ايمونوپارازيتولوژي اثرات ضد ليشمانيايي داروي ASA در موش هاي Balb/c حساس به ليشمانيا ماژور از طريق مكانيسم هاي NO و CRP

Immunoparasitologyc evaluation of ASA in Susceptible Balb/c Mice Infected with L. major via Nitric Oxide (NO) and C-Reactive Protein (CRP) pathways

Leishmaniasis is a zoonotic disease caused by Leishmania parasites, ranging from self-healing cutaneous lesion to severe and non-healing disseminated cutaneous or visceral leishmaniasis (VL). Cutaneous leishmaniasis (CL) is a chronic infectious and granulomatous disease caused by Leishmania parasites. NO is an inorganic free radical and versatile biological messenger that its biological roles especially as a cytotoxic anti-pathogenic agent released during an inflammatory response and involved in the microbicidal activity of macrophages against L.major as intracellular pathogens. CRP has been found in association with acute infections and a variety of inflammatory disorders. Aspirin can inhibit inflammatory reactions and platelet aggregation, but little is known about the effects of the ASA in leishmaniasis treatment. The purpose of this study was to evaluate of anti-leishmanial effect of ASA drug in susceptible Balb/c mice infected with L. major through its anti oxidant role with induction of immunity mediators such as NO and CRP in host, inhibition of visceralization of parasite and its effect on healing of leishmania lesion and proliferation of parasite in macrophages in compare with control groups. In order to carry out this investigation, mice were assigned into 4 groups as 2 groups of control and 2 groups of infected Balb/c. Experimental leishmaniasis was initiated by (s. c) injection of the 2*106 L. major promastigotes into the basal tail of infected groups. The appropriate of concentration of ASA was prepared in ethanol (60%) and after appearance of lesion it was inoculated to test groups as oral with gavage. The development of lesions was determined weekly by measuring the two diameters. After 13 weeks, all mice were killed humanly and target tissues including lymph node, spleen and liver from each mouse were removed, weighted and their impression smears were also prepared. Griess microassay method applied for measurement of NO in plasma and target organs. CRP was detected by a rapid latex agglutination test kit. In this study, ASA has some anti- leishmanial effect through changing of NO and CRP as immunity and inflammatory factors in Balb/c mice infected with L.major. It seems application of ASA could decrease parasite visceralization in target organs as well as declining its proliferation inside macrophages, however it has no effects on lesion size, survival rate and hepato/splenomegaly. ASA presented its ability to alter NO concentration in plasma during L.eishmania infection in mice, but it has no effects on liver and spleen NO levels. Although these alterations could affect the proliferation of amastigotes inside infected macrophages, however more studies are required to clarify this concept.