaction, Western blotting, and immunofluorescence to screen a variety of natural compounds, and found that Loureirin B (LrB) effectively promoted neuron polarization and axon regeneration in vitro and in vivo. LrB significantly inhibited ER stress and thereby promoted mitochondrial functions by regulating mitochondrial fusion. Further, LrB reactivated the Akt/GSK-3ß pathway, which plays critical roles in cell survival and microtubule stabilization. Taken together, our results suggest that the effects of LrB on neuron regeneration involve the inhibition of ER stress-induced mitochondrial dysfunction and activation of the Akt/GSK-3ß pathway, which further promotes microtubule stabilization. LrB may therefore be a promising candidate for facilitating recovery following SCI.

16.
Sleep Breath ; 23(1): 297-302, 2019 Mar.
Artigo em Inglês | MEDLINE | ID: mdl-30088240

RESUMO

OBJECTIVE: Glutamate is an excitatory neurotransmitter in the central nervous system that participates in initiation and maintenance of sleep and wakefulness. The mechanisms involved occur in the brainstem, lateral hypothalamus, and basal forebrain. Our previous study suggested that higher levels of glutamate in cerebrospinal fluid (CSF) contributed to poorer sleep quality. Smoking has been shown to be harmful to sleep quality. In the present study, we recruited non-smokers and heavy smokers and measured the concentration of CSF glutamate in order to investigate the associations among smoking status, sleep quality, and CSF glutamate levels. METHODS: We recruited 147 men (n = 68 non-smokers, 30.31 ± 9.10 years; n = 79 heavy smokers, 34.54 ± 10.71 years). Glutamate concentrations in CSF were measured by spectrophotometry, and subjective sleep quality was assessed using the Pittsburgh Sleep Quality Index (PSQI). RESULTS: PSQI total scores were significantly higher in heavy smokers than that in non-smokers (p < 0.001). Glutamate concentrations in CSF were lower in heavy smokers than that in non-smokers (p < 0.001). CSF glutamate levels positively correlated with PSQI total scores in the non-smokers group (r = 0.313, p = 0.011, effect size = 0.324). No correlation was found between CSF glutamate levels and PSQI total scores in the heavy smokers group (p > 0.05). Multivariable linear regression analysis showed that years of smoking was contributed to the PSQI total scores (p = 0.008), and cigarettes smoked per day contributed to the decreased CSF glutamate levels in heavy smokers (p = 0.001). CONCLUSION: Poorer subjective sleep quality and lower CSF glutamate concentrations were observed in the heavy smokers group than in the non-smokers group. In addition, lack of correlation was observed between CSF glutamate levels and PSQI scores in the heavy smokers.


Assuntos
Ácido Glutâmico/líquido cefalorraquidiano , Transtornos do Sono-Vigília/líquido cefalorraquidiano , Fumar/líquido cefalorraquidiano , Tabagismo/líquido cefalorraquidiano , Adulto , Correlação de Dados , Humanos , Masculino , Pessoa de Meia-Idade , Valores de Referência
17.
Cell Physiol Biochem ; 51(4): 1969-1981, 2018.
Artigo em Inglês | MEDLINE | ID: mdl-30513513

RESUMO

BACKGROUND/AIMS: Deregulation of microRNAs (miRNAs) has been associated with a variety of cancers, including colorectal cancer (CRC). Here, we investigated anomalous miR-142-3p expression and its possible functional consequences in primary CRC samples. METHODS: The expression of miR-142-3p was measured by quantitative RT-PCR in 116 primary CRC tissues and adjacent non-tumor tissues. The effect of miR-142-3p up- or down-regulation in CRC-derived cells was evaluated in vitro by cell viability and colony formation assays and in vivo by growth assays in xenografted nude mice. RESULTS: Using quantitative RT-PCR, we found that miR-142-3p was down-regulated in 78.4 % (91/116) of the primary CRC tissues tested when compared to the adjacent non-tumor tissues. We also found that the miR-142-3p mimic reduced in vitro cell viability and colony formation by inducing cell cycle arrest in CRC-derived cells, and inhibited in vivo tumor cell growth in xenografted nude mice. Inversely, we found that the miR-142-3p inhibitor increased the viability and colony forming capacity of CRC-derived cells and tumor cell growth in xenografted nude mice. In addition, we identified CDK4 as a potential target of miR-142-3p by predictions and dual-luciferase reporter assays. Concordantly, we found that miR-142-3p mimics and inhibitors could decrease and increase CDK4 protein levels in CRC-derived cells, respectively. CONCLUSION: From our results we conclude that miR-142-3p may act as a tumor suppressor in CRC and may serve as a tool for miRNA-based CRC therapy.


Assuntos
Neoplasias Colorretais/genética , Quinase 4 Dependente de Ciclina/genética , Regulação Neoplásica da Expressão Gênica , MicroRNAs/genética , Idoso , Pontos de Checagem do Ciclo Celular , Proliferação de Células , Neoplasias Colorretais/patologia , Regulação para Baixo , Feminino , Células HCT116 , Humanos , Masculino , Pessoa de Meia-Idade
18.
Psychiatry Res ; 270: 627-630, 2018 12.
Artigo em Inglês | MEDLINE | ID: mdl-30384282

RESUMO

Glutamate is involved in mental disorders and nicotine addiction. The aim of the present study was to evaluate the relationship between cerebrospinal fluid (CSF) glutamate levels and mental status in Chinese heavy smokers. Participants comprised 41 non-smokers and 77 heavy smokers (n = 118). Cerebrospinal fluid was extracted and glutamate levels were measured. We recorded age, years of education, BMI, the Barratt impulsiveness scale (BIS), the Beck Depression Inventory (BDI) and the Self-Rating Anxiety Scale (SAS). BIS action scores, total scores and BDI scores were significantly different between the groups. Partial correlation analyses with age and education years as covariates found that CSF glutamate levels negatively correlated with BDI scores, but did not correlate with SAS scores in heavy smokers. No correlation was found between CSF glutamate levels and BDI or SAS scores in non-smokers. In conclusion, heavy smokers had more impulsivity had lower levels of CSF glutamate and higher BDI scores. CSF glutamate levels negatively correlated with BDI scores in heavy smokers.


Assuntos
Transtorno Depressivo/líquido cefalorraquidiano , Ácido Glutâmico/líquido cefalorraquidiano , Escalas de Graduação Psiquiátrica/estatística & dados numéricos , Fumar/líquido cefalorraquidiano , Adolescente , Adulto , China , Correlação de Dados , Transtorno Depressivo/diagnóstico , Transtorno Depressivo/psicologia , Humanos , Masculino , Pessoa de Meia-Idade , Psicometria/estatística & dados numéricos , Valores de Referência , Fumar/efeitos adversos , Fumar/psicologia , Adulto Jovem
19.
Food Funct ; 9(11): 6020-6028, 2018 Nov 14.
Artigo em Inglês | MEDLINE | ID: mdl-30397690

RESUMO

Lactobacillus fermentum KP-3 was isolated from Korean pickle and used to ferment ginseng. The changes in the minor ginsenosides in the fermented ginseng were analyzed and the material was evaluated in high fat diet-fed mice. Total ginsenosides increased from 0.746 mg g-1 to 0.939 mg g-1 after fermentation, and the levels of minor ginsenosides (Rg2, Rg3, Rh1, Rh2, F2, and Ro) increased from 0.186 mg g-1 to 0.704 mg g-1. In an animal study, the serum TC and LDL levels in the HFD group were significantly higher than those of the control group. Compared with the HFD group, the probiotic-fermented ginseng significantly decreased the serum TC and LDL levels. In addition, the serum and liver ALT and AST levels were dramatically increased in the HFD group, but these increases were significantly inhibited by treatment with the probiotic-fermented ginseng. Furthermore, fermented ginseng reduced high fat diet-induced liver lipid accumulation. Overall, fermentation with L. fermentum KP-3 enhanced minor ginsenosides in ginseng and this probiotic-fermented ginseng ameliorated hyperlipidemia and liver injury induced by a high fat diet.


Assuntos
Ginsenosídeos/farmacologia , Hiperlipidemias/tratamento farmacológico , Lactobacillus fermentum/metabolismo , Hepatopatias/tratamento farmacológico , Panax/química , Alanina Transaminase/sangue , Animais , Aspartato Aminotransferases/sangue , Glicemia/metabolismo , Colesterol/sangue , Dieta Hiperlipídica , Fermentação , Microbiologia de Alimentos , Hiperlipidemias/sangue , Fígado/efeitos dos fármacos , Fígado/metabolismo , Hepatopatias/sangue , Masculino , Camundongos , Camundongos Endogâmicos C57BL , Extratos Vegetais/farmacologia , Probióticos , Triglicerídeos/sangue
20.
J Cell Mol Med ; 22(12): 6294-6303, 2018 12.
Artigo em Inglês | MEDLINE | ID: mdl-30320493

RESUMO

Diabetic nephropathy (DN) is one of general and common complication of diabetes, which severely affects the physical and mental health of diabetic patients. Fibroblast growth factor 1 (FGF1), an effective control agent of blood glucose, plays an effective treatment role on diabetes-induced renal injury. But the specific molecule mechanism underlying it is still unclear. Since induction of cellular stress is the main and common mechanism of diabetes-induced complication, we hypothesized that reduction of cellular stress is also the molecular mechanism of FGF1 treatment for DN. Here, we have further confirmed that FGF1 significantly ameliorated the diabetes-induced renal interstitial fibrosis and glomerular damage. The expression levels of collagen and α-smooth muscle actin (α-SMA) also dramatically induced in kidney from db/db mice, but these effects were blocked by FGF1 administration. Our mechanistic investigation had further revealed that diabetes significantly induced oxidative stress, nitrosative stress, and endoplasmic reticulum (ER) stress with upregulation of malondialdehyde (MDA), nitrotyrosine level, ER stress makers and downregulation of antioxidant capacity (AOC). FGF1 treatment significantly attenuated the effect of diabetes on cellular stress. We conclude that FGF1-associated glucose decreases and subsequent reduction of cellular stress is the another potential molecule mechanism underlying FGF1 treatment for DN.


Assuntos
Diabetes Mellitus Experimental/genética , Nefropatias Diabéticas/genética , Fator 1 de Crescimento de Fibroblastos/genética , Fibrose/genética , Animais , Antioxidantes/metabolismo , Glicemia/genética , Diabetes Mellitus Experimental/metabolismo , Diabetes Mellitus Experimental/patologia , Nefropatias Diabéticas/metabolismo , Nefropatias Diabéticas/patologia , Estresse do Retículo Endoplasmático/genética , Fibrose/metabolismo , Fibrose/patologia , Regulação da Expressão Gênica/genética , Humanos , Rim/metabolismo , Rim/patologia , Glomérulos Renais/metabolismo , Glomérulos Renais/patologia , Malondialdeído/metabolismo , Camundongos , Estresse Oxidativo/genética
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