Key result
Luteolin improved cardiac function and attenuated myocardial disorganization and fibrosis in diabetic rats by suppressing JNK/c-Jun-regulated miR-221 and reversing suppressed autophagy.
Why the study?
Does luteolin improve cardiac function and attenuate fibrosis in rats with diabetic cardiomyopathy?
Does luteolin improve cardiac function and attenuate fibrosis in rats with diabetic cardiomyopathy?
Luteolin demonstrates protective effects against diabetic cardiomyopathy in a rat model by modulating the JNK/c-Jun/miR-221 pathway and restoring autophagy.
Hypothesis-generating for luteolin in diabetic cardiomyopathy; clinical trials needed before practice consideration.
, i.g.) for 4 weeks. Histological and functional alterations in the diabetic heart were determined using HE staining, Masson staining and echocardiography. The expressions of myocardial miR-221, JNK, and c-Jun and autophagic vesicles in diabetes were evaluated by quantitative PCR, Western blotting and electron microscopy. Luteolin significantly improved cardiac function and attenuated myocardial disorganization and fibrosis in the diabetic rat accompanying the dose-dependent down-regulation of JNK, c-Jun, miR-221 and p62, increase of LC3-II/I and autophagic vesicles, and decrease of mitochondrial swelling in the diabetic heart. These data suggest that the protection of luteolin against DCM, at least, is related to suppressing JNK/c-Jun-regulated miR-221 and the subsequent blockage of autophagy.
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Xiao et al. (2023) studied Diabetic cardiomyopathy. Luteolin was evaluated on Cardiac function, myocardial disorganization and fibrosis. Luteolin improved cardiac function and attenuated myocardial disorganization and fibrosis in diabetic rats by suppressing JNK/c-Jun-regulated miR-221 and reversing suppressed autophagy.
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