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1.
Chinese Journal of Hepatology ; (12): 69-72, 2015.
Article in Chinese | WPRIM | ID: wpr-337046

ABSTRACT

<p><b>OBJECTIVE</b>To investigate the anti-oxidative stress and anti-fibrotic mechanisms of adiponectin by examining effects on oxidative stress levels and expression of fibrosis-related signaling factors, including transforming growth factor-beta 1 (TGFb1), collagen I (COL-1), and the adenosine monophosphate-activated protein kinase (AMPK) pathway by using an in vitro HSC-T6 cultured cell system.</p><p><b>METHODS</b>Activated HSC-T6 cells were pre-treated with 1.0 mug/mL adiponectin for 0, 30, 60 and 120 min, or left untreated to serve as controls, and both groups were then exposed to 5 mumol/L H2O2; a portion of the adiponectin-treated oxidative stress-induced cells were treated with an AMPK inhibitor (Compound C). The effects on mRNA levels of TGFb1. and COL-1 were analyzed by real-time PCR, in the levels of secreted TGF-b1 and COL-1 were detected by enzyme-linked immunosorbent assay of supernatants, and in the phosphoAMPK and AMPK protein expressions were detected by Western blotting.</p><p><b>RESULTS</b>Compared to the H2O2 group without adiponectin pre-treatment, the H2O2 group with adiponectin pre-treatment showed significantly increased activity of superoxide dismutase (SOD), decreased content of malondialdehyde (MDA), and decreased gene and protein expressions of TGF-b1 and COL-1 (P less than 0.05). Moreover, inhibition of the AMPK pathway inhibited these adiponectin-mediated effects. The H2O2 group with adiponectin pre-treatment also showed increased levels of phospho-AMPK protein expression, with the maximum effect detected after 120 min of the adiponectin pre-treatment (P less than 0.01).</p><p><b>CONCLUSION</b>Inhibition of oxidative stress is one of the mechanisms of the anti-fibrotic effects of adiponectin. Adiponectin can attenuate oxidative stress levels, resulting in down-regulation of TGFb1 and COL-1 expression through activation of the AMPK pathway.</p>


Subject(s)
Humans , AMP-Activated Protein Kinases , Adiponectin , Cell Line , Collagen Type I , Down-Regulation , Hepatic Stellate Cells , Hydrogen Peroxide , Oxidative Stress , RNA, Messenger , Signal Transduction , Transforming Growth Factor beta1
2.
Chinese Journal of Geriatrics ; (12): 872-874, 2013.
Article in Chinese | WPRIM | ID: wpr-436913

ABSTRACT

Objective To evaluate the clinical effect of exercise therapy on patients with osteoporosis according to osteoporosis quality of life scale(OQOLS)and the changes in biochemical markers of bone metabolism.Methods Totally 94 patients with primary osteoporosis were randomly divided into 2 groups:the intervention group [exercise therapy (Wu Xing Jian Gu Cao) with calcium/vitamin D supplementation for 90 days] and the control group (only calcium/vitamin D supplementation for 90 days].OQOLS and the changes in biochemical markers of bone metabolism were observed before and after treatment.Results Compared with before treatment,25-hydroxy vitamin D[25-(OH) D]levels were increased in control group (33 cases) and intervention group (29 cases) after treatment [(61.2± 11.1) mmol/L vs.(48.1±26.2)mmol/L,both P<0.001],and the enhanced level was higher in the intervention group than in the control group (P<0.05).Compared with before treatment,bone alkaline phosphatase (BALP) was decreased in control and intervention group after treatment (both P<0.05).There were significant differences in OQOLS in both groups between before and after treatment except for the function of physical activities in intervention group (P<0.05).Conclusions The basic and exercise therapy can both increase [25-(OH) D] level,reduce BALP,and have clinical effects on bone metabolism,while exercise therapy has an improvement in osteoporosis quality of life in patients with osteoporosis.

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