摘要
目的:探讨HIPK2对博来霉素诱导的肺纤维化小鼠的影响。方法:成功构建博来霉素诱导的肺纤维化小鼠模型,构建稳定过表达HIPK2腺病毒载体,设为对照组、模型组和过表达HIPK2组,每组各5只,对肺组织进行HE和Masson染色,并用RT-PCR、Western Blot法测定肺组织中HIPK2和α-SMA含量。结果:博来霉素诱导肺纤维化小鼠模型中HIPK2表达下调(P 【0.05),α-SMA表达上调(P 【0.05),且纤维化程度加重;过表达HIPK2可抑制成纤维细胞的激活,使α-SMA表达下调(P 【0.05),且肺纤维化程度减轻。结论:HIPK2缺乏在肺纤维化机制中具有重要作用,HIPK2可抑制成纤维细胞的激活,减轻肺纤维化。
Objective: To explore the effect of HIPK2 on bleomycin-induced pulmonary fibrosis in mice. Methods: A mouse model of bleomycin-induced pulmonary fibrosis was successfully constructed, and a stable overexpressing HIPK2 adenovirus vector was constructed. 15 mice were divided into Mock group, Ad-Control group, and Ad-HIPK2 group. HE Masson staining was performed on the lung tissue. The expression of mRNA and protein of HIPK2 and α-SMA were used RT-PCR, Western Blot method. Results: The expression of HIPK2 in Bleomycin-induced pulmonary fibrosis mouse was down-regulated (P
出处
《临床医学进展》
2020年第6期1091-1096,共6页
Advances in Clinical Medicine