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三七皂苷R1通过PI3K/Akt/mTOR信号通路抑制细胞凋亡和激活自噬，减轻葡萄糖诱导的足细胞损伤。

Notoginsenoside R1 attenuates glucose-induced podocyte injury via the inhibition of apoptosis and the activation of autophagy through the PI3K/Akt/mTOR signaling pathway.

作者信息

Huang Guodong, Zou Bingyu, Lv Jianzhen, Li Tongyu, Huai Guoli, Xiang Shaowei, Lu Shilong, Luo Huan, Zhang Yaping, Jin Yi, Wang Yi

机构信息

Department of Nephrology, Ruikang Hospital Affiliated to Guangxi University of Chinese Medicine, Nanning, Guangxi 530011, P.R. China.

Department of Gynecology, Sichuan Academy of Medical Science and Sichuan Provincial People's Hospital, Chengdu, Sichuan 610072, P.R. China.

出版信息

Int J Mol Med. 2017 Mar;39(3):559-568. doi: 10.3892/ijmm.2017.2864. Epub 2017 Jan 20.

DOI:10.3892/ijmm.2017.2864
PMID:28112381
原文链接:https://pmc.ncbi.nlm.nih.gov/articles/PMC5360354/
Abstract

Injury to terminally differentiated podocytes contributes ignificantly to proteinuria and glomerulosclerosis. The aim of this study was to examine the protective effects of notoginsenoside R1 (NR1) on the maintenance of podocyte number and foot process architecture via the inhibition of apoptosis, the induction of autophagy and the maintenance pf podocyte biology in target cells. The effects of NR1 on conditionally immortalized human podocytes under high glucose conditions were evaluated by determining the percentage apoptosis, the percentage autophagy and the expression levels of slit diaphragm proteins. Our results revealed that NR1 protected the podocytes against high glucose-induced injury by decreasing apoptosis, increasing autophagy and by promoting cytoskeletal recovery. The phosphoinositide 3-kinase (PI3K)/Akt/mammalian target of rapamycin (mTOR) signaling pathway was further investigated in order to elucidate the mechanisms responsible for the protective effects of NR1 on podocytes. Our data indicated that treatment with NR increased the phosphorylation levels of PI3K, Akt and mTOR, leading to the activation of the PI3K/Akt/mTOR signaling pathway in podocytes. To the best of our knowledge, this is the first in vitro study to demonstrate that NR1 protects podocytes by activating the PI3K/Akt/mTOR pathway.

摘要

终末分化足细胞的损伤对蛋白尿和肾小球硬化有显著影响。本研究的目的是通过抑制细胞凋亡、诱导自噬以及维持靶细胞中足细胞生物学特性，来研究三七总皂苷R1（NR1）对维持足细胞数量和足突结构的保护作用。通过测定细胞凋亡率、自噬率以及裂孔隔膜蛋白的表达水平，评估NR1在高糖条件下对条件性永生化人足细胞的影响。我们的结果显示，NR1通过降低细胞凋亡、增加自噬以及促进细胞骨架恢复，保护足细胞免受高糖诱导的损伤。为了阐明NR1对足细胞保护作用的机制，进一步研究了磷酸肌醇3激酶（PI3K）/蛋白激酶B（Akt）/雷帕霉素哺乳动物靶蛋白（mTOR）信号通路。我们的数据表明，NR处理可增加PI3K、Akt和mTOR的磷酸化水平，从而激活足细胞中的PI3K/Akt/mTOR信号通路。据我们所知，这是第一项在体外研究中证明NR1通过激活PI3K/Akt/mTOR通路来保护足细胞的研究。

https://cdn.ncbi.nlm.nih.gov/pmc/blobs/ba38/5360354/04aad809f4f3/IJMM-39-03-0559-g08.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/ba38/5360354/8fd4f7c8b029/IJMM-39-03-0559-g00.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/ba38/5360354/c806c08cc57d/IJMM-39-03-0559-g01.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/ba38/5360354/65d210fb2e96/IJMM-39-03-0559-g02.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/ba38/5360354/05b45bcb2ffc/IJMM-39-03-0559-g03.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/ba38/5360354/6c7fd5301f9a/IJMM-39-03-0559-g04.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/ba38/5360354/58dc34b27424/IJMM-39-03-0559-g05.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/ba38/5360354/196faa0861fd/IJMM-39-03-0559-g06.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/ba38/5360354/efc93b4e9b13/IJMM-39-03-0559-g07.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/ba38/5360354/04aad809f4f3/IJMM-39-03-0559-g08.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/ba38/5360354/8fd4f7c8b029/IJMM-39-03-0559-g00.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/ba38/5360354/c806c08cc57d/IJMM-39-03-0559-g01.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/ba38/5360354/65d210fb2e96/IJMM-39-03-0559-g02.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/ba38/5360354/05b45bcb2ffc/IJMM-39-03-0559-g03.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/ba38/5360354/6c7fd5301f9a/IJMM-39-03-0559-g04.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/ba38/5360354/58dc34b27424/IJMM-39-03-0559-g05.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/ba38/5360354/196faa0861fd/IJMM-39-03-0559-g06.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/ba38/5360354/efc93b4e9b13/IJMM-39-03-0559-g07.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/ba38/5360354/04aad809f4f3/IJMM-39-03-0559-g08.jpg

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