Role of N-acetylcysteine on fibrosis and oxidative stress in cirrhotic rats

Abstract

-Background -Hepatic cirrhosis is the final stage of liver dysfunction, characterized by diffuse fibrosis which is the main response to the liver injury. The inhalatory carbon tetrachloride is an effective experimental model that triggers cirrhosis and allows to obtain histological and physiological modifications similar to the one seen in humans. Aim -To investigate the effects of N-acetylcysteine (NAC) on the fibrosis and oxidative stress in the liver of cirrhotic rats, analyzing liver function tests, lipoperoxidation, activity of glutathione peroxidase enzyme, collagen quantification, histopathology, as well as the nitric oxide role. Methods -The animals were randomly in three experimentals groups: control (CO); cirrhotic (CCl4) and CCl4 + NAC. Evaluate the lipid peroxidation, the glutathione peroxidase enzyme, the collagen and the expression of inducible nitric oxide synthase (iNOS). Results -The cirrhotic group treated with N-acetylcysteine showed trough the histological analysis and collagen quantification lower degrees of fibrosis. This group has also shown less damage to the cellular membranes, less decrease on the glutathione peroxidase levels and less expression of inducible nitric oxide synthase when matched with the cirrhotic group without treatment. Conclusion -N-acetylcysteine seams to offer protection against hepatic fibrosis and oxidative stress in cirrhotic rat livers.

Effect of N-Acetylcysteine and Fructose-1,6-Bisphosphate in the Treatment of Experimental Sepsis

“…When the liver lesion parameters (AST and ALT) were analyzed, only the NAC-treated group presented a reduction in the AST plasma levels compared to the septic group, demonstrating its hepatoprotective role. This protective ability has been previously described in the literature, using carbon tetrachloride (CCl 4 )-induced cirrhotic animals, suggesting a protective effect related to the glutathione peroxidase, an endogenous antioxidant enzyme key in combating the ROS [49]. To verify that NAC would increase the cellular antioxidant defenses, we have also measured hepatic reduced glutathione levels.…”

Effects of albumin administration in serum liver enzymes of rats in the presence of extrahepatic biliary obstruction

“…Oxidative stress plays an important role in the activation of hepatic stellate cells. Antioxidants such as albumin, can prevent this activation and their subsequent role in liver fibrogenesis 7 . Studies show that there is a decrease in plasma levels of albumin in rats with common bile duct ligation, although they have conflicting results 8,9 , with two weeks of the beginning of the experiments, probably due to increased capillary permeability and a lack of compensation by increasing its hepatic synthesis, to a decrease of the same, and also by an increase in plasma volume after four weeks of the beginning of the experiment 10 .…”

Hepatotoxicity Implies Chemical-Driven Liver Damage Induced By Certain Medicinal and Other Chemical Agents

“…Ko et al, 1995 reported that certain natural extracts containing antioxidants protect against the CCl4-induced increased lipid peroxide levels and impairment in hepatic GSH status.Hepatic malondialdehyde (MDA) levels were also highly significantly increased in CCl4 treated group, showing an increased oxidative stress compared to control group. The increased MDA level suggests enhanced lipid peroxidation leading to tissue damage and failure of antioxidant defense mechanisms to prevent formation of excessive free radicals as described by (Pereira- Filho et al, 2008) and confirmed by (Kim et al, 2010).…”