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Fasudil hydrochloride prevents cisplatin-induced renal tubular epithelial cell apoptosis via Akt activation and PTEN inhibition / 中国病理生理杂志
Chinese Journal of Pathophysiology ; (12): 2254-2258, 2015.
Article in Chinese | WPRIM | ID: wpr-483836
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.

Full text: Available Index: WPRIM (Western Pacific) Language: Chinese Journal: Chinese Journal of Pathophysiology Year: 2015 Type: Article

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Full text: Available Index: WPRIM (Western Pacific) Language: Chinese Journal: Chinese Journal of Pathophysiology Year: 2015 Type: Article