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首页> 外文期刊>Cellular Physiology and Biochemistry >Carnosine prevents apoptosis of glomerular cells and podocyte loss in stz diabetic rats
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Carnosine prevents apoptosis of glomerular cells and podocyte loss in stz diabetic rats

机译：肌肽可预防stz糖尿病大鼠肾小球细胞凋亡和足细胞丢失

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摘要

We identified carnosinase-1 (CN-1) as risk-factor for diabetic nephropathy (DN). Carnosine, the substrate for CN-1, supposedly is a protective factor regarding diabetic complications. In this study, we hypothesized that carnosine administration to diabetic rats might protect the kidneys from glomerular apoptosis and podocyte loss. Methods: We examined the effect of oral L-carnosine administration (1g/kg BW per day) on apoptosis, podocyte loss, oxidative stress, AGEs and hexosamine pathway in kidneys of streptozotocin-induced diabetic Wistar rats after 3 months of diabetes and treatment. Results: Hyperglycemia significantly reduced endogenous kidney carnosine levels. In parallel, podocyte numbers significantly decreased (-21% compared to non-diabetics, p<0.05), apoptotic glomerular cells numbers increased (32%, compared to non-diabetic, p<0.05) and protein levels of bax and cytochrome c increased (175% and 117%). Carnosine treatment restored carnosine kidney levels, prevented podocytes loss (+23% compared to diabetic, p<0.05), restrained glomerular apoptosis (-34% compared to diabetic; p<0.05) and reduced expression of bax and cytochrome c (-63% and-54% compared to diabetics, both p<0.05). In kidneys of all diabetic animals, levels of ROS, AGEs and GlcNAc-modified proteins were increased. Conclusion: By inhibition of pro-apoptotic signaling and independent of biochemical abnormalities, carnosine protects diabetic rat kidneys from apoptosis and podocyte loss.
机译：我们确定肌肽酶-1（CN-1）为糖尿病肾病（DN）的危险因素。肌肽，CN-1的底物，可能是糖尿病并发症的保护因素。在这项研究中，我们假设对糖尿病大鼠使用肌肽可以保护肾脏免受肾小球凋亡和足细胞损失。方法：我们研究了口服左旋肌肽（每天1g / kg体重）对糖尿病和治疗3个月后链脲佐菌素诱导的糖尿病Wistar大鼠肾脏细胞凋亡，足细胞丢失，氧化应激，AGEs和己糖胺途径的影响。结果：高血糖症显着降低了内源性肾肌肽水平。同时，足细胞数量显着减少（与非糖尿病相比，-21％，p <0.05），凋亡性肾小球细胞数量增加（与非糖尿病相比，32％，p <0.05），并且bax和细胞色素c的蛋白质水平增加（175％和117％）。肌肽治疗可恢复肌肽肾水平，防止足细胞丢失（与糖尿病相比增加23％，p <0.05），抑制肾小球凋亡（与糖尿病相比-34％; p <0.05）并降低bax和细胞色素c的表达（-63％）和-54％与糖尿病患者相比，两者均p <0.05）。在所有糖尿病动物的肾脏中，ROS，AGEs和GlcNAc修饰蛋白的水平均升高。结论：肌肽通过抑制促凋亡信号传导并且独立于生化异常，可以保护糖尿病大鼠肾脏免于细胞凋亡和足细胞丢失。

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