Hepatoprotective Effects of Curcumin Against Diethyl Nitrosamine Induced Hepatotoxicity in Albino Rats

Abstract

Curcumin is widely used as a traditional medicine. This work was aimed to investigate its possible protective effect against chemically induced hepatocellular carcinoma (HCC) in rats. Fifty male albino rats were divided into five groups (n=10, each). The control group received a single dose of normal saline, the diethylnitrosamine (DENA) group received a single intra-peritoneal dose at 200mg/kg body weight, and the 3rd, 4th and 5th groups were given DENA and daily administrated curcunine (CUR) via intra-gastric intubation in doses of 300,200 and 100 mg/kg b.wt. respectively for 20 weeks. Serum, and liver samples were used for determination of alpha feto-protein (AFP), interleukin-2 (IL-2), interleukine-6 (IL-6), serum liver enzymes (AST, ALT, ALP and GGT) levels as well the activities and gene expression of glutathione peroxidise (GPx), glutathione reductase (GR), catalase (CAT) and super oxide dismutase (SOD). Curcumin significantly lowered the serum levels of AFP, IL-2 and IL-6, ALT, ALT, and malondialdehyde (MDA) as well gene expression of IL-2 and IL-6. In contrast it increased the gene expression and activities of Gpx, GRD, CAT and SOD. The protective effect of CUR against DEN-induced hepatocarcinogenesis in albino rats was proven.

Spices for Prevention and Treatment of Cancers

“…HIF-1α and HIF-2α protein levels were lowered by curcumin in hypoxia, and ARNT protein levels and HIF transcriptional activity were reduced in normoxia and hypoxia by curcumin, and survival of Hep3B hepatoma cells was negatively impacted [43]. Diethylnitrosamine (DENA)-induced hepatocarcinogenesis and damage were prevented and reversed by curcumin in rats [44,45]. Curcumin remarkably suppressed the serum levels of α feto-protein (AFP), interleukin-2 (IL-2), interleukine-6 (IL-6), alanine amino transferase (ALT), and malondialdehyde (MDA) as well as gene expression of IL-2 and IL-6, and increased the gene expression and activities of glutathione peroxidase (Gpx), glutathione reductase (GR), catalase (CAT) and super oxide dismutase (SOD) [44].…”

“…Diethylnitrosamine (DENA)-induced hepatocarcinogenesis and damage were prevented and reversed by curcumin in rats [44,45]. Curcumin remarkably suppressed the serum levels of α feto-protein (AFP), interleukin-2 (IL-2), interleukine-6 (IL-6), alanine amino transferase (ALT), and malondialdehyde (MDA) as well as gene expression of IL-2 and IL-6, and increased the gene expression and activities of glutathione peroxidase (Gpx), glutathione reductase (GR), catalase (CAT) and super oxide dismutase (SOD) [44]. Moreover, the overexpression of the angiogenic and anti-apoptotic factors transforming growth factor-β (TGF-β) and protein kinase B (PKB) were reduced, while caspase-3 expression was improved.…”

Baicalein and its underlying mechanism as a protector against liver injury induced by cisplatin in mice

“…Among them, GST is an important phase II enzyme which catalyses the conjugation of reactive metabolites with GSH [30]. GPx catalyses the GSH-dependent reduction of H 2 O 2 and hydroperoxides to non-toxic products and glutathione disulfide (GSSG), while GSSG can then be converted back to GSH by GR using NADPH (nicotinamide adenine dinucleotide phosphate) [31,32]. In the present study ( Figure 5), there was an obvious decrease in the liver activities of GPx, GST and GR in cisplatininduced mice compared to the controls (P < 0.001, P < 0.01, P < 0.01), whereas the activities of GPx, GST and GR significantly increased with baicalein (60 mg/kg) pretreatment (P < 0.01, P < 0.05, P < 0.05).…”

Hinokitiol-Ameliorated Diethylnitrosamine-Induced Hepatocarcinogenesis Through Antioxidant Mechanism in Rats: In Vitro and in Vivo Study

“…The portal triad consisted of hepatic artery, portal vein, and bile duct which constituted various zones surrounding these areas. DEN produced centrizonal necrosis, hydropic, and fatty changes with sinusoids congestion [41,42]. After treatment with HIOL, repaired the liver architecture and protected the hepatic tissue from degenerative and fatty alterations, by averting the toxic chemical reaction, OS, lipid peroxidation, molecular changes in the liver tissues, and micro-and macro-vesicular fatty changes ultimately leading to necrosis.…”