Qiang Wang1, Yi Yang2, Ken Chen1, Bing Tang1, Ke Peng1, Zhen Wang1, Ping Yang1, Dachun Yang1, Yongjian Yang1.
Abstract
BACKGROUND: Transient receptor potential melastatin subtype 8 (TRPM8) is a cold-sensing cation channel, mainly localized in the sensory neurons, which can be activated by menthol, a compound with a naturally cold sensation in mint. However, the effect of TRPM8 activation in inflammation and cardiac remodeling after myocardial infarction (MI) is not well defined.
METHODS: TRPM8 knockout (KO) mice (TRPM8-/-) and their wild-type littermates, aged 8 weeks, were randomly divided into sham and MI groups and were fed with chow or chow plus menthol.
RESULTS: Dietary menthol significantly attenuated MI injury, evidenced by decreased survival rates and plasma cardiac troponion I levels, reduced infarct size and cardiomyocytes, declined collagen deposition, and rescued cardiac function and hemodynamics. However, these effects of menthol disappeared when mice were lacking TRPM8. Furthermore, feeding of menthol ameliorated elevated expression of inflammatory cytokines and chemokines, and aggravated inflammation infiltration in the MI mice but not in TRPM8-/- mice. In addition, menthol treatment increased the release of calcitonin gene-related peptide (CGRP), which were absent in TRPM8-/- mice.
CONCLUSIONS: In conclusion, our results suggest that dietary menthol can protect against inflammation and cardiac remodeling after MI through activation of TRPM8. © American Journal of Hypertension, Ltd 2019. All rights reserved. For Permissions, please email: journals.permissions@oup.com.
BACKGROUND: Transient receptor potential melastatin subtype 8 (TRPM8) is a cold-sensing cation channel, mainly localized in the sensory neurons, which can be activated by menthol, a compound with a naturally cold sensation in mint. However, the effect of TRPM8 activation in inflammation and cardiac remodeling after myocardial infarction (MI) is not well defined.
METHODS: TRPM8 knockout (KO) mice (TRPM8-/-) and their wild-type littermates, aged 8 weeks, were randomly divided into sham and MI groups and were fed with chow or chow plus menthol.
RESULTS: Dietary menthol significantly attenuated MI injury, evidenced by decreased survival rates and plasma cardiac troponion I levels, reduced infarct size and cardiomyocytes, declined collagen deposition, and rescued cardiac function and hemodynamics. However, these effects of menthol disappeared when mice were lacking TRPM8. Furthermore, feeding of menthol ameliorated elevated expression of inflammatory cytokines and chemokines, and aggravated inflammation infiltration in the MI mice but not in TRPM8-/- mice. In addition, menthol treatment increased the release of calcitonin gene-related peptide (CGRP), which were absent in TRPM8-/- mice.
CONCLUSIONS: In conclusion, our results suggest that dietary menthol can protect against inflammation and cardiac remodeling after MI through activation of TRPM8. © American Journal of Hypertension, Ltd 2019. All rights reserved. For Permissions, please email: journals.permissions@oup.com.
Entities:
Keywords:
blood pressure; cardiac remodeling; hypertension; inflammation; menthol; myocardial infarction; transient receptor potential melastatin subtype 8
Mesh：
Substances：
Year: 2020
PMID： 31648306 DOI： 10.1093/ajh/hpz162
Source DB: PubMed Journal: Am J Hypertens ISSN： 0895-7061 Impact factor: 2.689