Inhibitory effect of glycyrrhizin on NF‐κB binding activity in CC1₄‐ plus ethanol‐induced liver cirrhosis in rats

Abstract

Liver ISSN 0106-9543Inhbitory effect binding activitv J 4 . 0 " 4 e . liver cirrhosis in ; of glycyrrhizin on NF-KB in CC1,-plus ethanol-induced rats Wang J-Y, Guo J-S, Li H, Liu S-L, Zern MA. Inhibitory effect of glycyrrhizin on NF-KB binding activity in CC14-plus ethanol-induced liver cirrhosis in rats.Abstract: Aims/Background: Potenlini is an injectable compound whose active component is glycyrrhizin, which is extracted from licorice. Previous studies showed that it could reduce liver injury, improve alanine aminotransferase (ALT) levels and act as an antifibrotic agent. However, the mechanism of its action remains unclear. The aim of this study was to determine the molecular mechanism of its action by investigating the effects of potenlini on nuclear factor-KB(NF-KB) binding activity in an animal model of liver cirrhosis. Methods: Rats were randomly allocated into a normal control group, a model control group, and a potenlini group. Rats in the latter two groups were treated with C C 4 and ethanol solution in order to induce chronic liver injury. Rats in the potenlini group were given potenlini treatment at the same time. Results: Serum ALT levels were significantly reduced in rats treated with potenlini compared with levels in rats of the model control group, which had dramatically increased ALT levels. Histologically, liver steatosis and fibrosis were severe in the rats of the model group, but were significantly improved in rats of the potenlini group. NF-KB binding activity was markedly increased in the liver specimens taken from the rats of the model control group in comparison with the binding of normal livers, but the binding levels were nearly normal in the livers of the potenlini group. Conclusions: The results suggest that potenlini can inhibit the NF-KB binding activity in CC14 and ethanol-induced chronic liver injury, and that effect may be a possible mechanism by which potenlini protects the liver from hepatotoxin- 180

Glycyrrhizin alleviates experimental allergic asthma in mice

“…NF-kB was found to be markedly activated which in turn regulates many of the inflammatory genes that are abnormally expressed in asthma [24,25]. Although GRZ has not been demonstrated to inhibit NF-kB binding in the airway or lung inflammation, however, it has been shown that it inhibited NF-kB binding activity in the rat liver cirrhosis model [26]. The recruitment of inflammatory cells from blood vessel to the airway needs various selectins and the blocking of these selectins has been demonstrated to inhibit antigen induced airway inflammation and late airway responsiveness in animal models [27,28].…”

Hepatic protection by glycyrrhizin and inhibition of iNOS expression in concanavalin A-induced liver injury in mice

“…It is known that the activation of NF-kappaB participates in Con A-induced hepatic iNOS expression [26]. GL has been reported to inhibit NF-KappaB binding activity in carbon tetrachloride and ethanol-induced chronic liver injury [32].…”

Antifibrotic effects of a herbal combination regimen on hepatic fibrotic rats

“…In a previous study, it was reported that Ligusticum chuanxiong (L) exerted antiproliferative effects on PDGF-stimulated HSC-T6 cells, with modulation of cell cycle regulatory proteins conducive to apoptosis (Lin et al, 2006a). In the literature, glycyrrhizin, an active principle of licorice (Glycyrrhiza glabra, G), has been reported to abrogate ethanol-plus CCl 4 -induced hepatic fibrosis in rats, possibly by interfering with NFκB pathways (Wang et al, 1998). The present study showed that SLG could reduce hepatic mRNA expression levels of iNOS and ICAM-1 genes in fibrotic livers.…”

“…(L) on the proliferation of HSC-T6 cells have been reported (Lin et al, 2006a). Glycyrrhizin, an active compound of licorice (Glycyrrhiza glabra, G) has also been shown to abrogate hepatic fibrosis in rats (Wang et al, 1998). This study investigated whether a herbal extract combination, SLG, could exert antifibrotic effects on DMN-induced rat hepatic fibrosis.…”