Entity

Time filter

Source Type

Shijiazhuang, China

Zhang H.-F.,Hebei Medical University | Shi L.-J.,Hebei Medical University | Song G.-Y.,Hebei Medical University | Cai Z.-G.,Hebei Medical University | And 2 more authors.
Food and Chemical Toxicology | Year: 2013

The present study was aimed to investigate the hepatoprotective effects of matrine against nonalcoholic steatohepatitis induced by a high-fructose diet. After being fed a high-fructose diet (HFD) for 4. weeks, male Wistar rats were orally administered matrine in three different doses (40, 80, or 160. mg/kg) once daily. Serum and liver samples were collected after treatment with matrine for 4. weeks. Lipid droplets within hepatocytes, infiltration of inflammatory cells, and necrotic foci in the liver were morphologically alleviated by matrine in a dose-dependent manner compared with the HFD group. ALT and AST in the blood and the triglyceride content in the liver also decreased. The increased malondialdehyde and depleted glutathione by HFD were ameliorated in a dose-related manner with matrine. Matrine promoted Nrf2 translocation to the nucleus with subsequently up-regulated antioxidative enzyme protein expression, and it enhanced antioxidant activities compared with the HFD group (p<. 0.05). The increased activity of nuclear factor-kappa B in the liver and the tumour necrosis factor-alpha levels in plasma induced by HFD were inhibited by matrine as well (p<. 0.05). In this study, we also found that matrine ameliorated HFD-induced hyperglycaemia and insulin resistance. Taken together, our findings demonstrate that matrine is effective in preventing conversion of high-fructose diet-induced hepatic steatosis into nonalcoholic steatohepatitis in rats. © 2013 Elsevier Ltd. Source


Wang G.,Hebei General Hospital
Zhonghua nan ke xue = National journal of andrology | Year: 2011

To explore the association of spermatogenic arrest with the expression of estrogen receptor alpha (ERalpha) in human testes. We examined the testicular biopsy specimens of 120 infertile men by HE staining, detected the expression of ERalpha in the specimens of those with spermatogenic arrest by the two-step immunohistochemical method, and compared the results with those of 10 healthy men. Of the 120 specimens from the infertile men, 31 (25.8%) met the diagnostic criteria of spermatogenic arrest. In the testis tissue of normal men, ERalpha expressed in Sertoli, myoid and Leydig cells, but not in spermatogenic cells, while in the testis tissues of those with spermatogenic arrest, ERalpha expressed lowly in Sertoli, myoid and Leydig cells, with statistically significant differences in immunostaining intensity between the two groups (P < 0.05). Androgen receptor (AR) and ERalpha may play a coordinating role in facilitating spermatogenesis. Spermatogenic arrest may be related to a complex series of disorders in cell signal transduction involving AR, ERalpha and HSP90. Source


Ma H.,Hebei General Hospital | Patti M.E.,Harvard University | Endocrinologist A.,Harvard University
Best Practice and Research: Clinical Gastroenterology | Year: 2014

Bile acids are increasingly recognized as key regulators of systemic metabolism. While bile acids have long been known to play important and direct roles in nutrient absorption, bile acids also serve as signalling molecules. Bile acid interactions with the nuclear hormone receptor farnesoid X receptor (FXR) and the membrane receptor G-protein-coupled bile acid receptor 5 (TGR5) can regulate incretin hormone and fibroblast growth factor 19 (FGF19) secretion, cholesterol metabolism, and systemic energy expenditure. Bile acid levels and distribution are altered in type 2 diabetes and increased following bariatric procedures, in parallel with reduced body weight and improved insulin sensitivity and glycaemic control. Thus, modulation of bile acid levels and signalling, using bile acid binding resins, TGR5 agonists, and FXR agonists, may serve as a potent therapeutic approach for the treatment of obesity, type 2 diabetes, and other components of the metabolic syndrome in humans. © 2014 Elsevier Ltd. All rights reserved. Source


Zhao Y.,Hebei Medical University | Feng G.,Hebei Medical University | Wang Y.,Hebei Medical University | Yue Y.,Hebei General Hospital | Zhao W.,Hebei Medical University
International Journal of Clinical and Experimental Pathology | Year: 2014

Objective: Long non-coding RNAs (lncRNAs) play important roles in diverse biological processes, such as transcriptional regulation, cell growth and tumorigenesis. However, little was known about whether lncRNA HIF 1 alpha-antisense RNA 1 (HIF1a-AS1) in regulating the proliferation and apoptosis of VSMCs in vitro and the expression of HIF1a-AS1 in serum of TAA patients. Methods: The cell viability was detected by the CCK8 assay. The cell apoptosis was assessed by annexin V-PI double-labeling staining. Expression of genes and proteins were analyzed by real-time PCR and western blotting respectively. Cells were transfected with siRNAs as a gene silencing methods. Results: In serum of TAA patients, the expression of HIF1a-AS1 was significantly increased (superior to 6 folds) compared to the normal control. Moreover, PA induced cell apoptosis in VSMCs in a time- and dose-dependent manner, and the proportion of the apoptotic cells had gained as compared to untreatment group. PA also induced upregulation expression of HIF1a-AS1. We also found that transfection of cells with HIF1a-AS1 siRNA decreased the expression of caspase3 and caspase8 and increased the expression of Bcl2, and protected PA-induced cell apoptosis in VSMCs. Conclusions: HIF1a-AS1 was overexpressed in the thoracoabdominal aorta aneurysm and the interaction between HIF1a-AS1 and apoptotic proteins plays a key role in the proliferation and apoptosis of VSMCs in vitro, which may contribute to the pathogenesis of thoracoabdominal aorta aneurysm. Source


Chen S.C.,Hebei General Hospital
Xi bao yu fen zi mian yi xue za zhi = Chinese journal of cellular and molecular immunology | Year: 2012

EPCs were cultured in high-glucose-medium to induce oxidative stress. Concentration of malonaldehyde (MDA) and nitrogen monoxidum (NO) in culture medium were measured. The function of EPCs and protein expression of GPx-1 and eNOS were determined. Antioxidant alpha lipoic acid (ALA) was used as an intervention factor to explore the mechanism by which glucose induces the damage of EPCs. EPCs were isolated and cultured from 15 Wistar rats (180-200 g). After planted for 4 days and 24 hours of attachment, cells were treated in 3 conditions: normal control group (NC) were cultured with 5 mmol/L glucose; high-glucose group (HS) were cultured with 30 mmol/L glucose; ALA group were cultured with 30 mmol/L glucose+ ALA(40 μg/L). Protein and gene expression of GPx-1 and eNOS were determined by Western blot and reverse transcription(RT-PCR); NO, MDA levels in culture medium were measured after 48 hours of treatment. (1) Effect of different treatment on the secretion of MDA in EPCs: MDA levels in medium treat with high glucose (HS group) after 48h was significantly higher than that in NC group (P<0.05) and decreased after ALA intervention. (2) Effect of different treatment on the protein expression of GPx-1 in EPCs: Protein expression of GPx-1 was significantly lower in EPCs treated with high glucose than that in NC group after 48 hours of treatment while significantly normalized after ALA intervention (P<0.05). (3) Effect of different treatment on eNOS expression and NO secretion: eNOS expression was significantly lower in EPCs treated with high glucose than that in NC group after 48 hours of treatment (P<0.05). NO levels in medium was lower in HS group than in NC group (P<0.05). eNOS expression and NO level were increased after ALA intervention compared with HS group(P<0.05). High-glucose culture induces oxidative stress in EPCs, EPCs cultured in high-glucose medium displays an impaired function shown as an lower anti-oxidative capacity, decreased eNOS expression and NO secretion, Impaired anti-oxidative capacity and NO secretion by high-glucose treatment can be improved by ALA intervention. Source

Discover hidden collaborations