Why the study?
Does the curcumin analogue C66 protect against diabetic cardiomyopathy through JNK2 inactivation in diabetic mice?
Does the curcumin analogue C66 protect against diabetic cardiomyopathy through JNK2 inactivation in diabetic mice?
The curcumin analogue C66 ameliorates diabetic cardiomyopathy in mice via a mechanism dependent on JNK2 inactivation.
C66 may protect diabetic hearts via JNK2; hypothesis-generating for clinical translation.
Aim Diabetic cardiomyopathy is an independent cardiac injury that can develop in diabetic individuals. Our previous study showed that C66, a curcumin analogue, protects against diabetes‐induced cardiac damage. The present study sought to reveal the underlying mechanisms of C66‐mediated cardioprotection. Methods An experimental diabetic model was established using JNK 2 −/− and wild‐type ( WT ) mice. C66 (5 mg/kg) was administered orally every other day for 3 months. Body weight, plasma glucose levels, cardiac function, and structure were measured. Masson trichrome and TUNEL staining were used to assess myocardial fibrosis and apoptosis, respectively. mRNA and protein levels of inflammation, fibrosis, oxidative stress, and apoptosis molecules were measured by quantitative PCR and Western blot, respectively. Results Neither C66 treatment nor JNK 2 knockout affected body weight or plasma glucose levels. Cardiac inflammation, fibrosis, oxidative stress, and apoptosis were increased in WT diabetic compared to WT control mice, all of which were attenuated by C66 treatment. However, these pathological and molecular changes induced by diabetes were eliminated in JNK 2 −/− diabetic mice compared to JNK 2 −/− control mice, and C66 treatment did not further affect these parameters in JNK 2 −/− diabetic mice. Conclusions Our results indicate that C66 ameliorates diabetic cardiomyopathy by inhibiting JNK 2 relative pathways.
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Li et al. (2018) studied this question.
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