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作 者:陈晓明[1] 张伟兵[1] 田晓彦[1] 刘长萍 张慧[1] 赵春雨[1] CHEN Xiao-ming ZHANG Wei-bing TIAN Xiao-yan LIU Chang-ping ZHANG Hui ZHAO Chun-yu(the Fourth Affiliated Hospital of Harbin Medical University, Harbin, Heilongjiang 150001, China)
机构地区:[1]哈尔滨医科大学附属第四医院老年病二科,黑龙江哈尔滨150001 [2]哈尔滨汽轮机厂职工医院内一科,黑龙江哈尔滨150001
出 处:《临床肺科杂志》2017年第3期526-531,共6页Journal of Clinical Pulmonary Medicine
摘 要:目的研究细胞凋亡在大鼠慢性阻塞性肺疾病(简称慢阻肺)形成过程中的作用机制,并探讨盐酸氨溴索对慢阻肺大鼠肺组织细胞凋亡和血清炎症因子的影响。方法 34只健康SD大鼠随机分为3组:A正常对照组、B盐酸氨溴索组、C模型组。采用免疫组化法检测Bcl-2(b cell lymphoma/lewkmia-2)蛋白、Bax(Bcl-2 associated x protein)蛋白及Caspase-3蛋白的表达;采用血清酶联免疫吸附测定法测定各组血清中炎症因子(LTB4、IL-8、SP-D)的浓度。结果与A组比较,C组中Bax蛋白、Caspase-3蛋白以及炎症因子表达增多,Bcl-2蛋白的表达及Bcl-2/Bax减少,差异均显著(P<0.05);与C组比较,B组Bax蛋白、Caspase-3蛋白以及炎症因子表达减少,Bcl-2蛋白的表达及Bcl-2/Bax增高,差异均显著(P<0.05)。结论慢阻肺的发病机制可能与细胞凋亡有关,盐酸氨溴索在慢阻肺肺组织中发挥抗细胞凋亡和抗炎作用,其机制可能在于调控死亡信号通路中Bax、Bcl-2、Caspase-3蛋白的表达以及抑制炎症因子的表达,起到肺保护的作用。Objective To study the mechanism of action of cell apoptosis in rats with chronic obstructive pulmonary disease (COPD) and to discuss the influence of ambroxol on cell apoptosis in lung tissue and serum in- flammatory factors in rats with chronic obstructive pulmonary disease. Methods 34 healthy SD rats were randomly divided into three groups. The normal control group was named A, the ambroxol group was named B, and the COPD model group named C. The expressions of apoptosis markers ( Bcl-2, Bax, Caspase-3) in each group were tested by immunohistochemistry, and the contents of the inflammatory factors ( LTB4, IL-8, SP-D) in each group were tested by ELISA. Results Compared with the group A, the group C had higher expression of Bax, Caspase-3 and inflam- matory factors, and lower expression of Bcl-2 and Bcl-2/Bax ( P 〈 0.05 ). Compared with the group C, the group B had lower expression of Bax, Caspase-3 and inflammatory factors, and higher expression of Bcl-2 and Bel-2/Bax (P 〈 0.05). Conclusion The mechanism of COPD may associate with cell apoptosis. The ambroxol has the effect of anti-apoptosis and anti-inflammatory, and it is probably that the ambroxol could regulate the expression of Bcl-2, Bax and Caspase-3 and inhibit the expression of inflammatory factors, and the protect lung.
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