三七皂苷Fc通过调节SIRT3/SOD2通路部分改善对乙酰氨基酚诱导的急性肾损伤中的肾小管损伤和线粒体损伤。
Notoginsenoside Fc ameliorates renal tubular injury and mitochondrial damage in acetaminophen-induced acute kidney injury partly by regulating SIRT3/SOD2 pathway.
作者信息
Wei Miaomiao, Gao Yuancheng, Cheng Dongsheng, Zhang Haiying, Zhang Wei, Shen Yilan, Huang Qunwei, An Xiaoning, Wang Bing, Yu Zhonghai, Wang Niansong, Chen Hongbo, Xu Youhua, Gui Dingkun
机构信息
College of Fisheries and Life Science, Shanghai Ocean University, Shanghai, China.
Department of Nephrology, Shanghai Sixth People's Hospital Affiliated to Shanghai Jiao Tong University School of Medicine, Shanghai, China.
出版信息
Front Med (Lausanne). 2023 Jan 6;9:1055252. doi: 10.3389/fmed.2022.1055252. eCollection 2022.
INTRODUCTION
Mitochondria dysfunction is one of the primary causes of tubular injury in acute kidney injury (AKI). Notoginsenoside Fc (Fc), a new saponin isolated from Panax notoginseng, exhibited numerous pharmacological actions. However, the beneficial effects of Fc on renal tubular impairment and mitochondrial dysfunction in AKI have not been fully studied.
METHODS
In this study, we established acetaminophen (APAP)-induced AKI model in mice to examine the therapeutic impacts of Fc on AKI.
RESULTS
Our results showed that Fc could decrease the levels of the serum creatinine (Scr), blood urea nitrogen (BUN) and Cystatin C in mice with AKI. Fc also ameliorated renal histopathology, renal tubular cells apoptosis and restored expression of apoptosis-related proteins such as Bax, Bcl-2 and caspase3 (C-caspase3). Additionally, Fc increased the protein expression of SIRT3 and SOD2 in kidneys from mice with AKI. studies further showed Fc reduced the apoptosis of HK-2 cells exposure to APAP, attenuated the loss of mitochondrial membrane potential and decreased the formation of mitochondrial superoxide. Fc also partly restored the protein expression of Bax, Bcl-2, C-Caspase3, SIRT3, and SOD2 in HK-2 cells exposure to APAP.
CONCLUSION
In summary, Fc might reduce renal tubular injury and mitochondrial dysfunction in AKI partly through the regulation of SIRT3/SOD2 pathway.
引言
线粒体功能障碍是急性肾损伤（AKI）中肾小管损伤的主要原因之一。三七皂苷Fc（Fc）是从三七中分离出的一种新皂苷，具有多种药理作用。然而，Fc对AKI肾小管损伤和线粒体功能障碍的有益作用尚未得到充分研究。
方法
在本研究中，我们建立了对乙酰氨基酚（APAP）诱导的小鼠AKI模型，以研究Fc对AKI的治疗作用。
结果
我们的结果表明，Fc可以降低AKI小鼠血清肌酐（Scr）、血尿素氮（BUN）和胱抑素C的水平。Fc还改善了肾脏组织病理学、肾小管细胞凋亡，并恢复了凋亡相关蛋白如Bax、Bcl-2和半胱天冬酶3（C-caspase3）的表达。此外，Fc增加了AKI小鼠肾脏中SIRT3和SOD2的蛋白表达。进一步研究表明，Fc减少了暴露于APAP的HK-2细胞的凋亡，减轻了线粒体膜电位的丧失，并减少了线粒体超氧化物的形成。Fc还部分恢复了暴露于APAP的HK-2细胞中Bax、Bcl-2、C-Caspase3、SIRT3和SOD2的蛋白表达。
结论
总之，Fc可能部分通过调节SIRT3/SOD2途径减轻AKI中的肾小管损伤和线粒体功能障碍。
Zotero 插件