Inhibitory effect of glycyrrhizin on NF-κB binding activity in CCl(4-) plus ethanol-induced liver cirrhosis in rats

Ji Yao Wang, Jin Sheng Guo, Hai Li, Shu Ling Liu, Mark A Zern

Research output: Contribution to journalArticle

61 Citations (Scopus)

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-κB (NF-κB) 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 CCl4 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-κB 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-κB binding activity in CCl4 and ethanol-induced chronic liver injury, and that effect may be a possible mechanism by which potenlini protects the liver from hepatotoxin-induced liver injury and cirrhosis.

Original languageEnglish (US)
Pages (from-to)180-185
Number of pages6
JournalLiver
Volume18
Issue number3
StatePublished - Jun 1998
Externally publishedYes

Fingerprint

Glycyrrhizic Acid
Liver Cirrhosis
Ethanol
Liver
Alanine Transaminase
Control Groups
Wounds and Injuries
Glycyrrhiza
Fatty Liver
Animal Models
Injections

Keywords

  • Cirrhosis
  • Glycyrrhizin
  • Liver injury
  • NF-κB
  • Potenlini

ASJC Scopus subject areas

  • Hepatology

Cite this

Wang, J. Y., Guo, J. S., Li, H., Liu, S. L., & Zern, M. A. (1998). Inhibitory effect of glycyrrhizin on NF-κB binding activity in CCl(4-) plus ethanol-induced liver cirrhosis in rats. Liver, 18(3), 180-185.

Inhibitory effect of glycyrrhizin on NF-κB binding activity in CCl(4-) plus ethanol-induced liver cirrhosis in rats. / Wang, Ji Yao; Guo, Jin Sheng; Li, Hai; Liu, Shu Ling; Zern, Mark A.

In: Liver, Vol. 18, No. 3, 06.1998, p. 180-185.

Research output: Contribution to journalArticle

Wang, JY, Guo, JS, Li, H, Liu, SL & Zern, MA 1998, 'Inhibitory effect of glycyrrhizin on NF-κB binding activity in CCl(4-) plus ethanol-induced liver cirrhosis in rats', Liver, vol. 18, no. 3, pp. 180-185.
Wang, Ji Yao ; Guo, Jin Sheng ; Li, Hai ; Liu, Shu Ling ; Zern, Mark A. / Inhibitory effect of glycyrrhizin on NF-κB binding activity in CCl(4-) plus ethanol-induced liver cirrhosis in rats. In: Liver. 1998 ; Vol. 18, No. 3. pp. 180-185.
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AU - Liu, Shu Ling

AU - Zern, Mark A

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N2 - 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-κB (NF-κB) 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 CCl4 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-κB 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-κB binding activity in CCl4 and ethanol-induced chronic liver injury, and that effect may be a possible mechanism by which potenlini protects the liver from hepatotoxin-induced liver injury and cirrhosis.

AB - 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-κB (NF-κB) 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 CCl4 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-κB 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-κB binding activity in CCl4 and ethanol-induced chronic liver injury, and that effect may be a possible mechanism by which potenlini protects the liver from hepatotoxin-induced liver injury and cirrhosis.

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