Abstract
BackgroundFulminant hepatic failure (FHF) is clinical syndrome with very poor prognosis and high mortality there is urgent need for the development of safe and non-toxic hepatoprotective agents for the adequate management of hepatitis. Hepatoprotective effect of the Lepidium sativum ethanolic extract (LSEE) was assessed by D-galactosamine-induced/lipopolysaccharide (400 mg/kg and 30 μg/kg) liver damage model in rats.MethodsHepatoprotective activity of LSEE (150 and 300 mg/kg) and silymarin on D-GalN/LPS induced FHF in rat was assessed using several liver function enzyme parameters. Antioxidant properties as antioxidant stress enzymes were assessed in hepatic Liver as well as mRNA expression of cytokines genes such as TNF-α, IL-6, and IL-10 and stress related genes iNOS and HO-1 were determined by RT-PCR. Protein expression of apoptotic genes were evaluated through western blot. MPO and NF-κB DNA-binding activity was analyzed by ELISA. The magnitude of hepatic impairment was investigated through histopathological evaluation.ResultsMarked amelioration of hepatic injuries by attenuation of serum and lipid peroxidation has been observed as comparable with silymarin (25 mg/kg p.o). D-GalN/LPS induced significant decrease in oxidative stress markers protein level, and albumin. LSEE significantly down-regulated the D-GalN/LPS induced pro-inflammatory cytokines TNFα and IL-6 mRNA expression in dose dependent fashion about 0.47 and 0.26 fold and up-regulates the IL-10 by 1.9 and 2.8 fold, respectively. While encourages hepatoprotective activity by down-regulating mRNA expression of iNOS and HO-1. MPO activity and NF-κB DNA-binding effect significantly increased and was mitigated by LSEE in a dose-dependent style as paralleled with silymarin.ConclusionOur data suggests that pretreatment of LSEE down regulates the caspase 3 and up-regulates the BCl2 protein expression. The above findings revealed that Lepidium sativum has significant hepatoprotective activity.Electronic supplementary materialThe online version of this article (doi:10.1186/s12906-016-1483-4) contains supplementary material, which is available to authorized users.
Highlights
Fulminant hepatic failure (FHF) is clinical syndrome with very poor prognosis and high mortality there is urgent need for the development of safe and non-toxic hepatoprotective agents for the adequate management of hepatitis
Assessment of biochemical markers A significant increase in serum biomarkers Aspartate Aminotransferase (AST), Alanine aminotransferase (ALT), Alkaline Phosphatase (ALP), γ-GT and bilirubin level was observed in animals administered with D-GalN/LPS, which is indicative of hepatic injuries
The possible activity of Lepidium sativum ethanolic extract (LSEE) may be due to the presence of glucosinolates, flavonoids and natural sterols. These findings established that LSEE mitigates hepatic injuries and structural damage through the decline of oxidative stress, inflammation, and apoptosis in the D-GalN/LPS induced liver damage
Summary
Fulminant hepatic failure (FHF) is clinical syndrome with very poor prognosis and high mortality there is urgent need for the development of safe and non-toxic hepatoprotective agents for the adequate management of hepatitis. Fulminant hepatic failure (FHF), a severe disease with very low prognosis and high mortality is caused by bacteria, hepatitis virus, alcohol, toxic drugs and is characterized by massive hepatocytes necrosis [1]. Administration of single dose of D-GalN results in dose dependent hepatic damage resembling viral hepatitis, with focal necrosis and periportal inflammation. It induces hepatitis by hindering the synthesis of RNA and protein via reduction in cellular UTP uptake that tips to the hepatic parenchyma necrosis [6, 7]. The quinones, flavones and carotenoids are well known antioxidants that are claimed to be hepatoprotective were evaluated by D-GaLN/LPS hepatic damage model [8, 9]
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