Abstract
BackgroundLiver 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.MethodsIn 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.ResultsDEX 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.ConclusionsDEX 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.
Highlights
Liver injury seriously threatens the health of people
oxygen and glucose deprivation (OGD) notably induced the apoptosis of WRL-68 cells, while the apoptotic effect of OGD was partially rescued in the presence of dexmedetomidine hydrochloride (DEX) (Fig. 1 c)
OGD treatment significantly inhibited the expression of Bcl-2 but increased the level of Bax in WRL-68 cells, while the effect of OGD on these two proteins was partially reversed by using DEX (Fig. 1d)
Summary
Liver injury seriously threatens the health of people. Dexmedetomidine hydrochloride (DEX) can protect against liver injury. The mechanism by which Dex mediates the progression of liver injury remains unclear. Liver injury is a common and serious injury in abdominal trauma. Its incidence ranks second only to spleen rupture, and there are many complications of liver injury [1, 2]. Liver injury usually results from the excessive consumption of alcohol, infections, and xenobiotics, et al [3]. It usually leads to liver failure and even death. Surgery is the main treatment for liver injury, while the mortality of liver failure has been maintained at a high level [4]. It is of great significance to explore the therapeutic targets against liver injury
Sign-in/Register to view highlights & summary Sign-in/Register to access full text options 
Talk to us
Join us for a 30 min session where you can share your feedback and ask us any queries you have
Schedule a callDisclaimer: All third-party content on this website/platform is and will remain the property of their respective owners and is provided on "as is" basis without any warranties, express or implied. Use of third-party content does not indicate any affiliation, sponsorship with or endorsement by them. Any references to third-party content is to identify the corresponding services and shall be considered fair use under The CopyrightLaw.
