Abstract
BackgroundSeptin4 (SEPT4) exists widely in human tissues and is related to mechanical stability, actin dynamics, membrane trafficking, viral replication and apoptosis. Data from many studies have suggested that SEPT4 plays a significant role in liver fibrosis. SEPT4 is down-regulated in the model of CCl4 and BDL treated liver fibrosis. However, it is up-regulated and peaked at 12 weeks post-infection (p.i.), and then decreased subsequently in Schistosoma japonicum (S. japonicum) egg-induced liver fibrosis. The aim of this study was to observe the dynamic alteration of SEPT4 after the treatment of praziquantel (PZQ) in ICR mice infected with S. japonicum.MethodsExpression of SEPT4 was determined by western blot, immunofluorescence and qRT-PCR. And pro-inflammatory cytokines IL-6 and TNF-α were detected by qRT-PCR. The number of eggs, the diameter of egg granulomas and fibrosis-associated genes were also measured.ResultsOur results showed that the granulomatous inflammation was reduced, whereafter the expression of SEPT4 on hepatic stellate cells (HSCs) was decreased after PZQ anti-schistosome therapy. And the variation tendency of SEPT4 had positive correlation with the inflammatory response in the area of S. japonicum egg granulomas.ConclusionsBased on these findings, the inhibition of the expression of the SEPT4 by PZQ might be due to alleviation of the inflammatory response at the chronic and advanced stage of S. japonicum infection.
Highlights
Septin4 (SEPT4) exists widely in human tissues and is related to mechanical stability, actin dynamics, membrane trafficking, viral replication and apoptosis
General histology and change of fibrosis-associated genes Granuloma induced by the schistosome egg is an inflammatory reaction and the diameter of egg granulomas reflects the degree of inflammatory response
Egg granulomas of S. japonicum egginduced liver fibrosis tissues at the acute stage were observed at 6 weeks p.i. and the diameter of egg granulomas were largest at this stage
Summary
Septin (SEPT4) exists widely in human tissues and is related to mechanical stability, actin dynamics, membrane trafficking, viral replication and apoptosis. Data from many studies have suggested that SEPT4 plays a significant role in liver fibrosis. SEPT4 is down-regulated in the model of CCl4 and BDL treated liver fibrosis. It is up-regulated and peaked at 12 weeks post-infection (p.i.), and decreased subsequently in Schistosoma japonicum (S. japonicum) egg-induced liver fibrosis. Following chronic injury to the liver, HSCs change from a quiescent form to an activated phenotype so that they lose the ability to store vitamin A, begin to express α-smooth muscle actin (α-SMA) and produce extracellular matrix (ECM) [2,8,9]. It has been identified that activated HSCs are shown to be present in the periphery of egg granulomas in murine and human S. japonicum infection [10]. HSCs play a pivotal role in S. japonicum-induced liver fibrosis [11]
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