Combination of Morroniside and Diosgenin Prevents High Glucose-Induced Cardiomyocytes Apoptosis.

Wen-Xia Pi,Xiao-Peng Feng,Li-Hong Ye,Bao-Chang Cai

doi:10.3390/molecules22010163

Wen-Xia Pi, Xiao-Peng Feng + Show 2 more

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https://doi.org/10.3390/molecules22010163

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Abstract

Cornus officinalis and Dioscorea opposita are two traditional Chinese medicines widely used in China for treating diabetes mellitus and its complications, such as diabetic cardiomyopathy. Morroniside (Mor) of Cornus officinalis and diosgenin (Dio) of Dioscorea opposita formed an innovative formula named M + D. The aims of the present study were to investigate myocardial protective effect of M + D on diabetic cardiomyopathy (DCM) through the inhibition of expression levels of caspase-3 protein, and identify the advantage of M + D compared with Mor, Dio, and the positive drug metformin (Met). We detected cell viability, cell apoptosis, intracellular reactive oxygen species (ROS) levels, and the expression levels of Bcl-2, Bax, and caspase-3 protein in rat cardiomyocytes. In result, Mor, Dio, and M + D increased cell viability, inhibited cell apoptosis and decreased ROS levels. Additionally, the expression of Bax and Bcl-2 protein was modulated and the expression levels of caspase-3 protein were markedly decreased. Among the treatment groups, M + D produced the most prominent effects. In conclusion, our data showed for the first time that Mor, Dio, and M + D prevented high glucose (HG)-induced myocardial injury by reducing oxidative stress and apoptosis in rat cardiomyocytes. Among all the groups, M + D produced the strongest effect, while Mor and Dio produced weaker effects.

Highlights

Diabetic cardiomyopathy (DCM), known as diabetic heart disease, was originally put forward by Rubler in 1972 [1]
At 72 h after high glucose injury in cardiomyocytes, in HG group, the proliferation of cardiomyocytes was markedly decreased compared with the CC group
The results of the MTT assay showed that MorH, DioH, and (M + D)H had an obviously protective effect on high glucose-induced cardiomyocytes injury

Summary

Introduction

Diabetic cardiomyopathy (DCM), known as diabetic heart disease, was originally put forward by Rubler in 1972 [1]. DCM has imposed an increasing social and economic burden with an increase in the number of diabetics. Increasing evidence demonstrates that hyperglycemia induces apoptotic of cardiomyocytes, resulting in the development of DCM through different mechanisms [2,3], including oxidative stress and the Bax pathway. Hyperglycemia may induce excessive production of reactive oxygen species (ROS) that is regarded as the most important contributor in the occurrence and progression of DCM [4], causing oxidative stress and eventually promoting cell apoptosis. Recent studies suggested that accumulation of advanced glycation end-products (AGEs) under hyperglycemic conditions contributed to the development of diabetic complications. AGEs exert their effects directly or by binding their member receptor, receptor for advanced glycation end-products (RAGE), to activate the downstream signaling pathway [5].

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