Puerarin mediates hepatoprotection against CCl4-induced hepatic fibrosis rats through attenuation of inflammation response and amelioration of metabolic function

Anti-Fibrotic Effect of Plumbagin on CCl4-Lesioned Rats

“…Many studies have suggested that fibrotic development can be controlled or inhibited through clinically therapeutic regimes [21]. In addition, plant-isolated active components, such as phloridzin [22], triterpenoid saponin [23] and puerarin [24], exert an effective antifibrotic role. Our data showed that body weight loss and hepatomegalia occurred in CCl 4 -injured rats, indicating that the signs of malnourishment were due to CCl 4 -induced hepatotoxicity.…”

Natural Products for the Prevention and Treatment of Hangover and Alcohol Use Disorder

“…The social interaction and locomotor activity were increased after withdrawal from 17 days of alcohol (7%) diet [47]. In addition, puerarin reduced hepatotoxicity in CCl 4 -induced hepatic fibrosis and chronic alcoholic liver injury in rats via the following underlying mechanisms: (a) regulated enzymes (ALT, AST), albumin, and total protein in blood; (b) inhibited Kupffer cells activation and attenuated TNF-α/NF-κB pathway for anti-inflammation response; and (c) improved metabolic function in liver tissue [48]. Additionally, owing to the antioxidant ability of Pueraria lobata, the activity of superoxide dismutase (SOD) was increased and the level of malondialdehyde (MDA) was decreased in liver [48,49].…”

“…In addition, puerarin reduced hepatotoxicity in CCl 4 -induced hepatic fibrosis and chronic alcoholic liver injury in rats via the following underlying mechanisms: (a) regulated enzymes (ALT, AST), albumin, and total protein in blood; (b) inhibited Kupffer cells activation and attenuated TNF-α/NF-κB pathway for anti-inflammation response; and (c) improved metabolic function in liver tissue [48]. Additionally, owing to the antioxidant ability of Pueraria lobata, the activity of superoxide dismutase (SOD) was increased and the level of malondialdehyde (MDA) was decreased in liver [48,49]. Therefore, the flowers of kudzu might have the ability to alleviate hangover and provide hepatoprotection while the root of kudzu was effective in reducing alcohol intake in several clinical population studies.…”

“…Mice Suppression of alcohol-induced liver steatosis by modulating the disturbance of the peroxisome proliferator-activated receptor α pathway and ameliorating mitochondrial function [42] Cells Suppression of alcohol-induced apoptosis in human neuroblastoma cells [43] Puerarin and daidzein Root Humans Reduced alcohol intake in a naturalistic setting [45] Humans Reduced alcohol consumption in a binge drinking paradigm [46] Rats Reduced anxiogenic effects of alcohol withdrawal via increased social interaction and locomotor activity [47] Rats Mitigation of liver damage (AST, ALT, GGT) and lipid deposition induced by chronic alcohol intake as well as TNF-α release, protein expression of endotoxin receptors [48] Fructus evodiae Dehydroevodiamine, evodiamine and rutaecarpine Dried and unripe fruit Mice Alleviation of hangover through stimulating the expression of hepatic alcohol metabolizing and antioxidant enzymes [50] Rats Prevention of alcohol-induced gastric mucosal lesions by strengthening the mucosal barrier integrity and increasing gastric mucosal nitric oxide (NO) synthesis [51] Trigonela foenum-graecum Polyphenols Seeds Cells Prevention of the toxic effects of alcohol through increased cell viability, reduced lactate dehydrogenase leakage and normalized GSH/GSSG ratios [53,55] Rats Suppressed alcohol-induced abnormalities in the liver through restoration of liver enzymes, ADH and ALDH activities [54] Rats Suppression of alcohol toxicity through prevention of enzymatic leakage, and improved lipid profiles [56][57][58] …”

Protective Effect of <b><i>Zingiber Officinale</i></b> against CCl₄-Induced Liver Fibrosis Is Mediated through Downregulating the TGF-ß1/Smad3 and NF-&#954;B/I&#954;B Pathways

“…Following hepatic inflammation and damage, hepatic stellate cells (HSCs) change to myofibroblast-like cells and produce a large amount of extracellular matrix (ECM) like type I collagen. The accumulation of collagen in the hepatic parenchyma further leads to fibrosis of the liver [3,4]. …”