The antiplatelet activity of camel milk in healthy and aluminum chloride-intoxicated rats.

This study examined the effect of camel milk on some marker of blood coagulation markers in aluminum chloride (ALCl)-treated rats. Rats (n = 6) were assigned as control, control + fresh camel milk (1 ml), ALCl (0.5 mg/kg), and ALCl + fresh camel milk (1 ml and 0.5 mg/kg, respectively). Treatments were conducted orally for 30 days and daily. Administration of camel milk to control and ALCl-intoxicated rats significantly increased platelet count, bleeding time, and collagen epinephrine (CEPI)-induced platelet aggregation. It also lowered plasma levels of thromboxane B2 and hepatic levels of glutathione (GSH) and the activities of antioxidant enzymes, catalase (CAT) and superoxide dismutase (SOD). While the treatment with camel milk has no effect on the liver structure, values of activated partial prothrombin time (aPPT), and levels of prothrombin time (PT) in control rats, it improved liver architectures and decreased serum levels alanine and aspartate aminotransferases (ALT and AST, respectively), and reduced values of both aPTT and PT in ALCl-intoxicated rats. In conclusion, camel milk inhibits platelets activity and aggregation in both control and ALCl-intoxicated rats.