Fig. 6

Effect of Vilda, DDS, and Vilda/DDS on α-SMA and MMP-9 as fibrotic markers on S. mansoni-infected mice. (a) Photomicrographs of immunohistochemical staining (IHC) of hepatic tissues with alpha-smooth muscle actin (α-SMA) (× 200, scale bar = 100µm) as follows: liver sections of normal control and normal treated groups (Control, Vilda, DDS, and Vilda/DDS) marked scarce hepatocytes with positive cytoplasmic reactivity to α-SMA antibody (arrow). Liver sections from (Infected to Inf + PZQ) highlighted positive expression of α-SMA along ova of Schistosoma (arrowhead), fibroblast encircling granuloma (circle), inflammatory cells with nuclear expression (cube), and surrounding hepatocytes with cytoplasmic reactivity (arrow). The expressions were graded as intense in the Infected group, high in Inf + DDS group, moderately high in Inf + PZQ group, moderately low in Inf + Vilda/DDS group, and few in Inf + Vilda group. (b) Quantitative analysis of hepatic α-SMA IHC expression; (c) Hepatic level of matrix metallopeptidase-9 (MMP-9) as a fibrotic marker. Data are presented as mean ± SEM, (n = 6) and analyzed by one-way ANOVA followed by Tukey multiple comparisons. ^aSignificantly different from the normal untreated group (Control), ^bSignificantly different from the S. mansoni-infected untreated group (infected), ^cSignificantly different from Inf + PZQ group, and ^dSignificantly different from Inf + Vilda/DDS group, at P < 0.05. Inf + PZO, infected mice treated with paraziquantel; Inf + Vilda/DDS, infected mice treated with a combination of vildagliptin and diaminodiphenyl sulphone; Inf + Vilda, infected mice treated with vildagliptin; Inf + DDS, infected mice treated with diaminodiphenyl sulphone. All treatments were administered for 14 consecutive days, except PZQ for two consecutive days.