Evaluation of muscular apoptotic changes and myogenin gene expression in experimental trichinosis after stem cells and atorvastatin added to ivermectin treatment.

Trichinosis is a common parasitic disease that affects the striated skeletal muscles, causing apoptotic and degenerative changes associated with myogenin expression in the affected myocytes. Hence, this study aimed to assess the ameliorative effects of stem cells and atorvastatin added to ivermectin on the infected myocytes during the muscular phase of murine trichinosis. 120 laboratory Swiss albino male mice were divided into 10 groups, and each group was subdivided into intestinal and muscular phases (each n = 6); uninfected control; untreated infected control; infected received ivermectin monotherapy; infected received atorvastatin monotherapy; infected received stem cells monotherapy; infected received ivermectin and atorvastatin dual therapy; infected received ivermectin and stem cells dual therapy; infected received atorvastatin and stem cells dual therapy; infected received ivermectin 0.2, atorvastatin 40, and stem cells triple therapy; and infected received ivermectin 0.1, atorvastatin 20, and stem cells triple therapy. Intestinal phase mice were sacrificed on the 5th day post-infection, while those of the muscular phase were sacrificed on the 35th day post-infection. Parasitological, histopathological, ultrastructural, histochemical, biochemical, and myogenin gene expression assessments were performed. The results revealed that mice that received ivermectin, atorvastatin, and stem cell triple therapies showed the maximum reduction in the adult worm and larvae burden, marked improvement in the underlying muscular degenerative changes (as was noticed by histopathological, ultrastructural, and histochemical Feulgen stain assessment), lower biochemical levels of serum NK-κB and tissue NO, and lower myogenin expression. Accordingly, the combination of stem cells, atorvastatin, and ivermectin affords a potential synergistic activity against trichinosis with considerable healing of the underlying degenerative sequel.

Ultrastructural changes and IgA modulatory effect of commercial prebiotic and probiotic in murine giardiasis.

Giardiasis, a parasitic infection of the gastrointestinal tract, is prevalent worldwide. The integrity of the intestinal epithelial barrier plays an important defensive role in giardiasis, and as Oral supplementation with prebiotics and probiotics is known to reinforce the intestinal barrier in many gastrointestinal diseases, this study assessed the effects of prebiotic and probiotic supplementation in giardiasis and compared the results with those obtained after nitazoxanide therapy. Swiss albino male lab-bred mice (n = 50) were divided into three major groups; Group I (control group), i.e., negative (noninfected nontreated) and positive controls (infected nontreated); Group II (preventive group), in which mice were provided prebiotic, probiotic, or a combination for 7 days before of infection, and Group III (therapy group), in which mice were administered prebiotic, probiotic, combined supplements and nitazoxanide from day 12 post-infection. The assessment was achieved through Giardia cyst count, histopathological examination and ultrastructure study. Also, Serological and immunohistochemical parameters were done to evaluate the modulation of IgA levels. Oral supplementation with prebiotic and probiotic, either before or after infection (in preventive or therapy groups respectively) resulted in a significant reduction in Giardia cyst shedding. Remarkable histological and ultrastructure improvement in the intestinal changes, along with a significant increase in the serological and immunohistochemical IgA levels, were seen in mice provided combined supplements and nitazoxanide (in therapy group). Thus, our results indicate that combined prebiotic and probiotic supplementation has promising anti-Giardia activity and that it can restore intestinal structures and modulate IgA response, apart from providing synergistic effects when added to nitazoxanide.