背景:Salidroside,一种来自中药红景天的活性成分,具有多种药理功能,包括抗炎,抗癌和抗氧化特性。然而,红景天苷是否在糖尿病肾病中发挥有益作用尚不清楚。
目的:这项工作的目的是研究红景天苷对糖尿病肾病的潜在作用和潜在的分子机制。
方法:对肥胖小鼠给予链脲佐菌素,制作糖尿病肾病动物模型。将红景天苷给予这些小鼠和蛋白尿,足细胞完整性,肾脏形态学和纤维化,线粒体生物发生进行了检查。
结果:我们的结果表明,红景天苷治疗可大大减轻糖尿病肾病,如尿白蛋白降低所证明,血尿素氮和血清肌酐。形态学分析表明红景天苷改善糖尿病肾病的肾脏结构。红景天苷明显逆转了nephrin和podocin表达的降低。此外,红景天苷在很大程度上预防了糖尿病肾病小鼠的肾纤维化。机械上,在红景天苷治疗的小鼠中,线粒体DNA拷贝和电子传递链蛋白显著增强。同时,在红景天苷存在下,糖尿病肾病中Sirt1和PGC-1α表达的降低几乎被完全抵消。
结论:我们的数据表明,红景天苷在小鼠糖尿病肾病中起着有益的作用,这可能是通过Sirt1/PGC-1α介导的线粒体生物发生。
BACKGROUND: Salidroside, an active component from Traditional Chinese Medicine Rhodiola rosea L., has various pharmacological functions including anti-inflammatory, anti-cancer and anti-oxidative properties. However, whether salidroside plays a beneficial role in diabetic nephropathy is still unclear.
OBJECTIVE: The objective of this work was to investigate the potential roles of salidroside against diabetic nephropathy and the underlying molecular mechanisms.
METHODS: Streptozocin was given to obese mice to generate diabetic nephropathy animal model. Salidroside was administered to these mice and proteinuria, podocyte integrity, renal morphology and fibrosis, mitochondrial biogenesis were examined.
RESULTS: Our results showed that salidroside treatment greatly attenuates diabetic nephropathy as evidenced by decreased urinary albumin, blood urea nitrogen and serum creatinine. Morphological analysis indicated that salidroside improves renal structures in diabetic nephropathy. The decreases in nephrin and podocin expression were markedly reversed by salidroside. Moreover, kidney fibrosis in diabetic nephropathy mice was largely prevented by salidroside. Mechanistically, in salidroside-treated mice, the mitochondrial DNA copy and electron transport chain proteins were significantly enhanced. Meanwhile, the reduced Sirt1 and PGC-1α expression in diabetic nephropathy was almost completely counteracted in the presence of salidroside.
CONCLUSIONS: Our data showed that salidroside plays a beneficial role against diabetic nephropathy in mice, which probably via Sirt1/PGC-1α mediated mitochondrial biogenesis.