Fasudil hydrochloride prevents cisplatin-induced renal tubular epithelial cell apoptosis via Akt activation and PTEN inhibition
10.3969/j.issn.1000-4718.2015.12.024
- VernacularTitle:盐酸法舒地尔通过活化 Akt 与抑制 PTEN 减轻顺铂导致的肾小管上皮细胞凋亡
- Author:
Deyang KONG
;
Jianbing HAO
;
Xiangmei YE
;
Jie TANG
;
Nana BAO
;
Donghua HOU
- Publication Type:Journal Article
- Keywords:
Fasudil hydrochloride;
Cisplatin;
Acute kidney injury;
Apoptosis;
Rho-associated protein kinase 1
- From:
Chinese Journal of Pathophysiology
2015;(12):2254-2258
- CountryChina
- Language:Chinese
-
Abstract:
AIM:To explore the protective effect of fasudil hydrochloride against cisplatin (CP)-induced renal tubular epithelial cell apoptosis via Akt activation and PTEN inhibition .METHODS:Healthy male Sprague-Dawley ( SD) rats were randomly divided into control group , CP group and CP+fasudil group .All animals were sacrificed 96 h after in-jection of 0.9%saline or CP .Blood samples and kidney tissues were collected to evaluate levels of blood urea nitrogen (BUN), serum creatinine (sCr) and morphological alteration of the kidneys , respectively.The apoptosis of renal tubular epithelium cells was detected by TUNEL.Protein levels of Rho-associated protein kinase 1 (ROCK1), PTEN and Akt were measured by Western blotting and immunohistochemistry .The protein level of p-Akt was analyzed by Western blotting . RESULTS:Compared with control group , the sCr and BUN levels , the expression of ROCK 1 and PTEN and TUNEL-posi-tive cells were increased , while the level of p-Akt was decreased in CP group and CP +fasudil group .The histological structure of the kidneys observed by PAS staining was developed marked structural damage in CP group (P<0.05).Com-pared with CP group, sCr level, the expression of ROCK1 and PTEN and TUNEL-positive cells were decreased, while the level of p-Akt was increased in CP+fasudil group (P<0.05).Very little structural damage was detected in fasudil-treated groups .CONCLUSION:Fasudil hydrochloride has a protective effect on CP-induced renal tubular epithelial cell apoptosis via Akt activation and PTEN inhibition 1.