Maslinic acid in the treatment of heart damage in obesity hypertension through activating Nrf2 pathway

Ailing Yang,Mei Hou,Mingguo Zhang,Ling Lin

doi:10.1590/fst.84821

Ailing Yang, Mei Hou + Show 2 more

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https://doi.org/10.1590/fst.84821

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Abstract

The present study is to explore the interventional effects and potential mechanisms of Maslinic acid on heart damage in obesity hypertension. The rats were given SHR high-fat diet for 16 weeks. WGA staining and Masson staining were applied to detect heart structure and heart fibrosis degree. WB method was used to detect the expressions of ANP, BNP, P-MHC, TGF-β1, CTGF, Collagen I, Collagen III, Fibronectin and other proteins in SHR heart tissue. ELISA method was used to detect serum TNF-α, IL-6, and PAI-1 content. IF method was employed to detect the expression of Nrf2 in heart tissue. Maslinic acid can significantly improve the morphology of the heart tissue, reduce the hypertrophy and swelling of cardiomyocytes, inhibit the deposition of collagen fibers, and significantly inhibit the expressions of ANP, BNP, MYH7, CTGF, TGFpl, Fibronectin, CollagenI and CollagenIII proteins in the heart tissue. Maslinic acid can effectively inhibit TNF-a, IL-6 and PAI-1 expression, reduce heart inflammation, and significantly elevate Nrf2 level in heart tissue. Maslinic acid can significantly improve the heart structure of obese SHR, inhibit myocardial hypertrophy, cardiac fibrosis, and cardiac inflammation. The underlying mechanism may be related to elevating the expression of Nrf2 protein in the cytoplasm of heart tissue, promoting Nrf2 to enter the nucleus, thereby promoting the expression and activity of mitochondria-function-related proteins. The capabilities to inhibit the expression of hypertrophy-related proteins are also related.

Highlights

The heart damage of obesity hypertension mainly characterizes myocardial hypertrophy and cardiac fibrosis, cardiac redox imbalance, cardiac tissue inflammation, myocardial mitochondrial dysfunction and energy metabolism imbalance, abnormal myocardial autophagy, myocardial cell necrosis and apoptosis
It is found that the expression and transcriptional activity of Nrf2 in heart tissue were significantly inhibited in the obese hypertension animal model
In obesity, diabetes and hypertension disease models induced by high-fat, high-sugar and high-salt diets for a long time, the expression and/or transcriptional activity of Nrf2 is often significantly inhibited, and the degree of inhibition of the expression and or transcriptional activity of Nrf2 is often positively correlated with the degree of heart damage

Summary

Introduction

The heart damage of obesity hypertension mainly characterizes myocardial hypertrophy and cardiac fibrosis, cardiac redox imbalance, cardiac tissue inflammation, myocardial mitochondrial dysfunction and energy metabolism imbalance, abnormal myocardial autophagy, myocardial cell necrosis and apoptosis. These pathological changes are independent and can influence each other to jointly promote the occurrence and development of heart damage (Termklinchan et al, 2019; Chen et al, 2019; Wang et al, 2019a). When Nrf knockout animals are fed with high fat, high sugar and high salt diet alone, their myocardial hypertrophy, fibrosis, peroxidation and inflammation will be more severe than wild-type animals (Liu et al, 2017; Wang et al, 2019b; Ding et al, 2015)

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