Protective activity of kudzu (Pueraria thunbergiana) vine on chemically-induced hepatotoxicity: in vitro and in vivo studies

Abstract

BackgroundKudzu (Pueraria thunbergiana) root has long been used in Traditional Chinese Medicine. However, the vine of the kudzu plant has been considered waste material. This study aimed to investigate the hepatoprotective properties of the kudzu vine.MethodsWe created 0 %, 30 %, 70 %, and 95 % ethanolic kudzu vine extracts. The isoflavone contents of kudzu vine extract were quantified by high-performance liquid chromatography. Tertiary-butylhydroperoxide (t-BHP) was added to human liver-derived HepG2 cells, and the production of reactive oxygen species was measured in the presence and absence of kudzu vine extract. Antioxidant activity was evaluated in all kudzu vine extracts using a hydroxyradical scavenging assay. Thirty-five male Sprague–Dawley rats were divided into seven groups (n = 5); two groups were not given any extract or drug, one group was treated with 50 mg/kg silymarin orally for 5 days, and the remaining four groups were respectively treated with 100 mg/kg of 0 %, 30 %, 70 %, or 95 % ethanolic extract of kudzu vine orally once daily for 5 days. On day 5 the treatment groups and one untreated group were fed 0.75 ml/kg carbon tetrachloride (CCl4) to induce liver damage. Blood and liver tissue samples were collected 24 h after CCl4 administration for measurement of plasma alanine aminotransferase and aspartate aminotransferase, and concentration of malondialdehyde and glutathione in liver tissue.ResultsPuerarin was the most abundant isoflavone in kudzu vine extract. Kudzu vine extract significantly reduced the cytotoxicity and production of reactive oxygen species induced by t-BHP in a dose-dependent manner. Treatment with 0 % and 30 % ethanolic extracts of kudzu vine significantly lowered the plasma levels of alanine aminotransferase and aspartate aminotransferase in a CCl4-induced hepatotoxicity rat model (P < 0.05). Glutathione was significantly elevated in the 30 % ethanolic extract-treated group (P < 0.05), while the malondialdehyde level in liver tissue was significantly decreased in the 0 % and 30 % ethanolic extract-treated groups (P < 0.05).ConclusionsThe kudzu vine is potentially highly beneficial in treating liver damage, as it scavenges reactive free radicals and boosts the endogenous antioxidant system.

Effects of DA-5513 on alcohol metabolism and alcoholic fatty liver in rats

“…The proprietary liquid DA-5513 formulation was developed using seven herbal extracts, including GMT-ALC-5L (fermented rice embryo and bean extract), Curcuma longa L. , Trapa japonica Flerov., Silybum marianum L. , Paullinia cupana Mart., Pueraria thunbergiana Benth., and honey. These natural products have been used in traditional oriental medicines to prevent alcohol-induced hangover and protect the liver against diverse hepatotoxins such as ethanol, carbon tetrachloride, antitubercular agents, and thioacetamide [ 14 15 16 17 18 19 20 ].…”

Fraxin Prevents Chemically Induced Hepatotoxicity by Reducing Oxidative Stress

“…Several studies have suggested that the antioxidant activity against free radicals may be an important mechanism of hepatoprotection [ 20 ]. Many natural products containing flavonoids, coumarins, and polyols have been investigated for the development as antioxidants [ 4 , 15 , 21 , 22 , 23 ].…”

“…CCl 4 is used to induce liver toxicity to allow the testing of drugs for their hepatoprotective activities. Silymarin is used as standard hepatoprotective compound since it is reported to have a protective effect on the hepatocytes [ 4 , 14 ]. In the present study, we also used CCl 4 to induce hepatotoxicity in rats.…”

“…According to Wang et al, Fraxin was orally administered to mice at 500 mg/kg and no toxicity was observed [ 13 ]. The positive controls were gavaged with silymarin (50 to 100 mg/kg) in CCl 4 induced hepatotoxicity rats [ 4 , 14 , 15 ]. We sought to evaluate the hepatoprotective effect of fraxin on the same dose as that of the positive control.…”

“…Hepatic damage can be attributed to various factors, such as infections, autoimmune disorders, chemical agents, and excessive alcohol consumption [ 1 , 2 , 3 , 4 ]. Chemical-induced hepatotoxicity accounts for approximately half of the cases of acute liver failure.…”