天津医药

天津医药 ›› 2015, Vol. 43 ›› Issue (3): 259-262.doi: 10.11958/j.issn.0253-9896.2015.03.010

• 实验研究 • 上一篇    下一篇

肌肽对局灶性脑缺血大鼠 bcl-2、 bax 表达的影响

朱洁， 马茜， 王辛， 刘翠梅， 王爱红   

  1. 南京中医药大学护理学院 （邮编 210023）
  • 收稿日期:2014-08-15 修回日期:2014-11-03 出版日期:2015-03-15 发布日期:2015-03-15
  • 通讯作者: 王爱红 E-mail:juliazhujie@126.com
  • 作者简介:朱洁 （1989）， 女， 硕士在读， 主要从事脑血管疾病的基础与临床方面研究
  • 基金资助:
    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）

The influence of carnosine in expression levels of bcl-2 and bax after focal cerebral ischemia in rats#br#

ZHU Jie， MA Qian， WANG Xin， LIU Cuimei， WANG Aihong   

  1. Institute of Nursing, Nanjing University of Chinese Medicine, Nanjing 210023, China
  • Received:2014-08-15 Revised:2014-11-03 Published:2015-03-15 Online:2015-03-15
  • Contact: WANG Aihong E-mail:juliazhujie@126.com

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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。

关键词: 肌肽, 脑缺血, 基因, bcl-2, bcl-2 相关 X 蛋白质, bcl-2/bax

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 randomly divided into 3 groups: sham-operated group, model group and carnosine treated group (n=10 for each group). The middle 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 saline (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 decreased while the expression of bax was increased in model group (P<0.05). Compared with model group, carnosine could significantly 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.

Key words: carnosine, brain ischemia, genes, bcl-2, bcl-2-associated X protein, bcl-2/bax