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首页> 外文期刊>American Journal of Physiology >Oxidative stress in the pathogenesis of experimental mesangial proliferative glomerulonephritis.
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Oxidative stress in the pathogenesis of experimental mesangial proliferative glomerulonephritis.

机译：氧化应激在实验性系膜增生性肾小球肾炎的发病机理中。

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摘要

Reactive oxygen species (ROS) are increasingly believed to be important intracellular signaling molecules in mitogenic pathways involved in the pathogenesis of glomerulonephritis (GN). We explored the effects of the antioxidants alpha-lipoic acid and N-acetyl-l-cysteine on ERK activation in cultured mesangial cells and the role of ERK activation in the severity of glomerular injury in a rat model of anti-Thy 1 GN. In cultured mesangial cells, growth factors stimulated ERK phosphorylation by 150-450%. Antioxidants reduced this increase by 50-60%. Induction of anti-Thy 1 nephritis in rats led to a 210% increase in glomerular ERK phosphorylation. This increase in phosphorylated ERK was reduced by 50% in animals treated with alpha-lipoic acid. Treatment with alpha-lipoic acid resulted in significant improvement of glomerular injury. Cellular proliferation was reduced by 100%, and the number of proliferating cell nuclear antigen-positive cells was reduced by 64%. The increased expression of glomerular transforming growth factor-beta1 protein and mRNA in rats with anti-Thy 1 nephritis was significantly attenuated and mesangial cell transformation into myofibroblasts was completely prevented by treatment with alpha-lipoic acid. The effects of alpha-lipoic acid were at least partially due to inhibition of oxidative stress. In rats with anti-Thy 1 nephritis, ROS production was increased 400-500%, and this increase was inhibited by 55% by treatment with alpha-lipoic acid. We suggest that ROS may mediate glomerular injury by inducing ERK phosphorylation. alpha-Lipoic acid should be considered a potential therapeutic agent in certain types of human GN.
机译：越来越多地认为，活性氧（ROS）是参与肾小球肾炎（GN）发病机理的有丝分裂途径中重要的细胞内信号分子。我们在抗Thy 1 GN大鼠模型中探索了抗氧化剂α-硫辛酸和N-乙酰基-1-半胱氨酸对系膜细胞ERK活化的影响以及ERK活化在肾小球损伤严重程度中的作用。在培养的系膜细胞中，生长因子刺激ERK磷酸化达150-450％。抗氧化剂使这种增加减少了50-60％。在大鼠中诱导抗Thy 1肾炎导致肾小球ERK磷酸化增加210％。在用α-硫辛酸治疗的动物中，磷酸化ERK的这种增加减少了50％。用α-硫辛酸治疗可显着改善肾小球损伤。细胞增殖减少了100％，增殖细胞核抗原阳性细胞的数量减少了64％。抗Thy 1肾炎大鼠肾小球转化生长因子β1蛋白和mRNA的表达明显减弱，用α-硫辛酸处理可完全阻止肾小球膜细胞转化为成纤维细胞。 α-硫辛酸的作用至少部分是由于抑制了氧化应激。在患有抗Thy 1肾炎的大鼠中，ROS的产生增加了400-500％，而用α-硫辛酸治疗后，ROS的产生被抑制了55％。我们建议ROS可能通过诱导ERK磷酸化来介导肾小球损伤。在某些类型的人类GN中，α-硫辛酸应被视为潜在的治疗剂。

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