Key result
Resveratrol treatment effectively suppressed cold exposure-induced cardiac hypertrophy, ultrastructure damage, and weakened heart functions in mice via inhibiting cardiomyocyte apoptosis.
Why the study?
Does resveratrol prevent cold exposure-induced cardiac hypertrophy and dysfunction in adult male mice?
Does resveratrol prevent cold exposure-induced cardiac hypertrophy and dysfunction in adult male mice?
Resveratrol attenuates low ambient temperature-induced myocardial hypertrophy and cardiac dysfunction in mice, partially by inhibiting cardiomyocyte apoptosis.
Resveratrol attenuates cold-induced cardiac damage in mice; hypothesis-generating for human cardioprotection and requires clinical validation.
BACKGROUND/AIMS: Low ambient temperature is an important risk factor for cardiovascular diseases, and has been shown to lead to cardiac hypertrophy. In this study, we aim to investigate if Resveratrol may inhibit cold exposure-induced cardiac hypertrophy in mice, and if so to clarify its molecular mechanism. METHODS: Adult male mice were randomly assigned to Control group (kept at room temperature), Cold group (kept at low air temperature range from 3°C to 5°C) and Resveratrol treatment group (100mg/kg/day) for eight weeks. HE staining, Masson staining and Transmission electron microscopy were employed to detect cardiac structure, fibrosis and myocardial ultrastructure, respectively. Echocardiogram was used to measure myocardial functions. Western blot was used to detect the expression of MAPK pathway and apoptotic proteins. TUENL assay was performed to evaluate cardiomyocyte apoptosis. qRT-PCR was employed to measure the mRNA level. RESULTS: Cold-treated mice showed a higher heart/body weight ratio and heart weight/tibia length ratio compared with control mice, and Resveratrol treatment may suppress these changes in cold-treated mice. Myocardial cross-section area and cardiac collagen volume were larger in cold group than control group, which also can be attenuated by Resveratrol treatment. Also, Resveratrol improved the ultrastructure damage of myocardium such as myofibril disarray in cold group. Echocardiogram measurement showed that EF and FS values in cold group declined apparently as compared to control group, and Resveratrol may improve the reduction of heart functions. The expression of p-JNK, p-p38 and p-ERK relative to total JNK, p38 and ERK in cold group was not altered in cold group and Resveratrol group as compared to control group. Cold-treated mouse hearts also showed the upregulation of hypertrophy-related miRNA-miR-328 but not miR-23a, and Resveratrol treatment can inhibit the increase of miR-328. Finally, Resveratrol treatment also may suppress apoptosis of myocardium in cold-treated mouse hearts via inhibiting Bax and caspase-3 activation. CONCLUSION: In summary, low ambient temperature can cause enlarged heart, ultrastructure damage of myocardium and weakened functions, and Resveratrol treatment effectively suppressed these changes at least partially via inhibiting cardiomyocyte apoptosis.
No takes yet. Share an insight, caveat, or question.
Yin et al. (2015) studied cold exposure-induced cardiac hypertrophy. Resveratrol vs. Cold group (low air temperature without Resveratrol) and Control group (room temperature) was evaluated on Cardiac hypertrophy, myocardial ultrastructure, and heart functions. Resveratrol treatment effectively suppressed cold exposure-induced cardiac hypertrophy, ultrastructure damage, and weakened heart functions in mice via inhibiting cardiomyocyte apoptosis.
Synapse has enriched 5 closely related papers on similar clinical questions. Consider them for comparative context: