Curcumin supplementation improves heat-stress-induced cardiac injury of mice: physiological and molecular mechanisms.

Heat stress (HS) causes serious physiological dysfunction associated with cardiovascular diseases. Curcumin (CUR) may increase animal survival and lifespan under HS. However, its effects and mechanism on mammal are underexplored. The goal of this study was to examine the protective effect of CUR on the cardiac health of mice exposed to HS. Mice were divided into six groups (n=8 per group): no-heat treatment (NHT), heat treatment (HT), aspirin, CUR 50 mg/kg/day, CUR 100 mg/kg/day and CUR 200 mg/kg/day. After administration for 4 weeks, except for NHT, other groups were exposed once to HS at 41°C for 20 min. After HS treatment, the physiological-related indexes of blood pressure, rectal temperature and heart rate were measured. Serum biochemical indexes and the levels of cardiac troponin I (cTn-I) in serum and angiotensin II (Ang II) in cardiomyocytes were analyzed. Furthermore, the mRNA and proteins levels of angiotensin receptor 1 (AT1), 78-kDa glucose-regulated protein (GRP78), C/EBP homologous protein (CHOP) and B-cell lymphoma 2 (Bcl-2) were measured. Our results indicated that CUR supplementation could alleviate HS-induced physiological disorders and the increasing of cTn-I and Ang II. The expression of AT1 gene in HT group was significantly higher than that of CUR groups, indicating the cardioprotective effects of CUR. Moreover, the levels of GRP78 and CHOP proteins in the HT group were significantly higher than those of CUR groups, indicating that CUR supplementation reversed the endoplasmic reticulum HS-mediated apoptosis. In summary, CUR supplementation alleviates physiological stress and cardiac damage caused by HS.
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