Tern of growth and attained a normal weight Naramycin A web PubMed ID:https://www.ncbi.nlm.nih.gov/pubmed/28381880 gain reaching 341.33 ?6.184 g over 8 weeks. The cirrhosis rats (Group 2) suffered growth retardation and had a significantly (P<0.05) lower weight than other groups. When the body weights were factored in, rats from Group 2 measured the highest liver index. Silymarin-treated rats (Group 3) and the rats treated with a high dose (500 mg/kg) of CLRE extract (Group 5) attained weights equivalent to Group 1, the normal rats. Rats treated with the low dose (250 mg/kg) of CLRE extract (Group 4) gained more weight than those of Group 2 but not as much as those attained in Group 3 and 5 (Table 3). These findings suggested thatSalama et al. BMC Complementary and Alternative Medicine 2013, 13:56 http://www.biomedcentral.com/1472-6882/13/Page 8 ofTable 4 Effect of CLRE on OHdG, Nitrotyrosine and MDA from rats at the end of 8 weeks studyTreatment Normal rats Cirrhosis rats Silymarin-treated Rats Low Dose CLRE-treated rats (250 mg/kg) High Dose CLRE-treated rats (500 mg/kg) 8-OH-dG (ng/mL) 2.17 ?0.33 5.40 ?0.34** 2.80 ?0.15* 2.83 ?0.33* 2.37 ?0.88* Nitrotyrosine (ng/mL) 1.06 ?0.07 3.87 ?0.13** 1.67 ?0.07* 1.40 ?0.20* 1.33 ?0.13* MDA (nM/mg protein) 2.17 ?0.33 5.40 ?0.34** 2.80 ?0.15* 2.83 ?0.33* 2.37 ?0.88*Data are expressed as mean ?SEM. *P<0.001 compared with the cirrhosis control Group 2. **P<0.001 compared with normal control Group 1. CLRE: C. longa rhizomes ethanolic extract.high dose CLRE could be optimal since it was as effective as Silymarin in attenuating cirrhosis progression.Specific liver markers and total protein, albumen and BilirubinThe plasma levels of specific liver enzymes and protein profile was measured to determine the liver function of each rat (Figures 3, 4 and 5). The liver damage induced by TAA toxicity significantly (P<0.001) elevated the plasma level of specific liver enzymes (AP, ALT, AST, bilirubin and prothrombin time ratio) and significantly (P<0.001) lowered protein and albumen levels in the hepatotoxic rats of Group 2 compared with the other groups. The high dose CLRE-treated rats (Group 5) resulted in comparable biochemical marker readings to those of normal control Group 1 and Silymarin-treated Group 3, and better than those recorded from the low dose CLRE-treated rats (Group 4). These data demonstrated that the effects of toxicity induced by TAA on the liver function could be effectively counterbalanced by CLRE treatment.significantly lower levels (P< 0.001) of liver MDA and nitrotyrosine compared with the cirrhosis rats of Group 2. In addition, low and high dose treated rats had significantly lower levels (P<0.001) of urinary 8-OH-dG contents in comparison to the cirrhosis rats. Moreover, there were no significant differences in the tested oxidative stress biomarkers between CLRE-treated animals and Silymarintreated animals. These results suggest that treatment with CLRE may protect hepatic cells from further damage during cirrhosis.Hepatocellular antioxidant enzymesHepatic CYP2E1 levelsAs shown in Figure 6, animals from the cirrhosis Group 2 had significantly (P<0.001) higher levels of CYP2E1 compared with the normal Group 1 and Silymarintreated Group 3. However, there was no difference between the low dose CLRE-treated animals of Group 4 and high dose CLRE-treated animals of Group 5 which had similar CYP2E1 levels, or between these groups and the cirrhosis Group 2.The loss of hepatocytes in the cirrhotic livers of animals was indirectly analyzed by the activity of the.
