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白藜芦醇通过一种依赖肾素-血管紧张素系统抑制的机制促进肾癌细胞的消退。

Resveratrol promotes regression of renal carcinoma cells via a renin-angiotensin system suppression-dependent mechanism.

作者信息

Li Jianchang, Qiu Mingning, Chen Lieqian, Liu Lei, Tan Guobin, Liu Jianjun

机构信息

Laboratory of Urology, Guangdong Medical University, Zhanjiang, Guangdong 524001, P.R. China.

出版信息

Oncol Lett. 2017 Feb;13(2):613-620. doi: 10.3892/ol.2016.5519. Epub 2016 Dec 20.

DOI:10.3892/ol.2016.5519
PMID:28356937
原文链接:https://pmc.ncbi.nlm.nih.gov/articles/PMC5351218/
Abstract

The aim of the present study was to investigate the effect of resveratrol on renal carcinoma cells and explore possible renin-angiotensin system-associated mechanisms. Subsequent to resveratrol treatment, the cell viability, apoptosis rate, cytotoxicity levels, caspase 3/7 activity and the levels of angiotensin II (AngII), AngII type 1 receptor (AT1R), vascular endothelial growth factor (VEGF) and cyclooxygenase-2 (COX-2) were evaluated in renal carcinoma cells. The effects of AngII, AT1R, VEGF and COX-2 on resveratrol-induced cell growth inhibition and apoptosis were also examined. The results indicated that resveratrol treatment may suppress growth, induce apoptosis, and decrease AngII, AT1R, VEGF and COX-2 levels in renal carcinoma ACHN and A498 cells. In addition, resveratrol-induced cell growth suppression and apoptosis were reversed when co-culturing with AT1R or VEGF. Thus, resveratrol may suppress renal carcinoma cell proliferation and induce apoptosis via an AT1R/VEGF pathway.

摘要

本研究的目的是探讨白藜芦醇对肾癌细胞的影响，并探索可能的肾素-血管紧张素系统相关机制。在白藜芦醇处理后，评估肾癌细胞的细胞活力、凋亡率、细胞毒性水平、半胱天冬酶3/7活性以及血管紧张素II（AngII）、血管紧张素II 1型受体（AT1R）、血管内皮生长因子（VEGF）和环氧合酶-2（COX-2）的水平。还研究了AngII、AT1R、VEGF和COX-2对白藜芦醇诱导的细胞生长抑制和凋亡的影响。结果表明，白藜芦醇处理可能抑制肾癌细胞ACHN和A498细胞的生长、诱导凋亡，并降低AngII、AT1R、VEGF和COX-2的水平。此外，与AT1R或VEGF共培养时，白藜芦醇诱导的细胞生长抑制和凋亡被逆转。因此，白藜芦醇可能通过AT1R/VEGF途径抑制肾癌细胞增殖并诱导凋亡。

https://cdn.ncbi.nlm.nih.gov/pmc/blobs/acd0/5351218/b16246aa14d1/ol-13-02-0613-g04.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/acd0/5351218/11c00d6da054/ol-13-02-0613-g00.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/acd0/5351218/69196fdc2976/ol-13-02-0613-g01.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/acd0/5351218/01342e19052a/ol-13-02-0613-g02.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/acd0/5351218/658136258c0d/ol-13-02-0613-g03.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/acd0/5351218/b16246aa14d1/ol-13-02-0613-g04.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/acd0/5351218/11c00d6da054/ol-13-02-0613-g00.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/acd0/5351218/69196fdc2976/ol-13-02-0613-g01.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/acd0/5351218/01342e19052a/ol-13-02-0613-g02.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/acd0/5351218/658136258c0d/ol-13-02-0613-g03.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/acd0/5351218/b16246aa14d1/ol-13-02-0613-g04.jpg

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