Protein Information

ID 8
Name superoxide dismutase
Synonyms IPO B; Indophenoloxidase B; MNSOD; Manganese superoxide dismutase; Manganese containing superoxide dismutase; Mangano superoxide dismutase; Mn superoxide dismutase; Mn SOD…

Compound Information

ID 1392
Name carbon tetrachloride
CAS tetrachloromethane

Reference

PubMed Abstract RScore(About this table)
19836219 Quan J, Yin X, Xu H: Boschniakia rossica prevents the carbon tetrachloride-induced hepatotoxicity in rat. Nutr J. 2006 Dec 2;5:31.
The present study was undertaken to investigate the hepatoprotective effect of Boschniakia rossica extract (BRE), rich in phenylpropanoid glycoside and iridoid glucoside, on CCl (4)-induced liver damage. Male Wistar rats were randomly divided into six groups of ten each. While the first group was maintained as normal control, groups II-VI were administered 0.5ml/kg CCl (4) (model), 100mg/kg BRE plus CCl (4), 200mg/kg BRE plus CCl (4), 50mg/kg silymarin plus CCl (4) and 200mg/kg BRE, respectively. CCl (4) challenge not only elevated the serum marker enzyme activities and reduced albumin (ALB) level but also increased liver oxidative stress, as evidenced by elevated lipid hydroperoxide (LOOH) and malondialdehyde (MDA) concentrations, combined with suppressed potential of hepatic antioxidative defense system including superoxide dismutase (SOD), glutathione peroxidase (GPx) activities and reduced glutathione (GSH) content. Furthermore, serum tumor necrosis factor-alpha (TNF-alpha), hepatic nitrite level, inducible nitric oxide synthase (iNOS) and cyclooxygenase-2 (COX-2) protein contents were elevated while cytochrome P450 2E1 (CYP2E1) expression and function were inhibited. Preadministration of BRE not only reversed the significant changes in serum toxicity markers, hepatic oxidative stress, xenobiotic metabolizing enzymes and proinflammatory mediators induced by CCl (4) but also restored liver CYP2E1 level and function. Interestingly, the protein expression of heme oxygenase-1 (HO-1) was further elevated by BRE treatment, which was markedly increased after CCl (4) challenge. These results demonstrate that BRE exhibits protective effect on CCl (4)-induced acute hepatic injury via, at least in part, reduced oxidative stress, suppressed inflammatory responses and induced HO-1 protein expression combined with improved CYP2E1 level and function in liver.
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