Praziquantel CAS 55268-74-1

Studies have shown that praziquantel can interfere with the Ca2+ internal environment of schistosomes. Praziquantel may change the permeability of worms to Ca2+, promote inflow and contracture of worms, or change the distribution of Ca2+ in cortical cytoplasm and muscle and cause cortical damage; It is manifested as the activity of the worm body, followed by the contraction of the worm body. These reactions depend on the existence of Ca2+ and are restricted by M. The schistosomiasis cultured in vitro can cause cortical damage after being treated with praziquantel for 5 minutes, white blood cells and macrophages It is easy to enter the insect body through the damaged part and further decompose the insect body.

The internal environment of Ca2+ in Schistosoma cells can be regulated by some cellular components, such as: voltage-gated calcium channels (Voltagegated calcium channels, VGCCs), ligand-gated calcium channels, second messenger-gated calcium channels, etc., these channels may become praziquantel Targets for regulation of Ca2+ homeostasis.

The mode of action of praziquantel may be as follows: ① Praziquantel can combine with the protein dimer of the same amount in the dimer interface groove to form crystals, thereby inhibiting the catalytic activity of schistosomal japonicum. ② Praziquantel can block the combination of poison and Schistosoma japonicum GST, so that the poison can accumulate in the worm. However, there are also studies that praziquantel does not inhibit the activity of Schistosoma japonicum GST, and is not the target molecule of praziquantel.

Actin is a highly conserved protein family that exists in all eukaryotic cells. It is the main component of the cytoskeleton and participates in cell division, movement, migration and shape maintenance. It mainly composes muscle filaments and completes muscle contraction.

Experiments showed that the molecular size of the membrane surface bound to praziquantel was 45 kDa, and amino acid sequencing showed that most of it was composed of actin. Praziquantel may bind to the lipid bilayer membrane of schistosomiasis and cause cortical damage, leading to antigen exposure, including actin exposure. The combination of praziquantel and actin of Schistosoma japonicum may cause changes in molecular conformation, affect the function of actin, severely damage the integrity of the cortex, and change the physiological traits of Schistosoma japonicum.

Praziquantel cannot kill Schistosoma japonicum eggs, but it can significantly reduce the granuloma of eggs or directly lead to the regression of granulomas, and it has a cellular immunosuppressive effect on the inflammatory cell reaction around Schistosoma japonicum eggs, so it can be considered as praziquantel Ketone directly inhibited egg granuloma, and the mechanism of inhibiting egg granuloma is likely to be the regulation of host immune function. Praziquantel, due to its short half-life, requires the subsequent engagement of the host immune system, otherwise the damaged schistosomiasis has the potential to recover.