Title of article :
Camel’s milk ameliorates TNBS-induced colitis in rats via downregulation of inflammatory cytokines and oxidative stress
Author/Authors :
Arab، نويسنده , , Hany H. and Salama، نويسنده , , Samir A. and Eid، نويسنده , , Ahmed H. and Omar، نويسنده , , Hany A. and Arafa، نويسنده , , El-Shaimaa A. and Maghrabi، نويسنده , , Ibrahim A.، نويسنده ,
Issue Information :
روزنامه با شماره پیاپی سال 2014
Pages :
9
From page :
294
To page :
302
Abstract :
Current treatment strategies for inflammatory bowel diseases (IBD) are associated with several adverse effects, and thus, the search for effective agents with minimal side effects merits attention. Camel’s milk (CM) is endowed with antioxidant/anti-inflammatory features and has been reported to protect against diabetes and hepatic injury, however, its effects on IBD have not been previously explored. In the current study, we aimed to investigate the potential alleviating effects of CM against TNBS-induced colitis in rats. CM (10 ml/kg b.i.d. by oral gavage) effectively suppressed the severity of colon injury as evidenced by amelioration of macroscopic damage, colon weight/length ratio, histopathological alterations, leukocyte influx and myeloperoxidase activity. Administration of CM mitigated the colonic levels of TNF-α and IL-10 cytokines. The attenuation of CM to colon injury was also associated with suppression of oxidative stress via reduction of lipid peroxides and nitric oxide along with boosting the antioxidant defenses through restoration of colon glutathione and total anti-oxidant capacity. In addition, caspases-3 activity, an apoptotic marker, was inhibited. Together, our study highlights evidences for the promising alleviating effects of CM in colitis. Thus, CM may be an interesting complementary approach for the management of IBD.
Keywords :
TNBS , Colitis , inflammation , oxidative stress , Camel’s milk , caspase-3
Journal title :
Food and Chemical Toxicology
Serial Year :
2014
Journal title :
Food and Chemical Toxicology
Record number :
2126993
Link To Document :
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