肌肽对局灶性脑缺血大鼠bcl-2、bax表达的影响
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[1000mg/(kg·d)],其余2组予等量生理盐水灌胃。分别于造模后清醒时、24h、72h通过神经功能缺损评分观察神经功能,于72h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72h较模型组降低(P〈0.05)...
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Published in | 天津医药 Vol. 43; no. 3; pp. 259 - 262 |
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Main Author | |
Format | Journal Article |
Language | Chinese |
Published |
南京中医药大学护理学院 邮编210023
2015
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Subjects | |
Online Access | Get full text |
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Summary: | 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[1000mg/(kg·d)],其余2组予等量生理盐水灌胃。分别于造模后清醒时、24h、72h通过神经功能缺损评分观察神经功能,于72h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72h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72h较模型组减小(p〈0.01);脑缺血后72h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。 |
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Bibliography: | carnosine ; brain ischemia; genes, bcl-2; bcl-2-associated X protein ; bcl-2/bax 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 Compare |
ISSN: | 0253-9896 |
DOI: | 10.3969/j.issn.0253-9896.2015.03.010 |