Abstract
This study was aimed to assess the therapeutic potential of camel milk on the carbon tetrachloride (CCl4)-induced hepatic injury in rats. A total of 24 Rats were randomized and divided into 4 groups (6 rats for each). Group 1: control untreated, group 2 was orally treated with camel milk (5 ml/rat/day) through gastric intubation with duration of 3 times weekly for 2 weeks and 5 times weekly for another 4 weeks. Group 3: CCl4 intoxicated rats (intraperitoneally injected with CCl4(1ml/kg b. w, 3 times weekly for 4 weeks). Group 4 was treated with CCl(4)and camel milk with the same dose and treatment protocol of the group 2 & 3. Blood samples were collected at the end of experiment for determination of serum levels of liver enzymes, albumin and total proteins. Determination of inflammatory cytokines (TNF-alpha and IL-1 beta) in liver homogenate was done and detection of the hepatic m-RNA expression of CYT p450 2E1. Other liver specimens were routinely fixed and processed for histopathological evaluationin addition, immunohistochemical evaluation of a-SMA expressionin hepatic sections was performed. Results revealed thatCCl(4)induced significant (P< 0.01) increase in serum hepatic enzymesand significant (P< 0.01) reduction of serum total proteins and albumin with elevated levels of TNF-alpha and IL-1 beta compared with control animals. Genetic results showed that the administration of CCl4 caused a significant down - regulation of the expression of CYP2E1 genes in liver tissue compared to control. On other hand the treatment with camel milk markedly improve serum hepatic functions and inhibit the down regulation of inflammatory cytokines and CYP2E1 genes in liver. Varioushistopathological alterations were detected in CCl4-intoxicated group that was markedly ameliorated by camel milk administration. Conclusion: the present study proved the therapeutic potential of camel milk against CCl4 - induced hepatic damage though improvement of hepatic function, decrease level of inflammatory cytokines and inhibit the down regulation of CYP2E1 genes in liver as well as markedly reduced hepatic histopathological alterations.