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SC in healthy mice led to a decrease in percentage of these cells in the spleen of female mice. Moreover, sildenafil was found to diminish serum levels of IL-6 in mice and demonstrated a tendency to increase IL-2. No influence of sildenafil on serum levels of IL-10, IL-1 ? or vascular endothelial grow factor (VEGF) was observed. Sildenafil revealed a considerable immunosuppressive effect in male as opposed to female mice [21]. The differences in immunological effects of the drug between females and males could be explained by endocrine and genetic differences between the sexes [22]. It should be noted that sildenafil in this study was used in large doses—20 mg/kg for 21 days. Ex vivo studies of the effects of sildenafil on isolated splenocytes from healthy mice confirmed a lack of influence on the cytotoxicity of mononuclear cells (CD8 + , NKT, and NK cells). SC did not affect either maturation or activation of dendritic cells (DC). But with respect to naive/memory phenotype of T cells sildenafil reduced the amount of CD8 + cells in whole population. Sildenafil at the concentration of 7.5 ? M after 24 h of culture increased the percentage of CD4 + T cells and reduced the percentage of B cells [21]. Szczypka and Obminska-Mrukowicz [23] investigated the effects of sildenafil on thymocytes, splenocytes, and T cells isolated from mice lymph nodes. Oral administration of sildenafil at a dose 1 mg/kg temporarily decreased the percentage of CD4 + CD8 + thymocytes and increased CD8 + cells. This effect was only observed after the fifth dose of the drug administrated at 24 h intervals. Among lymphocytes isolated from the mesenteric lymph nodes, the percentage of CD19 + cells decreased and a rise in the percentage of CD3 + cells was noted 72 h after the last dose of the drug. In another study researchers used the same protocol of administration of SC to investigate cytokine concentration in animals serum. Sildenafil decreased IL-2 level after 72 h from a single administration of 1 mg/kg and after 12 h enhanced temporarily the level of IL-5 (from 7 to 13 pg/mL) [24]. Szczypka and Obmiska-Mrukowicz [25] showed that sildenafil increased the production of IL-1 ? and nitric oxide (NO) by peritoneal macrophages ex vivo, increased the percentage of phagocytosing granulocytes, and decreased the percentage of phagocytosing monocytes. The Effect of Sildenafil on the Experimental Animals Immune System in Pathological Conditions. PDE5 is present in glial cells and neurons [26, 27]. [29] reported that immunomodulatory therapies can be particularly beneficial in the treatment of multiple sclerosis (MS), a disease in which the immune system reacts against the central nervous system (CNS) antigens, initiating a detrimental inflammatory cascade which leads to demyelination and axonal degeneration. [30], in their research on experimental autoimmune encephalomyelitis (EAE) as a model of MS, found that administration of sildenafil to mice (10 mg/kg, equivalent to a dose of 57 mg/day for a 70-kg human) for 7 days, at the onset of clinical symptoms, resulted in reduced cellular infiltration in spinal cord and white matter. Sildenafil treatment increased the number of cells expressing the forkhead box p3 (Foxp3) transcription factor, as well as the expression of mRNA of granzyme B (GrB) cluster proteins. CD4 + and CD8 + Treg cells are known to act by granzymes in the inhibition of T effectors cells and antigen presenting cells (APC). It was shown that GrB protein was upregulated in Treg cells [30]. Moreover, production of IL-2, IFN- ? , and IL-4 in cultures of splenocytes isolated from sildenafil-treated mice was reduced. A tendency to reduce the level of TNF- ? and IL-17 was also observed. Sildenafil did not change the level of inhibitory cytokine IL-10. In vitro proliferation of splenocytes from control group mice after stimulation with phytohemagglutinin (PHA) and exposure to sildenafil from 0.1 to 10 ? M/mL was decreased in the SC concentration-dependent manner [30]. Examination of sildenafil-treated EAE mice brains showed that infiltration of inflammatory cells to the brain was reduced due to a lower expression of the intracellular adhesion molecule-1 (ICAM-1). It was found that sildenafil also cialis 5 mg tablet price decreased the level of autoantibodies against myelin oligodendrocyte glycoprotein in the serum [31]. [32] confirmed a strong anti-inflammatory effect of sildenafil as a result of influence on TNF- ? , IFN- ? , IL-2, and IL-1 ? production in cerebella in sildenafil-treated MS mice. continued their research [33] in cuprizone- (CPZ-) induced demyelination in mice. Mice treated with sildenafil and CPZ for 15 days had decreased levels of IL-1 ? and TNF- ? in the serum compared to the CPZ group, but sildenafil did not affect concentration of IL-2. Expression of NO was significantly increased in animals treated with sildenafil, in comparison to the control group. Expression of IL-10 was higher in cerebella from sildenafil-treated mice than in CPZ group. [34] on placental and trophoblast cells from LPS-induced abortion mice provided insights into protective properties of sildenafil during pregnancy. Orally administered sildenafil blocks transcription of nuclear factor- ? B (NF- ? B) in nuclei of trophoblast cells and decreased the level of proinflammatory cytokines TNF- ? and IL-1 ? in placenta fragments. P-Selectin (P-Sel) expression was analyzed in the spongiotrophoblast area, where giant trophoblastic cells are predominant. The LPS-treated group had decreased expression of P-Sel. Sildenafil either alone or in combination with heparin was beneficial for maintaining higher levels of get cialis now P-Sel, similar to what was found in the control group [35]. Adhesion molecules such as P-selectin play a role in embryo implantation and placentation and can also be a marker of healthy placentas [36, 37]. [39] found that in tumor-bearing mice the inhibition of PDE5 with sildenafil prolongs survival of the animals through the augmentation of antitumor immunity.
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