The influence of carnosine in expression levels of bcl-2 and bax after focal cerebral ischemia in rats
10.3969/j.issn.0253-9896.2015.03.010
- VernacularTitle:肌肽对局灶性脑缺血大鼠bcl-2、bax表达的影响
- Author:
Jie ZHU
;
Qian MA
;
Xin WANG
;
Cuimei LIU
;
Aihong WANG
- Publication Type:Journal Article
- Keywords:
carnosine;
brain ischemia;
genes,bcl-2;
bcl-2-associated Xprotein;
bcl-2/bax
- From:
Tianjin Medical Journal
2015;(3):259-262
- CountryChina
- Language:Chinese
-
Abstract:
Objective To explore the effect of carnosine in the expression of B cell lymphomal/leukemia-2 (bcl-2) and bcl-2-associated X protein (bax) after focal cerebral ischemia in rats. Methods Thirty male SD rats (SPF scale) were ran?domly divided into 3 groups:sham-operated group, model group and carnosine treated group (n=10 for each group). The mid?dle cerebral artery occlusion model (MCAO) was induced in model group and carnosine treated group. Rats were received carnosine [1 000 mg/(kg·d), orally] in carnosine treated group, and the other rats were received the same volume of normal sa?line (NS) in shame-operated group and model group. The neurological deficit score was used to evaluate the neurological function at 24 h and 72 h after MCAO. Morphological changes were observed by HE staining. TCC staining was used to label infarct volume, and immunohistochemistry was used to detect the expression of bcl-2 and bax. Results Compared with model group, the score of neurological function and infarct volume were significantly declined in carnosine treated group at 72 h after injury (P<0.05 or P<0.01). The changes of ischemic impairment were lighter in carnosine treated group than that of model group. Compared with sham-operated group, the expression levels of bcl-2 and the ratio of bcl-2/bax were de?creased while the expression of bax was increased in model group (P<0.05). Compared with model group, carnosine could sig?nificantly increase the expression of bcl-2 and the ratio of bcl-2/bax, and reduce the expression of bax (P<0.01 or P<0.05). Conclusion Carnosine can enhance bcl-2 expression, decrease bax expression and increase the ratio of bcl-2/bax, which is likely to be one of the mechanisms of neuroprotection.
