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Apoptosis is closely associated with the occurrence and development of cardiovascular diseases and is considered as one of the crucial pathological processes of cardiomyopathy, sepsis, ischemia/reperfusion injury, myocardial infarction and heart failure. Hesperetin (HES), a flavanone glycoside found in citrus fruit peels, has been known to exhibit several key biological and pharmacological properties. Previous studies have demonstrated the anti-inflammatory, anti-oxidant and anti-tumor functions of HES. However, with regards to the pro- or anti-apoptotic functions of HES, there are several disagreements within the literature. To examine whether HES has protective effects in cardiac apoptosis, the present study examined the role of HES in lipopolysaccharide (LPS)-stimulated H9C2 cardiomyocytes, aiming to clarify the possible mechanisms underlying its effects. In the present study, HES reduced the percentage of viable apoptotic (VA) cells in a flow cytometry analysis. It had an anti-apoptosis function in LPS-stimulated H9C2 cells. To clarify whether HES alleviated LPS-stimulated apoptosis through the mitochondria-dependent intrinsic apoptotic pathway, certain indicators of this pathway were detected, including members of the caspase family. The data revealed that HES attenuated the activation of capase-3 and caspase-9. These results indicated HES has a mitochondria-dependent anti-apoptosis effect in LPS-stimulated H9C2 cells. To explore the possible mechanisms, the protein expression levels of certain markers in the possible signaling pathway were detected, including JNK and Bcl-2 family. As a result, HES downregulated the protein expression of Bax, upregulated the expression of Bcl-2 and attenuated the phosphorylation level of JNK. Therefore, the anti-apoptosis effects of HES were possibly mediated by the JNK/Bax signaling pathway. In conclusion, HES has a mitochondria-dependent anti-apoptosis effect in LPS-induced H9C2 cells via the JNK/Bax signaling pathway.

Hesperetin attenuates mitochondria-dependent apoptosis in lipopolysaccharide-induced H9C2 cardiomyocytes