Liver X Receptors Regulate H9C2Cells Apoptosis Induced By High Glucose Through Mitochondria-mediated Pathway

Objective：1.To observe the viability and apoptosis level of H9C2cells induced by highglucose.2.To investigate the effect of LXRs regulate apoptosis in H9C2cells inducedby high glucose through Mitochondria-mediated pathway.Methods:1. All researches were based on H9C2cells,and divied into five groups: lowglucose group (Control group);D-mannitol group;high glucose group;high glucose+T0901317group;high glucose+5CPPSS-50group.2. The rate of H9C2cells viability of each group were detected by CCK-8detection kit;the lever of ROS in H9C2cells were detected by DCFH-DA kit;themitochondrial membrane potential were detected by Rhodamine123kit;the mRNAexpression of Bax, Bcl-2were detected by qRT-PCR;the expression of CleavedCaspase3protein were detected by Western blot; the rate of H9C2cells apoptosis weredetected by Annexin V-FITC/PI kit.Results:1．The cells viability in high glucose group,high glucose+T0901317group andhigh glucose+5CPPSS-50group compared with that in control group weredecreased(P<0.05), there was no significance difference in D-mannitolgroup(P>0.05);compared with the high glucose group,the cells viability of highglucose+T0901317group was higher(P<0.05),and it was decreased in high glucose+5CPPSS-50group(P<0.05).2．Compared with the control group,the ROS lever in high glucose group,high glucose+T0901317group and high glucose+5CPPSS-50group werehigher(P<0.01),there was no significance difference in D-mannitol group(P>0.05).Compared with that in high glucose group, it was decreased in highglucose+T0901317group(P<0.01), and increased in high glucose+5CPPSS-50group(P<0.01). 3．Mitochondrial membrane potential were decreased in high glucose group,highglucose+T0901317group and high glucose+5CPPSS-50group compared with thecontrol group,there was no significance difference in D-mannitol group.Comparedwith that in high glucose group,it was higher in high glucose+T0901317group,andlower in high glucose+5CPPSS-50group (P<0.01).4．The expression of Bax mRNA were significantly up-regulated in high glucosegroup,high glucose+T0901317group and high glucose+5CPPSS-50group comparedwith the control group (P<0.01),there was no significance difference in D-mannitolgroup (P>0.05). Compared with that in high glucose group,it was decreased in highglucose+T0901317group (P<0.01),and up-regulated in high glucose+5CPPSS-50group(P<0.01).The expression of Bcl-2mRNA were significantly decreased in highglucose group,high glucose+T0901317group and high glucose+5CPPSS-50group,Compared with the control group(P<0.01),there was no significance difference inD-mannitol group （P>0.05).Compared with that in high glucose group, it wasup-regulated in high glucose+T0901317group(P<0.01),and decreased in highglucose+5CPPSS-50group(P<0.01).5．The expression of Cleaved Caspase3protein were significantly up-regulatedin high glucose group,high glucose+T0901317group and high glucose+5CPPSS-50group compared with the control group (P<0.01), there was no significance differencein D-mannitol group (P>0.05).Compared with that in high glucose group,it wasdecreased in high glucose+T0901317group(P<0.01),and up-regulated in highglucose+5CPPSS-50group(P<0.01).6．Apoptosis of H9C2cells significantly increased in high glucose group,highglucose+T0901317group and high glucose+5CPPSS-50group compared with thecontrol group (P<0.01),there was no significance difference in D-mannitol group(P>0.05). Compared with that in high glucose group,it was decreased in highglucose+T0901317group (P<0.01),and increased in high glucose+5CPPSS-50group(P<0.01).Conclusions:1. T0901317can improve the cell viability and reduce the apoptosis rate ofH9C2cells induced by high glucose;while inhibit the LXRs,damage effect more obvious in H9C2cells induced by high glucose.2. LXRs can regulate apoptosis in H9C2cells induced by high glucose throughMitochondria-mediated pathway.