The aim of the study was to investigate the antiinflammatory effects of naringenin in rats induced liver damage by exposure to ethanol. Rats were divided into four groups, groups 1 and 2 received isocaloric glucose; groups 3 and 4 received 20% ethanol equivalent to 6 g/kg body weight everyday for the total experimental period of 60 days. In addition, groups 2 and 4 were supplemented with naringenin (50 mg/kg p.o.) everyday for the last 30 days of the experiment. The results showed significantly elevated levels/activities/expression of serum aspartate and alanine transaminases, iron, ferritin, transforming growth factor-alpha (TNF-α), interleukin-6 (IL-6), nuclear factor-kappa B (NF-κB), cyclooxygenase-2 (COX-2), macrophage inflammatory protein 2 (MIP-2) and CD14 in ethanol fed rats as compared to those of the control. Ethanol-fed rats exhibited increased staining for the presence of inducible nitric oxide (iNOS) protein adducts in the liver. Supplementation with naringenin for the last 30 days to ethanol-fed rats, significantly decreased the levels/activities/expression of serum aspartate and alanine transaminases, iron, ferritin, TNF-α, IL-6, NF-κB, COX-2, MIP-2, CD14 and iNOS protein adducts in the liver as compared to the untreated ethanol fed rats. The inhibition of TNF-α, IL-6, NF-κB, COX-2, MIP-2, iNOS and CD14 by naringenin may contribute to its antiinflammatory activity in ethanol fed rats.

We have investigated the modulatory efficacy of naringenin on circulatory lipid peroxidation and anti-oxidant status, hepatic alcohol metabolizing enzymes in rats with ethanol induced hepatotoxicity. Rats were divided into four groups: groups 1 and 2 received isocaloric glucose and 0.5% carboxymethyl cellulose; groups 3 and 4 received 20% ethanol equivalent to 6 g/kg body weight everyday for the total experimental period of 60 days. In addition, groups 2 and 4 were given naringenin (50 mg/kg) everyday for the last 30 days of the experiment. The results showed significantly elevated levels/activities of bilirubin, alkaline phosphatase (ALP), lactate dehydrogenase (LDH), thiobarbituric acid reactive substances (TBARS), lipid hydroperoxides (LOOH), conjugated dienes (CD) and phase I enzymes, and significantly lowered the activities of alcohol dehydrogenase (ADH), aldehyde dehydrogenase (ALDH), superoxide dismutase (SOD), catalase (CAT) and phase II enzymes in ethanol-fed rats as compared to those of the control. Supplementation with naringenin for the last 30 days of the experiment to ethanol-fed rats, significantly decreased the levels/activities of bilirubin, ALP, LDH, TBARS, LOOH, CD and phase I enzymes, and significantly elevated the activities of ADH, ALDH, SOD, CAT and phase II enzymes as compared to control rats. These findings suggest that naringenin can effectively modulate the hepatic alcohol metabolizing enzymes in rats with ethanol induced liver injury.

Taken together these findings suggest that naringenin has a therapeutic potential in the abatement of ethanol-induced hepatotoxicity.

These data provide new insights into the therapeutic approach of d-limonene against the development of the metabolic syndrome associated with NAFLD.

Our aim was to investigate the effect of naringenin on hyperlipidemia induced by ethanol. Groups 1 and 2 rats received isocaloric glucose and 0.5% carboxymethyl cellulose (CMC); groups 3 and 4 received 20% (6 g/kg body weight p.o.) ethanol everyday for 60 days. Groups 2 and 4 rats received naringenin (50 mg/kg body weight/day in 0.5% CMC) everyday during the last 30 days of the experiment. There were increased levels of plasma total cholesterol (TC), triglycerides (TG), free fatty acids (FFA), very low density lipoproteins (VLDL), low density lipoproteins (LDL) and tissue TC, TG, FFA, HMG CoA reductase and alterations in collagen content of ethanol‐fed rats, which on naringenin supplementation showed decreased levels of plasma and tissue TC, TG and FFA, HMG CoA reductase and collagen content. There was a significant decrease in the levels of plasma high density lipoprotein (HDL), lipoprotein lipase (LPL) and lecithin cholesterol acyltransferase (LCAT) of ethanol‐fed rats, which on naringenin supplementation showed an increase in the levels of HDL and LPL with ethanol alone–fed rats. Naringenin can efficiently prevent the accumulation of plasma lipids and lipoproteins. PRACTICAL APPLICATIONS Alcohol abuse, alcohol intolerance, alcohol dependence and other alcohol related disabilities are some of the most challenging public health problems. A phytotherapeutic approach in the new drug development can provide many valuable drugs from traditional plant sources. The use of herbal medicines for the treatment of hepatotoxicity has gained importance throughout the world. Renewed attention to alternative medicine and natural therapies has stimulated new wave of research interest in traditional practice, and there is a need to look for more potent agents with lesser side effects. The present study is aimed to identify the efficacy of naringenin by uncovering its underlying mechanism of action against alcohol‐induced liver disease for effective therapy. Naringenin, an important flavonoid, is widely present in fruits and vegetables. Naringenin is known to possess a number of significant beneficial properties. If the biochemical and histological findings are positive, indicating the marked hepatoprotective efficacy of naringenin, it could be subjected to human trials in the future.