RESUMO
AIM: To analyze the role and mechanism of PDGF/AKT pathway in pressure overload-induced ventricular remodeling. METHODS: A total of 55 C57BL/6 female mice were selected to establish aortic arch narrowing model. Forty-five models were successfully modeled. The randomized digital table method was used to divide the models into sham operation group, DMSO group and experimental group. The sham operation group was opened after chest operation. The suture was performed without aortic coarctation (TAC). After 24 hours of thoracotomy, 200 μL of PBS solution and 50 μL of DMSO were administered. The DMSO group was given 200 μL of PBS solution and 50 μL of DMSO 24 h after operation. The experimental group was given PBS solution 200 μL plus AG1296 50 μL 24 h after TAC to observe the heart function and myocardial histopathology of mice. Lentiviral infection was established to identify and culture HUVEC cells with different expression of PDGF gene. According to different treatments, the cells were divided into control group, PDGF group, shRNA group and PDGF+IMA group to detect the expression of p-AKT and t-AKT protein in HUVEC cells. RESULTS:LVESV, LVEDV, LVESD and LVEDD were increased in DMSO group as compared with sham operation group, while EF and FS of DMSO group were lower than those in sham operation group. LVESV, LVEDV, LVESD and LVEDD were lower in experimental group than those in DMSO group, while EF and FS in experimental group were higher than those in DMSO group. The difference was statistically significant (P<0.05). The sham operation group had neatly arranged myocardial tissue and normal interstitial; the DMSO group had irregular morphology, inflammatory cell infiltration, cell gap was enlarged, and the nucleus was deeply stained. The number of expanded or necrotic cells in experimental group decreased, the gap became smaller, and the inflammatory infiltration decreased. The cross-sectional area of myocardial cells in DMSO group was higher than that in sham operation group. The cross-sectional area of the myocardial cells in experimental group was lower than that in DMSO group (P<0.05). The expression of p-AKT and t-AKT protein in PDGF+IMA group was significantly higher than that in PDGF group and shRNA group, the difference was statistically significant (P<0.05). CONCLUSION:PDGF can accelerate ventricular remodeling induced by pressure overload and promote the formation of myocardial fibrosis, while inhibiting PDGF/AKT pathway can improve myocardial cell hypertrophy.
RESUMO
Objective:To investigate Th17,Treg and related factors before and after myocardial infarction ,and explore the cor-relations among them.Methods:Extracted mononuclear cell in peripheral blood ,and used fluorescence-activated cell sorting analysis to detect the contect of Th17 and Treg.Enzyme-linked immunosorbent assay was used to detect cytokine production of IL-17 and TGF-β;real-time PCR was used to detect the contect of RORγT and Foxp3.Results: Compared with the control group , experimental group (both before and after thrombolysis) had increased expressions of Th17,IL-17 and RORγT(P<0.05);the expressions of Treg,TGF-βand Foxp3 had decreased(P<0.05).Compared with the group of before thrombolysis ,the group of after thrombolysis 7 d had decreased expressions of Th17,IL-17 and RORγT(P<0.05);increased expressions of Treg,TGF-βand Foxp3(P<0.05).Conclusion:Compared with the control group,patients with myocardial infarction have the high levels of Th 17 and the related factors,the decreased levels of Treg and the related factors.Thrombolytic therapy can decrease the levels of Th 17 and the related factors,and increase levels of Treg and the related factors.