Hydrogen Sulfide Protects Human Cardiac Fibroblasts Against Tunicamycin-induced Stress Damage
Objective To explore the protective effects of hydrogen sulfide(H2 S)against endoplasmic reticulum stress-in-duced cellular damage and to investigate the mechanisms involving the Caspase3/Bax/Bcl-2 signaling pathway.Methods Human cardiac fibroblasts(HCFs)were randomly divided into four groups:control,sodium hydrosulfide(NaHS),tunica-mycin,and NaHS+tunicamycin.Reactive oxygen species(ROS)levels were detected with DHE staining.Mitochondrial membrane potential was measured using the JC-1 fluorescent probe.Lysosomal activity was assessed using LysoTracker Deep Red.The expressions of Caspase 3,Bax,and Bcl-2 were determined by Western blot,and apoptosis was assessed by Annexin V.Results Compared with the control group,the tunicamycin group had increased ROS levels,lysosomal activity,and cell apoptosis,alongside decreased mitochondrial membrane potential,enhanced expressions of Caspase 3 and Bax,and lowered expression of Bcl-2.Compared with the tunicamycin group,NaHS in the NaHS+tunicamycin group reduced cellular ROS production,lysosomal activity,cell apoptosis,and prevented loss of membrane potential,with decreased ex-pressions of Caspase 3 and Bax while increased expression of Bcl-2.Conclusion H2 S provides protection against tunicamy-cin-induced cellular damage in human cardiac fibroblasts.Its mechanism is associated with preserving mitochondrial func-tion and inhibiting the Caspase 3/Bax/Bcl-2 signaling pathway.
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