Borneol attenuates inflammation and inhibits cardiac remodeling after myocardial infarction in mice via TRPM8.

AIM: To examine the effects of borneol on inflammation and myocardial remodeling after myocardial infarction (MI) in mice, and to investigate the underlying mechanisms. METHODS: Eight-week-old wild-type (WT) C57BL/6 mice and transient receptor potential cation channel subfamily M member 8 (TRPM8) gene knockout ( TRPM8^-/-) mice were randomly divided into sham and MI groups, and were subsequently treated with normal saline (control group) or borneol (borneol group) via gavage. Survival curves were plotted for WT and TRPM8mice with MI treated with or without borneol. After 28 d, cardiac function of the mice was assessed through echocardiography, and haemodynamic indexes were evaluated using a multi-channel physiological instrument. Infarct size, myocardial hypertrophy and interstitial fibrosis were assessed via pathological staining. In addition, inflammatory response in the peri-infarct region was detected. RESULTS: The TRPM8 expression was up-regulated in the peri-infarct region of the mice with MI (P<0. 05), and borneol had no effect on TRPM8 expression (P>0. 05). Borneol increased the survival rate, reduced the infarct size, inhibited cardiac remodeling and improved cardiac function in WT mice with MI (P<0. 05 or P<0. 01). However, it did not affect the survival rate, infarct size, myocardial hypertrophy, myocardial fibrosis or cardiac function in TRPM8mice (P>0. 05). Furthermore, borneol reduced inflammatory cell infiltration and the expression of inflammatory cytokines, tumor necrosis factor-α (TNF-α ), interleukin-1β (IL-1β), IL-6 and monocyte chemotactic protein-1 (MCP-1), in WT mice (P<0. 05 or P<0. 01) but not in TRPM8^-/- mice (P>0. 05). CONCLUSION: Borneol attenuates inflammation, inhibits cardiac remodeling and improves cardiac function in mice with MI via TRPM8. [ABSTRACT FROM AUTHOR]