High temperature requirement A3 attenuates hypoxia/reoxygenation induced injury in H9C2 cells via suppressing inflammatory responses.

High temperature requirement A3 (HtrA3) belongs to the HtrA family, and its role in inflammation and myocardial ischemia-reperfusion injury remains unknown. Herein, the study aimed to explore the role of HtrA3 in inflammatory cytokine secretion and the nuclear factor kappa B (NF-κB) signaling pathway in hypoxia-reoxygenation (H/R)-induced H9C2 cardiomyoblasts. H9C2 cells were treated with H/R to mimic myocardial ischemia-reperfusion in vitro. Results showed that HtrA3 expression was significantly downregulated and the expression of inflammatory cytokines was regulated in response to H/R. HtrA3 overexpression decreased the secretion of inflammatory cytokines, whereas HtrA3 knockdown led to increase levels of inflammatory cytokines. And H/R-induced inflammation in H9C2 cells was inhibited by the regulation of the NF-κB signaling pathway. Our findings demonstrate that HtrA3 alleviates H/R-induced inflammatory responses in H9C2 cardiomyoblasts, possibly by suppressing the pro-inflammatory NF-κB signaling pathway. [ABSTRACT FROM AUTHOR]