ABSTRACT
Wei Kang Su (WKS) is an antioxidant-enriched herbal product manufactured on the basis of Shengmai San, a well-known traditional Chinese herbal formula. In the present study, we investigated the effects of WKS co-treatment on chronic ethanol toxicity in rats. WKS co-treatment protected against chronic ethanol-induced hepatotoxicity, as evidenced by the suppression of plasma enzyme activities and reactive oxygen metabolite levels, as well as the inhibition of hepatic mitochondrial malondialdehyde production in chronic ethanol-intoxicated rats. The hepatoprotection afforded by WKS co-treatment in chronic ethanol-intoxicated rats was associated with a reversal of altered hepatic mitochondrial antioxidant status and adenosine triphosphate (ATP) generation capacity, as well as heat shock protein 25/70 production. Therefore, WKS may offer the prospect of preventing ethanol-associated liver damage by increasing the resistance of mitochondria to oxidative stress.
Subject(s)
Drugs, Chinese Herbal/therapeutic use , Liver Diseases/drug therapy , Adenosine Triphosphate/metabolism , Animals , Antioxidants/metabolism , Chronic Disease , Drug Combinations , Drugs, Chinese Herbal/pharmacology , Ethanol , Female , HSP27 Heat-Shock Proteins/metabolism , HSP70 Heat-Shock Proteins/metabolism , Mitochondria/drug effects , Mitochondria/metabolism , Rats , Rats, Sprague-DawleyABSTRACT
Wei Kang Su (WKS) is a commercial herbal product based on a Chinese herbal formula, Shengmai San. Here, we investigated the effects of long-term treatment with WKS on mitochondrial antioxidant status and functional ability, as well as heat shock protein (Hsp) 25/70 production, in various tissues of rats. WKS treatment enhanced mitochondrial antioxidant status and ATP generation capacity, as well as Hsp 25/70 production in various rat tissues. WKS treatment suppressed plasma reactive oxygen metabolite levels and protected against carbon tetrachloride hepatotoxicity in rats. Long-term WKS treatment may prevent diseases by enhancing the resistance of mitochondria to oxidative stress.