Schistosomiasis remains a major global public health concern. Currently, the control of this
neglected tropical disease still depends on
chemotherapy to reduce the prevalence and intensity of the
parasite infection. It has been widely accepted that
praziquantel is highly effective against all species of Schistosoma, and this agent is virtually the only
drug of choice for the treatment of human
schistosomiasis.
Mass drug administration (MDA) with
praziquantel has been shown to be effective in greatly reducing the prevalence and morbidity due to
schistosomiasis worldwide. In addition to antischistosomal activity, a large number of experiential and clinical evidence has demonstrated the action of
praziquantel against
fibrosis caused by S. mansoni and S. japonicum
infections through decreasing the expression of fibrotic
biomarkers such as α-smooth muscle actin (α-SMA),
collagen,
matrix metalloproteinase (
MMP), and
tissue inhibitor of metalloproteinase (TIMP), and inhibiting the expression of proinflammatory
cytokines such as
interleukin (IL)-6,
tumor necrosis factor (TNF)-α, and
transforming growth factor (TGF)-β, as well as
chemokines, and similar antifibrotic activity was observed in mouse models of
fibrosis induced by
carbon tetrachloride (CCl4) and
concanavalin A (Con-A). In this review, we discuss the role of
praziquantel in the prevention and treatment of
fibrosis associated with
schistosomiasis and the possible mechanisms. We call for randomized, controlled clinical trials to evaluate the efficacy and safety of
praziquantel in the treatment of
schistosomiasis-induced hepatic
fibrosis, and further studies to investigate the potential of
praziquantel against
fibrosis associated with alcohol consumption, viruses, and toxins seem justified.