Oral Rg1 supplementation strengthens antioxidant defense system against exercise-induced oxidative stress in rat skeletal muscles

Yu, Szu Hsien; Huang, Hui Yu; Korivi, Mallikarjuna; Hsu, Ming Fen; Huang, Chih Yang; Hou, Chien-Wen; Kao, Chung Lan; Lee, Ru Ping; Lee, Shin-Da; Kuo, Chia‐Hua

doi:10.1186/1550-2783-9-23

Cited by 33 publications

(30 citation statements)

References 31 publications

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“…Exercise-induced ROS may rapidly attack lipids in the cell, leading to lipid peroxidation chain reactions and the production of peroxidation byproducts including MDA. In previous studies, increased MDA levels during exhaustive swimming were confirmed to increase oxidative stress (8,11,16). In the present study, the administration of SBE decreased MDA levels after exhaustive swimming, suggesting that SBE can inhibit the lipid peroxidation induced by exhaustive exercise.…”

Section: Discussionsupporting

confidence: 80%

“…During exhaustive exercise, fat is typically used as the primary energy source, thus sparing glycogen stores, which in turn retards fatigue. However, substantial production of ROS occurs via fatty acid oxidation during the utilization of fat (8,36,41). Excessive oxygen consumption by strenuous and exhaustive exercise generates O 2…”

Section: Discussionmentioning

confidence: 99%

“…However, strenuous and exhaustive exercise can cause overwhelming production of reactive oxygen species (ROS), which leads to an imbalance between ROS production and antioxidant defense by cellular antioxidants and enzymes such as catalase (CAT), glutathione peroxidase (GPx), and superoxide dismutase (SOD), as well as the non-enzymatic antioxidant, reduced glutathione (7). This imbalance eventually damages biological molecules, key cellular components, and processes such as lipid peroxidation and enzyme inactivation, in addition to causing oxidative DNA damage (8), leading to deteriorated cellular function. Deteriorating function in skeletal muscle is tightly related to lower exercise capacity (9)(10)(11)(12).…”

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confidence: 99%

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<i>Sasa borealis</i> Extract Efficiently Enhanced Swimming Capacity by Improving Energy Metabolism and the Antioxidant Defense System in Mice

You

Kim

Yoon

et al. 2015

J Nutr Sci Vitaminol

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SummaryThis study was conducted to determine the effects of 50% ethanolic extract from Sasa borealis leaves (SBE) on swimming capacity and oxidative metabolism in mice. The mice were divided into 2 groups with similar swimming times and body weights; Ex-Control and Ex-SBE were orally administered with distilled water and 250 mg/kg body weight/d of SBE. Exhaustive swimming times were prolonged by 1.5-fold in the Ex-SBE group compared to the Ex-Control. The Ex-SBE group displayed lower lactate and higher non-esterified fatty acid levels 15 min after swimming and the hepatic and muscle glycogen levels were significantly higher than that in the Ex-Control. SBE potentially enhanced mRNA expression of citrate synthase (CS), carnitine palmitoyltransferase (CPT-1), and b-hydroxyacyl coenzyme A dehydrogenase (b-HAD) in skeletal muscle. The activities and mRNA expression of catalase (CAT), glutathione peroxidase (GPx), and superoxide dismutase (SOD) were elevated in the Ex-SBE compared with the Ex-Control after exhaustive swimming. These results suggest that SBE might be used as an effective agent to enhance swimming capacity by utilization of energy substrates and might ameliorate physical exhaustion by facilitating energy-generating metabolic genes and enhancing endogenous antioxidants.

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Section: Discussionsupporting

confidence: 80%

Section: Discussionmentioning

confidence: 99%

mentioning

confidence: 99%

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<i>Sasa borealis</i> Extract Efficiently Enhanced Swimming Capacity by Improving Energy Metabolism and the Antioxidant Defense System in Mice

You

Kim

Yoon

et al. 2015

J Nutr Sci Vitaminol

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“…Lipid peroxidation can cause fluidity loss and permeability increase of membranes, leading to the loss of cytosolic proteins [33]. Inhibition of lipid peroxidation is essential for maintaining normal cell function [34]. MDA is one of the end products of the unsaturated fatty acid peroxidation in phospholipids, and has been widely used as a marker of oxidative stress [4].…”

Section: Discussionmentioning

confidence: 99%

Polysaccharides from Polygonatum odoratum strengthen antioxidant defense system and attenuate lipid peroxidation against exhaustive exercise-induced oxidative stress in mice

Yang¹,

Zhang²

2017

Trop. J. Pharm Res

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“…It has been demonstrated that ginsenoside Rg1 has an anti-inflammatory effect on human skeletal muscle during exercise (31). Yu et al (32) have also demonstrated that the antioxidant defense system against exercise-induced oxidative stress is strengthened by oral supplements of Rg1 in rat skeletal muscle. However, the function of Rg1 in the resistance to muscle atrophy remains unclear (33)(34)(35)(36)(37)(38).…”

Section: Introductionmentioning

confidence: 99%

Ginsenoside Rg1 prevents starvation-induced muscle protein degradation via regulation of AKT/mTOR/FoxO signaling in C2C12 myotubes

Peng

et al. 2017

Experimental and Therapeutic Medicine

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Abstract. Skeletal muscle atrophy is often caused by catabolic conditions including fasting, disuse, aging and chronic diseases, such as chronic obstructive pulmonary disease. Atrophy occurs when the protein degradation rate exceeds the rate of protein synthesis. Therefore, maintaining a balance between the synthesis and degradation of protein in muscle cells is a major way to prevent skeletal muscle atrophy. Ginsenoside Rg1 (Rg1) is a primary active ingredient in Panax ginseng, which is considered to be one of the most valuable herbs in traditional Chinese medicine. In the current study, Rg1 was observed to inhibit the expression of MuRF-1 and atrogin-1 in C2C12 muscle cells in a starvation model. Rg1 also activated the phosphorylation of mammalian target of rapamycin (mTOR), protein kinase B (AKT), and forkhead transcription factor O, subtypes 1 and 3a. This phosphorylation was inhibited by LY294002, a phosphatidylinositol 3-kinase inhibitor. These data suggest that Rg1 may participate in the regulation of the balance between protein synthesis and degradation, and that the function of Rg1 is associated with the AKT/mTOR/FoxO signaling pathway. IntroductionMuscle atrophy is characterized by an increase in protein degradation and reduction in protein synthesis. It is associated with a number of human diseases and catabolic conditions, including fasting, disuse, aging, cancer, neuromuscular diseases, stroke, chronic obstructive pulmonary disease, chronic heart failure, HIV-acquired immunodeficiency syndrome and sepsis (1-5). Muscle volume shrinking and muscle weakness induced by muscular dystrophy typically disrupt and adversely affect the life of patients (3,6-8). Therefore, it is essential to understand the mechanism by which skeletal muscle atrophy is regulated.A large amount of protein hydrolysis has previously been identified to occur during muscle atrophy and the ubiquitin-proteasome system (UPS) has been demonstrated to be involved in this process (9)(10)(11)(12)(13)(14). In this system, the proteins are first conjugated into multiple molecules of ubiquitin. The 26S proteasome then recognizes and degrades the ubiquitinated proteins (15,16). Multiple enzymes regulate the protein ubiquitination; these include E1, the ubiquitin-activating enzyme, E2, the ubiquitin conjugating enzyme and E3 ubiquitin ligases (17,18). E3 ubiquitin ligases serve a major role in the specificity of protein degradation, because the specific binding between the protein substrate and E3 occurs prior to the reaction with ubiquitin (18,19).It has been demonstrated that the insulin-signaling pathway is involved in the inhibition of UPS (20). In this pathway, the phosphorylation of insulin receptor substrate is stimulated when insulin binds its receptor. Phosphatidylinositol 3-kinase (PI3K), an intracellular intermediate, is recruited to phosphorylate a serine/threonine kinase, protein kinase B (AKT) during this process. AKT then phosphorylates the forkhead box class O transcription factors, subtype 1 and 3a (FoxO1 and FoxO3a), which pre...

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Oral Rg1 supplementation strengthens antioxidant defense system against exercise-induced oxidative stress in rat skeletal muscles

Cited by 33 publications

References 31 publications

<i>Sasa borealis</i> Extract Efficiently Enhanced Swimming Capacity by Improving Energy Metabolism and the Antioxidant Defense System in Mice

<i>Sasa borealis</i> Extract Efficiently Enhanced Swimming Capacity by Improving Energy Metabolism and the Antioxidant Defense System in Mice

Polysaccharides from Polygonatum odoratum strengthen antioxidant defense system and attenuate lipid peroxidation against exhaustive exercise-induced oxidative stress in mice

Ginsenoside Rg1 prevents starvation-induced muscle protein degradation via regulation of AKT/mTOR/FoxO signaling in C2C12 myotubes

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