摘要
目的检测高迁移率族蛋白B1(HMGB1)和α平滑肌肌动蛋白(α-SMA)在博莱霉素(BLM)致小鼠肺纤维化模型肺内的表达水平,探讨HMGB1在肺纤维化发病机制中的作用。方法取20只4.6周龄C57BL/6雄性小鼠,随机分为BLM组和生理盐水(NS)对照组,每组10只。分别向气管内灌注BLM(3mg/kg)和NS,10d后处死小鼠。应用RT—PCR法检测两组肺组织HMGB1和α—SMA的mRNA表达水平,应用免疫组织化学检测两组肺组织中HMGB1和α-SMA的蛋白表达水平。结果RT-PCR半定量和免疫组织化学半定量分析结果显示,BLM组HMGB1的mRNA和蛋白表达均较NS对照组显著增加(0.61±0.08比0.15±0.02,13.12±1.33比7.92±1.10,P均〈0.01);BLM组α—SMA的mRNA和蛋白表达均较NS对照组显著增加(0.89±0.12比0.60±0.07,13.66±1.01比8.18±1.33,P均〈0.01)。结论在BLM诱导的肺纤维化中肺组织的HMGB1和α—SMA表达增加。肺纤维化病理过程可能与HMGB1表达增加并活化α—SMA的表达有关。
Objective To investigate the expression of high mobility group protein-B1 (HMGBI) and α-smooth muscle actin (α-SMA) in Bleomycin induced pulmonary fibrosis in mice. Methods Twenty C57BL/6 male mice were randomly divided into a Bleomycin group and a control group. The Bleomycin group was treated with Bleomycin(3 mg/kg) by endotracheally injection to induce pulmonary fibrosis. The control group were treated with normal saline(NS). Then they were sacrificed by abdominal aortic bleeding 10 days after the injection. The right lung was stained with hematoxylin-eosin and Masson trichrome respectively for pathological examination. Immunohistochemistry and RT-PCR were performed to identify the protein and mRNA levels of α-SMA and HMGB1 respectively. Results The mRNA (0. 89 ± 0. 12,0. 61 ± 0. 08) and protein( 13.66 ± 1.01,13.12 ± 1.33) expressions of α-SMA and HMGB1 in the Bleomycin group were all significantly higher than those of the control group ( mRNA:0. 60 ± 0. 07,0. 15 ± 0. 02 ; protein :8. 18 ± 1.33, 7. 92 ± 1.10 ; all P 〈 0. 01 ). Conclusions The expressions of HMGB1 and α-SMA are increased in Bleomyein induced pulmonary fibrosis. HMGB1 participates in the pathological process of pulmonary fibrosis probably by activation of the α-SMA expression.
出处
《中国呼吸与危重监护杂志》
CAS
2009年第2期181-185,共5页
Chinese Journal of Respiratory and Critical Care Medicine
基金
国家自然科学基金(编号:30340029)