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苏木乙酸乙酯提取物对慢性病毒性心肌炎模型小鼠Bcl-2、Bax的影响
引用本文:刘志平,周亚滨,陈会君,张轶铭,崔欣美.苏木乙酸乙酯提取物对慢性病毒性心肌炎模型小鼠Bcl-2、Bax的影响[J].中华中医药学刊,2022(1).
作者姓名:刘志平  周亚滨  陈会君  张轶铭  崔欣美
作者单位:;1.黑龙江中医药大学;2.黑龙江中医药大学附属第一医院;3.黑龙江中医药大学附属第二医院;4.黑龙江省嘉润医院
基金项目:国家自然科学基金青年科学基金(81102590);黑龙江省中医药科研项目(ZHY19-016);黑龙江中医药大学科研基金(201835)。
摘    要:目的观察苏木乙酸乙酯提取物对慢性病毒性心肌炎(VMC)小鼠Bcl-2、Bax的影响,从而探讨其在慢性病毒性心肌炎抗细胞凋亡的作用机制,为治疗慢性病毒性心肌炎提供客观的理论依据。方法采用雄性Balb/c小鼠腹腔反复注射柯萨奇病毒B3(Coxsackieviruses B3,CVB3)的方式,建立慢性病毒性心肌炎动物模型。145只雄性Balb/c小鼠,随机选取10只,作为空白组,其余135只腹腔反复注射CVB3,45 d后成活小鼠随机分为3组,环孢素组给予环孢素溶液初始剂量30 mg/(kg·d),维持剂量20 mg/(kg·d)灌胃;苏木组给予苏木乙酸乙酯提取物溶液700 mg/(kg·d)灌胃;空白组及模型组给予0.2%羧甲基纤维素钠0.2 mL/d灌胃,各组小鼠给药20 d后,分别采用心脏超声检测小鼠心脏功能变化、苏木素-伊红(HE)染色法观察小鼠心肌病理形态改变及免疫组化法检测心肌细胞Bcl-2、Bax蛋白表达水平。结果 (1)与模型组相比,环孢素组、苏木组的左心室射血分数(EF)、左心室短轴缩短率(FS)均明显增加,与环孢素组相比,苏木组的EF、FS均明显增加。(2)与模型组相比,环孢素组、苏木组心肌组织病理损伤程度较轻。(3)与模型组相比,环孢素组、苏木组的Bcl-2蛋白表达明显增加;而环孢素组、苏木组的Bax蛋白均明显降低。与环孢素组相比,苏木组Bcl-2表达增强,而Bax表达降低。结论苏木乙酸乙酯提取物能抑制VMC小鼠心肌细胞凋亡。

关 键 词:苏木乙酸乙酯提取物  病毒性心肌炎  细胞凋亡  BCL-2  BAX

Effects of Ethyl Acetate Extract of Sappanwood on Expressions of Bcl-2 and Bax Proteins in Chronic Viral Myocarditis Mice
LIU Zhiping,ZHOU Yabin,CHEN Huijun,ZHANG Yiming,CUI Xinmei.Effects of Ethyl Acetate Extract of Sappanwood on Expressions of Bcl-2 and Bax Proteins in Chronic Viral Myocarditis Mice[J].Chinese Archives of Traditional Chinese Medicine,2022(1).
Authors:LIU Zhiping  ZHOU Yabin  CHEN Huijun  ZHANG Yiming  CUI Xinmei
Institution:(Heilongjiang University of Chinese Medicine,Harbin 150040,Heilonfyiang,China;The Firsl Hospital Affiliated to Heilongjiang University of Chinese Medicine,Harbin 150040,Heilongjiang,China;The Second Hospital Affiliated to Heilongjiang University of Chinese Medicine,Harbin 150001,Heilongjiang,China;Heilongjiang Jiarun Hospital,Harbin 150001,Heilongjiang,China)
Abstract:Objective To observe the effect of ethyl acetate extract of sappanwood on Bcl-2 and Bax in mice with chronic viral myocarditis, so as to explore its mechanism of action against apoptosis in chronic viral myocarditis and provide objective theoretical basis for the treatment of chronic viral myocarditis. Methods Male Balb/c mice were intraperitoneally injected repeatedly with Coxsackieviruses B3(CVB3) to establish an animal model of chronic viral myocarditis. Ten male Balb/c mice were randomly selected as the blank group, and the remaining 135 male Balb/c mice were intraperitoneally injected with CVB3 repeatedly. After 45 days, the surviving mice were randomly divided into 3 groups. The cyclosporin group was given an initial dose of cyclosporin solution of 30 mg/(kg·d) and a maintenance dose of 20 mg/(kg·d). The sappanwood group was given 700 mg/(kg·d) of ethyl acetate extract solution of sappanwood by gavage. The blank group and the model group were given 0.2% sodium carboxymethyl cellulose 0.2 mL/d by gavage, and the mice in each group were given the drug for 20 days. The cardiac ultrasound was used to detect the changes of cardiac function in mice. HE staining was used to observe the pathological morphological changes of mice myocardium, and immunohistochemical method was used to detect the expression levels of Bcl-2 and Bax proteins in myocardial cells, respectively. Results(1)Compared with those of the model group, EF and FS of the cyclosporine and sappanwood groups were significantly increased, and those of the cyclosporine and sappanwood groups were significantly increased.(2)Compared with those of the model group, the degree of pathological damage of myocardial tissue in the cyclosporine group and sappanwood group was less.(3)Compared with those of the model group, the Bcl-2 protein expression in the cyclosporine group and sappanwood group was significantly increased. The Bax protein in the cyclosporine group and sappanwood group was significantly decreased. Compared with that of the cyclosporine group, the Bcl-2 expression was enhanced in sappanwood group, while the Bax expression was decreased. Conclusion Ethyl acetate extract of sappanwood can inhibit the apoptosis of myocardial cells in VMC mice.
Keywords:ethyl acetate extract of sappanwood  viral myocarditis  cell apoptosis  Bcl-2Bax
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