摘要
目的研究肌肽对局灶性脑缺血大鼠缺血皮质区B淋巴细胞瘤/白血病-2(bcl-2)、bcl-2相关蛋白X(bax)表达的影响。方法 30只SPF级雄性SD大鼠随机分为假手术组、模型组和肌肽组,每组10只。模型组和肌肽组以线栓法制作大鼠永久性脑缺血模型,肌肽组于造模后予肌肽水溶液灌胃[1 000 mg/(kg·d)],其余2组予等量生理盐水灌胃。分别于造模后清醒时、24 h、72 h通过神经功能缺损评分观察神经功能,于72 h采用2,3,5-三苯基氯化四氮唑(TTC)染色观察脑梗死体积、HE染色观察病理形态学改变,并用免疫组化法检测bcl-2和bax表达。结果肌肽组神经功能评分72 h较模型组降低(P<0.05);脑组织缺血损伤病理学改变轻于模型组;脑梗死体积72 h较模型组减小(P<0.01);脑缺血后72 h与假手术组相比,模型组bcl-2表达下降、bax表达上升、bcl-2/bax比值下降(均P<0.05);经肌肽处理后bcl-2表达上升、bax表达下降,bcl-2/bax比值上升(P<0.01或P<0.05)。结论肌肽处理能提高bcl-2表达、降低bax表达及提高bcl-2/bax比值,这可能是肌肽发挥神经保护作用的分子机制之一。
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 bct-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.
出处
《天津医药》
CAS
2015年第3期259-262,I0004,共5页
Tianjin Medical Journal
基金
江苏省青蓝工程项目资助
江苏省优势学科项目资助项目(YSHL0201-26)
