TRPC5在间歇性低氧诱导的心肌细胞损伤中的作用OA

Objective To explore the effects and possible mechanisms of transient receptor potential channel 5(TRPC5)on cardio-myocyte injury under intermittent hypoxia(IH)conditions.Methods A total of 100 snoring patients(aged 18-75 years)admitted to the First Affiliated Hospital of Xinjiang Medical University from January 2023 to June 2024 were included.Participants underwent polysomnography(PSG)and were divided into obstructive sleep apnea-hypopnea syndrome(OSAHS)group(n=50)and non-OSAHS group(n=50).Demographic data,laboratory results,and echocardiographic parameters were collected.TRPC5 mRNA levels in pe-ripheral blood mononuclear cells(PBMCs)and serum interleukin-1β(IL-1β),IL-18,and TNF-α levels were measured.Spearman cor-relation analysis was used to assess the relationships between TRPC5 and sleep monitoring parameters,echocardiographic indices,and inflammatory cytokines.In vitro experiments,an intermittent hypoxia(IH)cell model was established to simulate OSAHS.H9C2 cardiomyocytes were transfected with lentiviral vectors to construct TRPC5-overexpressing(TRPC5 OE)and empty vector control(TRPC5 NC)models.Cells were exposed to normoxia or IH and divided into four groups:normoxia+TRPC5 NC group,normoxia+TRPC5 OE group,IH+TRPC5 NC group,and IH+TRPC5 OE group.Flow cytometry was used to detect cardiomyocyte apoptosis rate.ELISA was performed to measure IL-1β,IL-18,and TNF-α levels in cell supernatants.Western blotting was applied to analyze pro-tein expressions of TRPC5,NLRP3,Caspase-1,and GSDMD in H9C2 cells.Results Compared with non-OSAHS controls,TRPC5 mRNA expression was significantly elevated in PBMCs,and serum IL-1β,IL-18,and TNF-α levels were increased in OSAHS patients(all P<0.05).Spearman analysis revealed TRPC5 was positively correlated wtih apnea-hypopnea index(AHI),oxygen desatu-ration index(ODI),left atrial diameter(LAD),and IL-1β(P<0.05),while negatively correlated with E/A ratio(P=0.013)and mean oxygen saturation(MSaO2,P=0.015).Compared with normoxia group,the apoptosis rate of H9C2 cells significantly increased in IH group,and the levels of TRPC5,IL-1β,IL-18,TNF-α,NLRP3,Caspase-1,and GSDMD were upregulated(all P<0.05).Compared with IH+TRPC5 NC group and normoxia+TRPC5 OE group,the cardiomyocyte apoptosis was enhanced and the levels of IL-1β,IL-18,TNF-α,NLRP3,Caspase-1,and GSDMD were elevated in IH+TRPC5 OE group(all P<0.05).Conclusion IH promotes the cardiomyocyte injury and inflammatory cytokine release.Overexpression of TRPC5 aggravates IH-induced cardiomyocyte injury by en-hancing the inflammatory response.