同源结构域相互作用蛋白激酶2 (HIPK2)对博来霉素诱导小鼠肺纤维化的影响

The Effect of HIPK2 on Bleomycin-Induced Pulmonary Fibrosis in Mice

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。

Abstract: 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 < 0.05), α-SMA expression up-regulated (P < 0.05), and the degree of fibrosis increased; overexpression of HIPK2 can inhibit fibroblast activation, down-regulate the expression of α-SMA (P < 0.05), and the degree of pulmonary fibrosis was reduced. Conclusion: HIPK2 deficiency plays an important role in the mechanism of pulmonary fibrosis. HIPK2 can inhibit the activation of fibroblasts and reduce pulmonary fibrosis.