Tetrahydrocurcumin exhibited protective potential against septic cardiomyopathy in a mouse model by reducing oxidative stress and inflammation through the regulation of JNK/ERK signaling.
Does tetrahydrocurcumin prevent myocardial dysfunction in a lipopolysaccharide-induced mouse model of sepsis?
Tetrahydrocurcumin demonstrates protective effects against septic cardiomyopathy in a preclinical mouse model by reducing oxidative stress, inflammation, and apoptosis via JNK/ERK signaling.
BACKGROUND: Acute myocardial dysfunction in patients with sepsis is attributed to oxidative stress, inflammation, and cardiomyocyte loss; however, specific drugs for its prevention are still lacking. Tetrahydrocurcumin (THC) has been proven to contribute to the prevention of various cardiovascular diseases by decreasing oxidative stress and inflammation. This study was performed to investigate the functions and mechanism of action of THC in septic cardiomyopathy. METHODS: After the oral administration of THC (120 mg/kg) for 5 consecutive days, a mouse model of sepsis was established via intraperitoneal lipopolysaccharide (LPS, 10 mg/kg) injection. Following this, cardiac function was assessed, pathological section staining was performed, and inflammatory markers were detected. RESULTS: expression. Furthermore, upon THC treatment, Bcl-2 expression was significantly increased, along with a decline in Bax and cleaved caspase-3 expression, which reduced cardiomyocyte loss. CONCLUSION: Our findings indicate that THC exhibited protective potential against septic cardiomyopathy by reducing oxidative stress and inflammation through the regulation of JNK/ERK signaling. The findings of this study provide a basis for the further evaluation of THC as a therapeutic agent against septic cardiomyopathy.
Zhu et al. (Sat,) conducted a other in Septic cardiomyopathy. Tetrahydrocurcumin (THC) was evaluated on Cardiac function, pathological section staining, and inflammatory markers. Tetrahydrocurcumin exhibited protective potential against septic cardiomyopathy in a mouse model by reducing oxidative stress and inflammation through the regulation of JNK/ERK signaling.