Objective To observe the effects of radiation on the growth and expression of cysteine-rich 61(Cyr61/CCN1) of L929 cells and investigate the relationship between CCN1 expression and radiation injury.Methods L929 cells were cultured and divided into 2 groups,cells irradiated with 4 Gy ?-irradiation as radio-group and untreated cells as control group.The cell proliferation was measured by MTT assay and plate colony formation testing.Flow cytometry was utilized to quantify the cell cycle distribution.CCN1 expression at protein and mRNA levels were determined by immunocytochemistry(ICC) and RT-PCR respectively.Results Significant inhibition of proliferation(P

Objective To study the role of Cysteine-rich 61 ( Cyr61/CNN1) in repair of combined injury by observing whether exogenous CCN1 promotes the proliferation and migration of radiation-injured L929 cells. Methods A radiation model of L929 cells was induced by ? ray at a dose of 4 Gy. The irradiated L929 cells were cultured in a medium containing 2 ml adenovirus plasmids of CCN1 or RFP at 37 ℃ in an atmosphere containing 5% CO2,which served as a CCN1 group and a RFP group,respectively. Irradiated L929 cells cultured in a blank control medium served as a blank control group. Effects of CCN1 on proliferation and migration of radiation-injured L929 cells were detected by MTT assay,plate colony formation assay,cell cycle analysis,and scratch test of wound healing. Results The proliferation and colony formation rates of L929 cells cultured in a medium containing CCN1 were significantly higher than in RFP and control groups [colony formation rate:( 34. 4 ?3. 6) % vs ( 24. 5 ?2. 9) % and ( 29. 5 ?3. 5) %,P

Metabolic dysfunction-associated fatty liver disease （MAFLD） is a common chronic liver disease with the pathological feature of lipid accumulation in the liver， and it is closely associated with liver metabolic disorders. The latest research has shown that the pathogenesis of MAFLD is associated with the abnormal expression of specific genes， especially the fat mass and obesity-associated （FTO） gene. The abnormal activity of the FTO gene may lead to an imbalance in liver lipid metabolism， which manifests as the increase in fatty acid synthesis and the reduction in fatty acid oxidation， thereby promoting liver fat deposition and inflammatory response. Therefore， regulating the expression or activity of the FTO gene is considered one of the potential strategies for the treatment of MAFLD. At present， drug research targeting the function of the FTO gene has achieved preliminary results， and inhibition of the activity of the FTO gene can help to regulate liver lipid metabolism and alleviate liver inflammatory injury. This article reviews the mechanism of action of the FTO gene in the development and progression of MAFLD， summarizes the advances in drug research on the FTO gene and related metabolic pathways in recent years， and analyzes their application prospect in research and treatment.