Role And Significance Of IGFBP-3 In Rat Myocardial Fibrosis And Myocardial Fibroblast Activation And Proliferation

Objective Myocardial fibrosis is the main pathological process shared by many serious cardiovascular diseases,but the detailed mechanism of the pathogenesis of the disease is still unclear.In recent years,it has been found that the IGFBP family has a certain influence on the progression of organ fiber diseases.IGFBP and IGF in the circulation combine to affect the propagation of signal pathways inside and outside the cell,and have a corresponding biological effect on cell growth.In the human body,IGFBP-3occupies the largest proportion in the IGFBP family,and the content in the circulation is more abundant,which occupies a very important position in the body.Therefore,in this experiment,an animal model of rat myocardial fibrosis and a cell model of myocardial fibroblast proliferation and activation were artificially established to detect and discuss the expression of insulin-like growth factor binding protein-3(IGFBP-3)in the model to explore the possible role of IGFBP-3 in the pathogenesis of myocardial fibrosis.Methods Forty SD male rats with the same growth and development conditions were randomly divided into a model group and a control group,with 20 rats in each group.In the model group,rats were injected subcutaneously with isoproterenol to establish a biological model of the myocardial tissue fibrosis process.In the control group,rats were injected with equal-quality medical saline,and both groups were injected subcutaneously for 2 weeks.At the same time,transforming growth factor β1(TGF-β1)was added to the cell culture medium to stimulate the CFs of suckling rats,so as toproliferate and activate them to prepare a cell model as a model group.The model group is further divided into two groups with different durations of stimulation at 24 h and 48 h under the same stimulation conditions,while the control group is normal CFs that have not been stimulated and the model group is cultured for the same duration.The myocardial tissue of the completed rat myocardial fibrosis model was detected by HE and Masson staining to detect myocardial pathological changes and calculate its collagen volume fraction(CVF).The CCK-8 experimental technique was used to determine the degree of proliferation and activation of the CFs model.Western blot and q RT-PCR techniques were used to detect the expression of IGFBP-3,α-smooth muscle actin(α-SMA)and type I collagen procollagen A1(COL1A1)m RNA and protein molecules in myocardial tissues and cell models of animal models In the circumstances,the myocardial tissue and CFs of the control group were subjected to the same experimental operations as the model group,and the experimental results were collated and statistically analyzed.Results Compared with the control group,most of the myocardial cells in the animal model group were disordered,collagen fiber hyperplasia and collagen volume fraction increased,indicating that the pathological changes of the myocardial tissue fibrosis in the model group were obvious,and the IGFBP-3,α-SMA and COL1A1 protein and m RNA expression were significantly increased in the myocardial tissue.After adding TGF-β1 to the cell model group to stimulate CFs for 24 h and 48 h,the degree of proliferation and activation of CFs cells was obvious.Compared with the control group,the expression of protein molecules and m RNA of IGFBP-3,α-SMA and COL1A1 after CFs were stimulated 24 h and 48 h,the level has also been significantly improved.Conclusion The expression of IGFBP-3 in rat fibrotic myocardial tissue and activatedCFs is significantly increased,suggesting that IGFBP-3 may play a relevant regulatory role in the process of myocardial fibrosis,in order to further explore myocardial fibrosis the pathogenesis of the disease provides clues.