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Aim:To explore whether overexpression of the small heat shock protein HSP20 inrat cardiomyocytes protects against simulated ischemia/reperfusion(SI/R)injury.Methods:Recombinant adenovirus expressing HSP20 was used to infect rat H9c2cardiomyocytes at high efficiency,as assessed by green fluorescent protein.H9c2cells were subjected to SI/R stress;survival was estimated through assessment oflactate dehydrogenase and cell apoptosis through caspase-3 activity.Results:Overexpression of HSP20 decreased lactate dehydrogenase release by 21.5% andcaspase-3 activity by 58.8%.Pretreatment with the protein kinase C inhibitor Ro-31-8220(0.1 μmol/L)for 30 min before SI/R canceled the protective effect of HSP20.The selective mitochondrial K+awP channel inhibitor 5-hydroxydecanoate(100 μmol/L)had a similar effect.However,the non-selective K~+_(ATP)channel inhibitorglibenclamide(100 μmol/L)had no significant effect.Conclusion:These dataindicate that the protective effect of HSP20 in vitro is primarily due to reducednecrotic and apoptotic death of cardiomyocytes,possibly via the protein kinaseC/mitochondrial K~+ATP pathway.
Aim: To explore whether overexpression of the small heat shock protein HSP20 inrat cardiomyocytes protects against simulated ischemia / reperfusion (SI / R) injury. Methods: Recombinant adenovirus expressing HSP20 was used to infect rat H9c2 cardiomyocytes at high efficiency, as assessed by green fluorescent protein .H9c2cells were subjected to SI / R stress; survival was estimated through assessment of lactate dehydrogenase and cell apoptosis through caspase-3 activity. Results: Overexpression of HSP20 decreased lactate dehydrogenase release by 21.5% and caspase-3 activity by 58.8% .Pretreatment with the protein kinase C inhibitor Ro-31-8220 (0.1 μmol / L) for 30 min before SI / R canceled the protective effect of HSP20. The selective mitochondrial K + awP channel inhibitor 5-hydroxydecanoate (100 μmol / L) had a similar effect. However, the non-selective K ~ + (ATP) channel inhibitorglibenclamide (100 μmol / L) had no significant effect. Conlusion: These dataindicate that the protective effect of HSP20 in vitro is primaril y due to reduced necrotic and apoptotic death of cardiomyocytes, possibly via the protein kinase C / mitochondrial K ~ + ATP pathway.