Background

The root of Rehmannia glutinosa (R. glutinosa) is commonly used in various traditional Chinese herbal formulae to ameliorate nephropathy; however, little is known about its active component(s) and mechanisms.

Aim

In the present study, we examined the protective effect and potential mechanism of rehmapicrogenin, a monomeric compound extracted from R. glutinosa, against Adriamycin (ADR)-induced nephropathy (AN) in vivo and in vitro.

Methods

In this study, an ADR-induced kidney injury model was employed to investigate the nephroprotective effects of rehmapicrogenin in mice. In vivo, ELISA kits, flow cytometry, haematoxylin-eosin staining, immunofluorescence techniques, and western blotting were used to evaluate the effect of rehmapicrogenin on kidney injury in mice. In vitro, the effects of rehmapicrogenin on NRK-52E cellular damage induced by ADR were determined using the 3-(4,5-dimethylthiazolyl-2-yl)-2,5-diphenyltetrazolium bromide (MTT) method. The mechanism was investigated using ELISA kits, flow cytometry and In-Cell Western™ blotting.

Results

In vivo, rehmapicrogenin treatment significantly attenuated the pathological changes in the kidney induced by ADR; rescued weight, serum creatinine (Scr), blood urea nitrogen (BUN) and urine albumin (U-ALB) levels; reduced reactive oxygen species (ROS) accumulation; and decreased oxidative stress, the apoptosis rate, and cell survival in ADR-treated mice. Importantly, both in vivo and in vitro experimental results demonstrated that rehmapicrogenin regulates the Nrf2/ARE signalling pathway, the most important pathway for oxidative stress. Rehmapicrogenin attenuated ADR-induced kidney damage by reducing oxidative stress through the oestrogen receptor pathway. Moreover, after treatment with ICI 182780 (the oestrogen receptor-nonspecific antagonist Faslodex), the improvement induced by rehmapicrogenin was significantly reversed.

Conclusions

In conclusion, rehmapicrogenin attenuates kidney damage by reducing inflammatory factor release through the oestrogen signalling pathway.

中文翻译：

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Rehmapicrogenin的肾脏保护作用和机制包括体内和体外通过雌激素样途径抑制ROS

背景

熟地黄（R. glutinosa）的根通常用于各种传统中草药配方中以改善肾病。然而，对其活性成分和机制知之甚少。

目的

在本研究中，我们检查了保护作用和rehmapicrogenin，从提取的单体化合物的潜在机制地黄，对阿霉素（ADR）诱导的肾病（AN）在体内和体外。

方法

在这项研究中，采用ADR诱导的肾脏损伤模型来研究rehmapicrogenin对小鼠的肾脏保护作用。在体内，使用ELISA试剂盒，流式细胞仪，苏木精-伊红染色，免疫荧光技术和Western印迹法来评估rehmapicrogenin对小鼠肾脏损伤的作用。在体外，使用3-（4,5-二甲基噻唑基-2-基）-2,5-二苯基四唑溴化物（MTT）方法测定了瑞克帕克罗丁菌素对ADR诱导的NRK-52E细胞损伤的影响。使用ELISA试剂盒，流式细胞仪和In-Cell Western™印迹对机理进行了研究。

结果

在体内，Rehmapicrogenin治疗可显着减轻ADR所致肾脏的病理变化。挽救体重，血清肌酐（Scr），血尿素氮（BUN）和尿白蛋白（U-ALB）水平；减少活性氧（ROS）积累；降低了ADR处理的小鼠的氧化应激，凋亡率和细胞存活率。重要的是，在体内和体外实验结果表明，rehmapicrogenin调节Nrf2 / ARE信号传导途径，这是氧化应激最重要的途径。Rehmapicrogenin通过减少通过雌激素受体途径的氧化应激而减轻了ADR诱导的肾脏损害。此外，在用ICI 182780（雌激素受体非特异性拮抗剂Faslodex）治疗后，rehmapicrogenin引起的改善显着逆转。

结论

总之，Rehmapicrogenin通过减少通过雌激素信号传导途径释放的炎症因子来减轻肾脏损害。