阿司匹林对慢性阻塞性肺疾病大鼠气道平滑肌细胞增殖和凋亡的影响及机制Effects of aspirin on the proliferation and apoptosis of airway smooth muscle cells in rats with chronic obstructive pulmonary disease and its mechanism
李晓华,王慧敏,温霞
LI Xiaohua,WANG Huimin,WEN Xia
摘要(Abstract):
目的 探讨阿司匹林对慢性阻塞性肺疾病大鼠气道平滑肌细胞增殖和凋亡的影响。方法 选取30只SD大鼠作为研究对象,随机取10只作为对照组,其余20只建立慢性阻塞性肺疾病大鼠模型,造模成功后随机均分为模型组及阿司匹林组,阿司匹林组给予100 mg/kg的阿司匹林灌胃,对照组与模型组给予等量生理盐水灌胃,连续30 d;灌胃结束后,提取大鼠肺组织进行苏木精-伊红(HE)染色法观察肺组织受损情况,采用Western blot实验检测其凋亡蛋白B淋巴细胞瘤-2蛋白(Bcl-2)、BCL2-Associated X的蛋白质(Bax)的表达;取大鼠气道平滑肌细胞(ASMCs),采用MTT检测细胞活力、Western blot实验检测增殖细胞核抗原(PCNA)、Bcl-2及Bax的表达,采用流式细胞术检测细胞凋亡水平。结果 HE染色结果证明阿司匹林对肺部气道平滑肌组织具有较好的保护作用;MTT检测发现阿司匹林可以抑制慢性阻塞性肺疾病大鼠ASMCs细胞的增殖能力;Western blot实验发现模型组ASMCs中PCNA蛋白表达水平较对照组升高,阿司匹林组ASMCs中PCNA蛋白表达水平较模型组降低(P<0.05);流式细胞术和Western blot实验证明,模型组ASMCs中Bcl-2/Bax比值较对照组升高,阿司匹林组ASMCs中Bcl-2/Bax比值较模型组降低(P<0.05)。结论 阿司匹林可以抑制慢性阻塞性肺疾病大鼠气道平滑肌的增殖并诱导细胞凋亡,还可改善气道重塑以达到延缓慢性阻塞性肺疾病的病程。
Objective The purpose of this study was to investigate the effects of aspirin on the proliferation and apoptosis of airway smooth muscle cells in rats with chronic obstructive pulmonary disease(COPD). Methods Thirty SD rats were selected, with 10 rats randomly assigned to the control group and the remaining 20 rats used to establish the COPD rat model. After successful modeling, the rats were randomly divided into the model group and the aspirin group. The aspirin group received oral administration of 100 mg/kg aspirin, while the control group and the model group received an equivalent amount of saline orally for 30 consecutive days. After oral administration, the airway smooth muscle tissue protein of the rats in each group was extracted and observed for lung tissue damage using Hematoxylin-Eosin staining(HE staining). The expression of apoptosis proteins B-cell lymphoma-2(Bcl-2) and BCL2-Associated X protein(Bax) in the airway smooth muscle tissue of the rats was detected by Western blot. The viability of airway smooth muscle cells(ASMCs) in the three groups was measured by MTT assay, and the expression of proliferating cell nuclear antigen(PCNA) was detected by Western blot. Cell apoptosis of ASMCs was detected by flow cytometry, and the expression of apoptosis proteins Bcl-2 and Bax was detected by Western blot. Results HE staining results showed that aspirin had a protective effect on lung tissue. MTT assay revealed that aspirin inhibited the proliferation of ASMCs in rats with COPD. Western blot analysis showed that the expression of PCNA protein in the model group was increased compared to the control group, while the expression in the aspirin group was downregulated(P<0.05). Flow cytometry and Western blot analysis confirmed that the Bcl-2/Bax ratio was higher in the model group than in the control group, and the Bcl-2/Bax ratio in the aspirin group was downregulated compared to the model group(P<0.05). Conclusion Aspirin can inhibit the proliferation of airway smooth muscle cells in rats with COPD and induce cell apoptosis, thereby improving airway remodeling, and delaying the progression of COPD.
关键词(KeyWords):
阿司匹林;慢性阻塞性肺疾病;气道平滑肌细胞;增殖;凋亡;增殖细胞核抗原
aspirin;chronic obstructive pulmonary disease;airway smooth muscle cell;proliferation;apoptosis;proliferating cell nuclear antigen
基金项目(Foundation): 内蒙古自治区科技计划项目(201802119)
作者(Author):
李晓华,王慧敏,温霞
LI Xiaohua,WANG Huimin,WEN Xia
DOI: 10.19367/j.cnki.2096-8388.2023.09.007
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