The Effects Of Lentivirus-mediated LXRs Overexpression On High Glucose-induced Apoptosis In H9C2Cells

Objective:To observe the affect of high glucose to H9C2cells on the expression of Bax, Bcl-2,NF-κB, caspase3and cell apoptosis;To investigate the intervention of lentiviraloverexpression LXRs on high glucose-induced apoptosis in H9C2cells andmechanisms.Methods:H9C2cells were cultured in low sugar(5.5mmol/L glucose as normal control),mannitol (5.5mmol/L glucose+27.5mmol/L mannitol) and high glucose (33mmol/Lglucose) respectively in vitro; The H9C2cells cultured in high glucose were infectedwith lentiviral of GV287-Nr1h3, GV287-Nr1h3and empty vector; The proliferationinhibition rate of H9C2cells was detected by CCK-8; The mRNA expression of Bax, Bclwere detected by qRT-PCR; The Western blot were employed to detect the expression ofNF-κB, cleaved caspase3protein; Hoechst33342staining were used to detect cellsapoptosis rate.Results:1. H9C2cell derived from embryonic rat heart able to normal adherent andgrown in10%normal FBS.2. Compared with control group, there was no significance difference inmannitol group（P>0.05）, the inhibition rate of of H9C2cells were highest in highglucose group and GFP group（P<0.01）; compared with high glucose group, therewas no significance difference in GFP group（P>0.05）, the inhibition rate were lowerin LXRα and LXRβ group（P<0.05）.3. Compared with control group, there was no significance in mannitol group（P>0.05）, the mRNA levels of Bax were higher in high glucose group and GFPgroup（P<0.01）; compared with high glucose, there was no significance in GFP group（P>0.05）, the mRNA levels of Bax were lower in LXRα and LXRβ group（P<0.05）.Compared with control group, there was no significance in mannitolgroup（P>0.05）, the mRNA levels of Bcl-2were lower in high glucose group and GFP group（P<0.01）; compared with high glucose, there was no significance in GFPgroup（P>0.05）, the mRNA levels of Bcl-2were higher in LXRα and LXRβ group（P<0.05）.4. Compared with control group, there was no significance in mannitol group（P>0.05）, the NF-κB, Bax,cleaved caspase3protein were higher in high glucosegroup and GFP group（P<0.01）; Compared with high glucose, there was nosignificance in GFP group（P>0.05）, the NF-κB, Bax,cleaved caspase3protein werelower in LXRα and LXRβ group（P<0.05）.The Bcl-2protein were lower in highglucose group and GFP group（P<0.01）; Compared with high glucose, there was nosignificance in GFP group（P>0.05）, the Bcl-2protein were lower in LXRα andLXRβ group（P<0.05）.5. Compared with control group, there was no significance in mannitol group（P>0.05）, the H9C2cells apoptosis rate were higher in high glucose group and GFPgroup（P<0.01）; Compared with high glucose, there was no significance in GFPgroup（P>0.05）, the apoptosis rate were lower in LXRα and LXRβ group（P<0.05）.Conclusion:(1) High glucose via NF-κB activation induce H9C2cells apoptosis.(2) LXRs overexpression can improve the apoptosis of H9C2cell induced byhigh glucose.(3) LXRs overexpression improve high glucose-induced H9C2cell apoptosis, itmay be related to suppressed high sugar induced NF-κB activation.