Hepatorenal protective effect of Antistax(®) against chemically-induced toxicity.

Atallah F Ahmed, Hanan M Al-Yousef, Jawaher H Al-Qahtani, Mansour S Al-Said, AbdelKader E Ashour, Mohammed Al-Sohaibani, Syed Rafatullah

文献索引：Pharmacogn. Mag. 11 , S173-81, (2015)

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摘要

Antioxidant natural products and chemoprevention are considered nowadays as an effective approach against health various disorders and diseases induced by oxidative stress or free radicals.The aim of this study was to assess the hepato- and nephroprotective activity of a standardized red vine leaf aqueous extract AS195 (Antistax(®)).The protective activity of AS195 (100 mg/kg) was investigated on carbon tetrachloride (CCl4)-intoxicated rats in comparison with silymarin. The flavonoid/proanthocyanidin nature of AS195 was identified by phytochemical and nuclear magnetic resonance (NMR) analyses, while its total phenol/proanthocyanidin/flavonoid content and antioxidant activity were determined by Folin-Ciocalteau, vanillin-sulfuric acid, AlCl3, and 2, 2-diphenyl-2-picrylhydrazyl radical scavenging assays, respectively.Relative to the control CCl4 -intoxicated group, pretreatment with AS195 could significantly suppressed the elevated serum levels of alanine aminotransferase, alkaline phosphatase, γ-glutamyl transferase, total cholesterol, low-density lipoprotein cholesterol, very low-density lipoprotein cholesterol, triglycerides, bilirubin, creatinine, uric acid, and calcium, whereas it significantly increased the diminished serum levels of high-density lipoprotein cholesterol, albumin and total protein. Moreover, AS195 significantly decreased malondialdehyde formation in the tissues of liver and kidney, whereas it significantly elevated and nonprotein sulfhydryl groups, compared with the intoxicated control. The improvement in biochemical parameters by AS195 was obviously observed and further confirmed by restoration of normal histological features in the two organs.The results of the present study revealed the capacity of AS195 to enhance the recovery from xenobiotic-induced hepatorenal toxicity initiated by free radicals.