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Protective effect of resveratrol on renal damage in spontaneously hypertensive rats and the related mechanisms
Authors:Huang Xinzhong  Zhang Dingwu  Dai Houyong  Yuan Li  Zhang Yide  Chen Xiaolan  Shi Hui  Fan Yaping
Institution:Department of Nephrology, Affiliated Hospital of Nantong University, Nantong 226001, China; Corresponding author: Fan Yaping, Email: fanyp19107@medmail.com.cn
Abstract:Objective To investigate the protective effect of resveratrol (RSV) on renal damage in spontaneously hypertensive rats (SHR) and the related mechanisms on interleukin-6 (IL-6) and intercellular adhesion molecule-1 (ICAM-1). Methods Twelve male spontaneously hypertensive rats were randomly divided into two groups: model group (SHR, n=6)and RSV group (RSV, n=6). Six male Wistar-Kyoto rats served as control group (WKY, n=6). RSV (20 mg·kg-1·d-1) or vehicle were gavaged for 20 weeks. Microalbuminuria and urinary β2-microglobulin were determined by urine collection from 8:00 to 16:00 at 20th week. Scr, BUN and the renal pathological changes were measured after 20 weeks. Immunohistochemistry staining of fibronectin, collagenⅠ, IL-6 and ICAM-1 were used to analysis the changes of renal fibrosis and inflammation. Real-time PCR and Western blotting were used to measure the expression of IL-6 and ICAM-1 in kidneys. Results Compared with the control group, SHR significantly increased the level of microalbuminuria, urinary β2-microglobulin (P<0.05), but they were diminished in RSV group (P<0.05). The expressions of fibronectin, collagenⅠ, IL-6 and ICAM-1 by immunohistochemistry staining were augmented in SHR group, and were significantly inhibited in RSV group. Compared with the control group, the expressions of renal IL-6, ICAM-1 mRNA and protein were significantly increased in SHR group (P<0.05), and RSV treatment significantly inhibited the up-regulation (P<0.05). Conclusions RSV treatment can attenuate microalbuminuria, urinary β2-microglobulin and renal fibrosis in SHR rats. This renal protective effect is associated with the inhibition of IL-6, ICAM-1 expression, which suggesting that inflammation may be a potential therapeutic target of hypertensive renal damage.
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