Effect of Genistein Supplementation on Exercise-Induced Inflammation and Oxidative Stress in Mice Liver and Skeletal Muscle.

Cong Wu,Sihui Ma,Siyi Zhou,Katsuhiko Suzuki

doi:10.3390/medicina57101028

Abstract

Background and objectives: The purpose of this study was to investigate the influences of oral high-dose genistein (GE) administration on exercise-induced oxidative stress, inflammatory response and tissue damage. Materials and Methods: Thirty-two mice were randomly divided into control group (Con; sedentary/0.5% CMC-Na), GE administrated group (GE; sedentary/GE dosed), exercise group (Ex; exercise/0.5% CMC-Na), or GE administrated plus exercise group (GE + Ex; exercise/GE dosed), mice in the GE and GE + Ex group were given GE orally at the dose of 200 mg/kg weight. Results: Plasma aspartate aminotransferase (AST), alanine aminotransferase (ALT) levels, liver interleukin (IL)-6, IL-1β, superoxide dismutase 1 (SOD1), catalase (CAT), hemeoxygenase-1 (HO-1) gene expression levels and skeletal muscle IL-6, nuclear factor erythroid 2-related factor (Nrf2), and HO-1 gene expression levels increased immediately after exhaustive exercise. GE supplementation increased liver protein carbonyl concentrations. On the other hand, GE supplementation significantly decreased SOD1, CAT gene expression levels in the liver and Nrf2, and HO-1 gene expression levels in the skeletal muscles. Conclusions: Acute exercise induced organ damage, inflammation, and oxidative stress in skeletal muscles and the liver. However, a single dose of GE supplementation before exercise did not lead to favorable antioxidant and anti-inflammatory effects in this study.

Highlights

Publisher’s Note: MDPI stays neutral with regard to jurisdictional claims in Oxidative stress is defined as a kind of imbalance caused by electronically excited states and reactive oxygen species (ROS) in organisms [1]
As the main finding of this study, we revealed that GE administration failed to relieve oxidative stress, but increased oxidative stress in the liver, which is shown by the increase of protein carbonyl, and might be associated with the failure to regulate nuclear factor erythroid 2-related factor (Nrf2) gene expression
We examined TBARS and protein carbonyl concentrations to assess the effect of GE administration on antioxidant capacity and gene expression of superoxide dismutase 1 (SOD1) and CAT to evaluate the effect of GE administration on enzymatic antioxidant capacity

Summary

Introduction

Oxidative stress is defined as a kind of imbalance caused by electronically excited states and reactive oxygen species (ROS) in organisms [1]. When the production rate of ROS exceeds the system’s detoxification and repair capacity, oxidative stress can result in cellular damage [1]. Physical exercise is widely considered as an effective way to maintain health status [3,4]. According to Suzuki et al and Radak et al [5,6], when the intensity of exercise is moderate, organisms can adapt to the mild burst of ROS; this kind of adaptation is called hormesis. The purpose of this study was to investigate the influences of oral high-dose genistein (GE) administration on exercise-induced oxidative stress, inflammatory re-sponse and tissue damage. Materials and Methods: Thirty-two mice were randomly divided into control group (Con; sedentary/0.5% CMC-Na), GE administrated group (GE; sedentary/GE dosed), exercise group (Ex; exercise/0.5% CMC-Na), or GE administrated plus exercise group (GE + Ex; ex-ercise/GE dosed), mice in the GE and GE + Ex group were given GE orally at the dose of 200 mg/kg weight

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Methods

Results

Discussion

Conclusion