Liver injury seriously threatens the health of people. Meanwhile, dexmedetomidine hydrochloride (DEX) can protect against liver injury. However, the mechanism by which Dex mediates the progression of liver injury remains unclear. Thus, this study aimed to investigate the function of DEX in oxygen and glucose deprivation (OGD)-treated hepatocytes and its underlying mechanism. In order to investigate the function of DEX in liver injury, WRL-68 cells were treated with OGD. Cell viability was measured by MTT assay. Cell apoptosis was detected by flow cytometry. Inflammatory cytokines levels were measured by ELISA assay. The interaction between miR-194 and TUG1 or SIRT1 was detected by dual-luciferase reporter. Gene and protein levels were measured by qPCR or western blotting. DEX notably reversed OGD-induced inflammation and apoptosis in WRL-68 cell. Meanwhile, the effect of OGD on TUG1, SIRT1 and miR-194 expression in WRL-68 cells was reversed by DEX treatment. However, TUG1 knockdown or miR-194 overexpression reversed the function of DEX in OGD-treated WRL-68 cells. Moreover, TUG1 could promote the expression of SIRT1 by sponging miR-194. Furthermore, knockdown of TUG1 promoted OGD-induced cell growth inhibition and inflammatory responses, while miR-194 inhibitor or SIRT1 overexpression partially reversed this phenomenon. DEX could suppress OGD-induced hepatocyte apoptosis and inflammation by mediation of TUG1/miR-194/SIRT1 axis. Therefore, this study might provide a scientific basis for the application of DEX on liver injury treatment.

中文翻译：

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盐酸右美托咪定通过激活lncRNA TUG1 / miR-194 / SIRT1信号通路抑制肝细胞凋亡和炎症

肝损伤严重威胁着人们的健康。同时，右美托咪定盐酸盐（DEX）可以预防肝损伤。但是，Dex介导肝损伤进展的机制仍不清楚。因此，本研究旨在研究DEX在氧和葡萄糖剥夺（OGD）处理的肝细胞中的功能及其潜在机制。为了研究DEX在肝损伤中的功能，用OGD处理WRL-68细胞。通过MTT测定法测量细胞活力。通过流式细胞术检测细胞凋亡。通过ELISA测定法测量炎性细胞因子水平。通过双荧光素酶报告基因检测到miR-194与TUG1或SIRT1之间的相互作用。基因和蛋白质水平通过qPCR或蛋白质印迹法测量。DEX显着逆转了OGD诱导的WRL-68细胞炎症和凋亡。同时，通过DEX处理逆转了OGD对WRL-68细胞中TUG1，SIRT1和miR-194表达的影响。然而，在OGD处理的WRL-68细胞中，TUG1敲低或miR-194过表达逆转了DEX的功能。此外，TUG1可以通过使miR-194海绵化来促进SIRT1的表达。此外，敲低TUG1促进了OGD诱导的细胞生长抑制和炎症反应，而miR-194抑制剂或SIRT1过表达则部分逆转了这一现象。DEX可以通过TUG1 / miR-194 / SIRT1轴的介导抑制OGD诱导的肝细胞凋亡和炎症。因此，本研究可能为DEX在肝损伤治疗中的应用提供科学依据。TUG1敲低或miR-194过表达逆转了OGD处理的WRL-68细胞中DEX的功能。此外，TUG1可以通过使miR-194海绵化来促进SIRT1的表达。此外，敲低TUG1促进了OGD诱导的细胞生长抑制和炎症反应，而miR-194抑制剂或SIRT1过表达则部分逆转了这一现象。DEX可以通过TUG1 / miR-194 / SIRT1轴的介导抑制OGD诱导的肝细胞凋亡和炎症。因此，本研究可能为DEX在肝损伤治疗中的应用提供科学依据。TUG1敲低或miR-194过表达逆转了OGD处理的WRL-68细胞中DEX的功能。此外，TUG1可以通过使miR-194海绵化来促进SIRT1的表达。此外，敲低TUG1促进了OGD诱导的细胞生长抑制和炎症反应，而miR-194抑制剂或SIRT1过表达则部分逆转了这一现象。DEX可以通过TUG1 / miR-194 / SIRT1轴的介导抑制OGD诱导的肝细胞凋亡和炎症。因此，本研究可能为DEX在肝损伤治疗中的应用提供科学依据。而miR-194抑制剂或SIRT1过表达可部分逆转此现象。DEX可以通过TUG1 / miR-194 / SIRT1轴的介导抑制OGD诱导的肝细胞凋亡和炎症。因此，本研究可能为DEX在肝损伤治疗中的应用提供科学依据。而miR-194抑制剂或SIRT1过表达可部分逆转此现象。DEX可以通过TUG1 / miR-194 / SIRT1轴的介导抑制OGD诱导的肝细胞凋亡和炎症。因此，本研究可能为DEX在肝损伤治疗中的应用提供科学依据。