Hepatitis is a serious clinical problem caused by exposure to different agents such as viruses, alcohol, and chemicals, and by autoimmune diseases. Hepatitis may occur with limited or no symptoms and often leads to anorexia, jaundice, and hepatic carcinoma. Although extensive studies into the treatment of liver disease with several oral hepatoprotective agents have been carried out, few beneficial liver drugs are currently available in the clinic. d-Galactosamine (GalN) is a specific hepatotoxicant that depletes the uridine triphosphate pool and thereby inhibits macromolecule synthesis, inducing hepatotoxicity that resembles that of human viral and drug-induced hepatitis In GalN-induced acute liver injury, overproduction of reactive oxygen species from hepatocytes, infiltrated leukocytes, and activated Kupffer cells, accompanied by enhanced activity of the proinflammatory cytokine signaling pathway, contributes to liver damage. Heme oxygenase (HO)-1 is an endogenous cytoprotective enzyme induced in response to cellular and environmental stresses. The critical role of HO-1 in the protection against in vivo and in vitro inflammatory disease models has been reported, and upregulation of HO-1 exerts an anti-inflammatory effect in experimental settings of hepatic ischemia/reperfusion and acute hepatitis

Panax ginseng Meyer (Araliaceae) is a medicinal herb that has been used worldwide for > 5,000 yrs. P. ginseng has been widely used for treatment of inflammation, cardiovascular diseases, trauma, and bleeding caused by injury. Several investigators have reported the biologic role of P. ginseng in experimental models of liver diseases, including fatty liver disease, liver fibrosis, hepatic carcinoma, and chemical-induced liver injury. However, the yield of active components from natural sources can be highly variable depending on the source plant, location, season of harvest, and the prevailing environmental conditions. The objective of this study is to investigate the cytoprotective effects of wild ginseng CMCs against GalN-induced acute liver injury, particularly the modulation of inflammatory responses.

Panax ginseng has a wide range of biological activities including anti-inflammatory, antioxidant, and immunomodulatory functions. Wild ginseng cambial meristematic cells (CMCs) were obtained from P. ginseng cambium. This study examined the protective mechanism of wild ginseng CMCs against d-galactosamine (GalN)-induced liver injury. GalN, a well-known hepatotoxicant, causes severe hepatocellular inflammatory damage and clinical features similar to those of human viral hepatitis in experimental animals.

Hepatotoxicity was induced in rats using GalN (700 mg/kg, i.p.). Wild ginseng CMCs was administered orally once a day for 2 wks, and then 2 h prior to and 6 h after GalN injection.

Wild ginseng CMCs attenuated the increase in serum aminotransferase activity that occurs 24 h after GalN injection. Wild ginseng CMCs also attenuated the GalN-induced increase in serum tumor necrosis factor-α, interleukin-6 level, and hepatic cyclooxygenase-2 protein and mRNA expression. Wild ginseng CMCs augmented the increase in serum interleukin -10 and hepatic heme oxygenase-1 protein and mRNA expression that was induced by GalN, inhibited the increase in the nuclear level of nuclear factor-kappa B, and enhanced the increase in NF-E2-related factor 2.

Our findings suggest that wild ginseng CMCs protects liver against GalN-induced inflammation by suppressing proinflammatory mediators and enhancing production of anti-inflammatory mediators.

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