Gracillin inhibits apoptosis and inflammation induced by lipopolysaccharide (LPS) to alleviate cardiac injury in mice via improving miR-29a.

Gracillin inhibits apoptosis and inflammation induced by lipopolysaccharide (LPS) to alleviate cardiac injury in mice via improving miR-29a.

Model: Lipopolysaccharide-induced acute cardiac injury (sepsis), with parallel cardiomyocyte culture experiments

Gracillin improved cardiomyocyte viability, reduced lactate dehydrogenase release and apoptosis, preserved cardiac function and suppressed NF-kappaB-driven inflammation in lipopolysaccharide-challenged mice. Protection depended on miR-29a, since the benefit was abrogated by miR-29a suppression.

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