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Damage to the cultured rat mesangial cells by constant and intermittent high glucose / 中华内分泌代谢杂志
Chinese Journal of Endocrinology and Metabolism ; (12): 1063-1066, 2010.
Article in Chinese | WPRIM | ID: wpr-385317
ABSTRACT
Objective To study the impairment and the expression of receptor of advanced glycation endproduct (RAGE) in cultured rat glomerular mesangial cells ( GMC ) induced by constant and intermittent high glucose, and to investigate the pathogenesis of diabetic nephropathy. Methods After being cultured under constant and intermittent high glucose with different concentrations for 24 and 48 hours, the morphological changes of rat mesangial cells were observed, the proliferation of GMC was detected by MTT assay, the activity of superoxide dismutase (SOD)and the level of malondialdehyde (MDA)in supernatant were measured by spectrophotometer,and the expressions of RAGE mRNA were evaluated by RT-PCR. Results ( 1 ) Compared with the control group,the cellular morphology was changed in case of constant and intermittent high glucose. The damage of GMC with intermittent high glucose concentrations was more serious. (2)The activity of SOD was decreased and the level of MDA was raised in case of intermittent high glucose concentrations compared with the constant high glucose concentrations (P<0.05). (3)The expression of RAGE mRNA with intermittent high glucose concentrations was significantly higher than that with constant high glucose concentrations ( P<0. 01 ). Conclusions The damaging effects and increased expression of RAGE in cultured rat GMC induced by blood glucose fluctuation was much worse than that with constant high glucose. The blood glucose fluctuation may be one of the causes that induce diabetic nephropathy.

Full text: Available Index: WPRIM (Western Pacific) Language: Chinese Journal: Chinese Journal of Endocrinology and Metabolism Year: 2010 Type: Article

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Full text: Available Index: WPRIM (Western Pacific) Language: Chinese Journal: Chinese Journal of Endocrinology and Metabolism Year: 2010 Type: Article