Schistosoma japonicum is one of the major causative agents of schistosomiasis. The pairing of males and females leads to female sexual maturation and maintains this mature state. However, the mechanisms by which pairing facilitates sexual maturation are yet to be investigated.

Chemotherapy for schistosomiasis has been around for 100 years. During the past century, great efforts have been made to develop new antischistosomal drugs from antimonials to nonantimonials, and some of these have been used extensively in clinical treatment. With the exception of a few drugs, such as oxamniquine and metrifonate, most of the antischistosomals developed in the pre-praziquantel period have variable limitations with respect to safety and efficacy. Although oxamniquine and metrifonate have been used for schistosomiasis control, they are only effective against Schistosoma mansoni and S. haematobium, respectively. Currently, praziquantel is the only drug used for treatment of all five species of human schistosomes. In this review, the pharmacological and immunological effects of praziquantel against S. japonicum are summarized and discussed. From the end of the 1970s until the 2000s, scientists have conducted a series of experimental studies on the effects of praziquantel against S. japonicum. These have included examining its unique pharmacological action on schistosomes, the characteristics in susceptibility of the different developmental stages of schistosomes to the drug, the relationship between plasma concentration of the drug and efficacy, the impact of host factors on cidal action of the drug, prevention and early treatment of schistosomal infection, as well as praziquantel-resistant schistosomiasis. The effects of praziquantel against S. japonicum, as elucidated by the experimental studies that are reviewed in this paper, may have some reference significance for the development of new antischistosomals.

Neuritin (Nrn1) is a neurotrophin that plays an important role in nervous system plasticity and repair following nerve injury. MicroRNAs (miRNAs) are a type of small non‐coding RNA that regulate nearly all aspects of nerve development and survival, including apoptosis. Here it was found that miR‐204 negatively regulates Nrn1 protein expression through direct interaction with Nrn1 transcript. Moreover, miR‐204 activates cleaved caspase‐3, enhancing the sensitivity of RSC96 Schwann cells to H₂O₂‐induced oxidative stress and apoptosis. Thus, miR‐204 expressed at a low level may create a microenvironment suitable for the repair of injured nerves by relieving the inhibition of Nrn1 transcription and stimulating the anti‐apoptotic function of Schwann cells. These results provide novel insights into the roles of miR‐204 in nerve injury and repair.