摘要
目的探讨丹参酮对脂多糖(LPS)诱导的肺泡Ⅱ型上皮细胞损伤的影响及其可能作用机制。方法采用LPS诱导的肺泡Ⅱ型上皮细胞建立急性肺损伤模型,随机分组:空白对照组、LPS组、LPS+丹参酮L组、LPS+丹参酮M组、LPS+丹参酮H组、LPS+si-NC组、LPS+si-DLX6-AS1组、LPS+丹参酮+pcDNA-DLX6-AS1组;MTT法、流式细胞术分别就检测细胞增殖及凋亡;ELISA法检测白细胞介素-6(IL-6)、白细胞介素-10(IL-10)、肿瘤坏死因子-α(TNF-α)的水平;qRT-PCR法检测DLX6-AS1的表达量。结果与空白对照组比较,LPS组细胞增殖抑制率和细胞凋亡率升高(P<0.05),IL-6、IL-10、TNF-α的水平升高(P<0.05),DLX6-AS1的表达量升高(P<0.05);与LPS组相比,LPS+丹参酮H组、LPS+丹参酮L组、LPS+丹参酮M组细胞增殖抑制率和细胞凋亡率降低(P<0.05),IL-6、IL-10、TNF-α的水平降低(P<0.05),DLX6-AS1的表达量降低(P<0.05),且呈剂量依赖性;与LPS组、LPS+si-NC组比较,LPS+si-DLX6-AS1组细胞增殖抑制率和细胞凋亡率降低(P<0.05),IL-6、IL-10、TNF-α的水平降低(P<0.05);与LPS+丹参酮组比较,LPS+丹参酮+pcDNA-DLX6-AS1组细胞增殖抑制率和细胞凋亡率升高(P<0.05),IL-6、IL-10、TNF-α的水平升高(P<0.05)。结论丹参酮可通过抑制DLX6-AS1的表达而促进细胞增殖及抑制细胞凋亡、炎症反应从而减轻LPS诱导的肺泡Ⅱ型上皮细胞损伤。
Objective:To explore the effect of tanshinone on lipopolysaccharide(LPS)-induced alveolar typeⅡepithelial cell damage and its possible mechanism.Methods:LPS-induced alveolar typeⅡepithelial cells were used to establish an acute lung injury model,and they were randomly divided into groups:con group,LPS group,LPS+tanshinone L group,LPS+tanshinone M group,LPS+tanshinone H group,LPS+si-NC group,LPS+siDLX6-AS1 group,LPS+tanshinone+pcDNA-DLX6-AS1 group.MTT method and flow cytometry respectively were used to detect cell proliferation and apoptosis.ELISA method was used to detect the levels of IL-6,IL-10,and TNF-α;qRT-PCR was used to detect the expression of DLX6-AS1.Results:Compared with the con group,the cell proliferation inhibition rate and apoptosis rate in the LPS group were increased(P<0.05),the levels of IL-6,IL-10,and TNF-αwere increased(P<0.05),and the expression of DLX6-AS1 was increased(P<0.05).Compared with the LPS group,the cell proliferation inhibition rate and apoptosis rate of the LPS+tanshinone H group,LPS+tanshinone L group and LPS+tanshinone M group were decreased(P<0.05),and the levels of IL-6,IL-10,and TNF-αwere decreased(P<0.05),the expression of DLX6-AS1 was decreased(P<0.05),and was dose-dependent.Compared with the LPS group and LPS+si-NC group,the cell proliferation inhibition rate and apoptosis rate of the LPS+si-DLX6-AS1 group were reduced(P<0.05),and the levels of IL-6,IL-10,and TNF-αwere reduced(P<0.05).Compared with the LPS+tanshinone group,the cell proliferation inhibition rate and apoptosis rate of the LPS+tanshinone+pcDNA-DLX6-AS1 group were increased(P<0.05),and the levels of IL-6,IL-10,and TNF-αwere increased(P<0.05).Conclusion:Tanshinone can promote cell proliferation and inhibit cell apoptosis and inflammation by inhibiting the expression of DLX6-AS1,thereby reducing LPS-induced alveolar typeⅡepithelial cell damage.
作者
余淑菁
余莉萍
李旭成
崔金涛
Yu Shujing;Yu Liping;Li Xucheng;Cui Jintao(Wuhan Special Care Hospital of Hubei Province,Hubei,Wuhan 430021,China.)
出处
《中国中医急症》
2022年第2期225-227,241,共4页
Journal of Emergency in Traditional Chinese Medicine
基金
国家中医药管理局全国名老中医药专家传承工作室建设项目(国中医药人教函【2019】41号)
湖北省卫生健康委员会中医药科研项目(ZY2019M048)。
