Abstract
Despite regular exercise benefits, acute exhaustive exercise elicits oxidative damage in liver. The present study determined the hepatoprotective properties of ginsenoside-Rg1 against exhaustive exercise-induced oxidative stress in rats. Forty rats were assigned into vehicle and ginsenoside-Rg1 groups (0.1 mg/kg bodyweight). After 10-week treatment, ten rats from each group performed exhaustive swimming. Estimated oxidative damage markers, including thiobarbituric acid reactive substance (TBARS) (67%) and protein carbonyls (56%), were significantly (P < 0.01) elevated after exhaustive exercise but alleviated in ginsenoside-Rg1 pretreated rats. Furthermore, exhaustive exercise drastically decreased glutathione (GSH) content (∼79%) with concurrent decreased superoxide dismutase (SOD), catalase (CAT), and glutathione peroxidase (GSH-Px) activities. However, these changes were attenuated in Rg1 group. Additionally, increased xanthine oxidase (XO) activity and nitric oxide (NO) levels after exercise were also inhibited by Rg1 pretreatment. For the first time, our findings provide strong evidence that ginsenoside-Rg1 can protect the liver against exhaustive exercise-induced oxidative damage.
Highlights
It is well documented that regular exercise has many health beneficial effects including improvement of antioxidant status in liver [1, 2]
Lipid peroxidation widely considered as an oxidative stress marker, caused by excessive amount of free radicals attacking on membrane components of the cell
An important finding of the present study is that exercise-induced elevated thiobarbituric acid reactive substance (TBARS) levels were significantly controlled in ginsenoside-Rg1 pretreated rats
Summary
It is well documented that regular exercise has many health beneficial effects including improvement of antioxidant status in liver [1, 2]. ROS are scavenged by a sophisticated antioxidant defense system, which includes enzymes, superoxide dismutase (SOD), catalase (CAT) and glutathione peroxidase (GSHPx), and nonenzyme glutathione (GSH) [5]. When ROS exceeds the normal physiological coping range during exhaustive exercise, accumulation of ROS and decrease in antioxidant status could be resulted. This scenario increased oxidative stress and leads to modification of lipid and protein structures that compromises the cellular functions in liver [3, 4, 6, 7]
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