Conclusion
Our findings revealed that HES attenuated the LPS-mediated inflammation and apoptosis of H9c2 cells by activating the AMPK/P53 signaling pathway, suggesting that HES may be a potential cardioprotective agent.
Methods
Cell viability was assessed through MTT assay. Tumor necrosis factor (TNF)-α and interleukin (IL)-β expression were quantified through RT-qPCR assay. Secondly, the apoptosis rate was assessed by Terminal deoxynucleotidyl transferase-mediated dUTP nick end labeling assay. Finally, B-cell lymphoma 2 (Bcl-2)- associated X protein (Bax), adenosine monophosphate-activated protein kinase (AMPK), and P53 expression were quantified through western blot assay.
Results
Our results demonstrated that LPS stimulation decreased the cell viability, increased IL-1β and TNF-α expression in H9c2 cells. However, HES treatment significantly increased the cell viability, decreased IL-1β and TNF-α expression in LPS-induced H9c2 cells. In addition, HES significantly increased the phosphorylation level of AMPK. Meanwhile, HES prevented against LPS-mediated the P53 and Bax protein upregulation, and Bcl-2 protein downregulation in H9c2 cells. More interestingly, compound C (an AMPK inhibitor) treatment eliminated the protective effects of HES.