Objective To study the protein expressions of Fas-associated death domain protein (FADD) and caspase-8 in rats with intracerebral hemorrhage ,and the effects of erythropoietin tp reveal the mechanism of neu-m-protection by EPO. Methods 126 male SD rats were randomly divided into three groups: Sham-operated group, intracerebral hemorrhage group, and EPO group. Each group was divided into seven subgroups according to the differ-ent time points (3,6,12,24,48,72 h and 7 d). The model of intracerebral hemorrage was established in rats by in-tracerebral injection of autogenous blood. The protein expressions of FADD and caspas-8 in rats tissue around the hemorrhagic and the normal brain tissue were detected by immunohistochemistry. Results The protein expressions of FADD and caspase-8 were increased [(4.66±0.46 ) and ( 15.89±1.81)] at 3 h after intracerebral hemorrhage, and peaked at 48 h [ (35.88±4.24 ) and (45.04±3.99)], the expressions of FADD and caspas-8 in the region around hematoma in EPO group significantly decreased compared with model group[ (3.92±0.64) and (28.24±1.90), (13.32±2.01 ) and (35.08±2.82)] at 3 h and 48 h. Conclusion The protein expressions of FADD and easpase-8 are markedly increased after intracerebral hemorrhage. EPO can protect the neurons by signifi-cantly reducing the expressions of FADD and caspase-8.

Female ; Granulosa Cell Tumor ; diagnosis ; surgery ; Humans ; Infant ; Ovarian Neoplasms ; diagnosis ; surgery

BACKGROUND:In recent years,the incidence of hyperuricemia caused by purine metabolism disorders has been increasing,which can induce inflammatory responses and lead to renal injury. OBJECTIVE:To explore the role and mechanism of solute carrier family 2 member 12(SLC2A12)in hyperuricemia-related renal injury. METHODS:Renal tubular cells(HK2 cells)were divided into five groups:HK2 group,HK2+uric acid group,HK2+uric acid+NC group,HK2+uric acid+siSLC2A12 group,and HK2+uric acid+siSLC2A12+MK-2206 group.HK2 cells were treated with uric acid and transfected with siRNA SLC2A12,followed by MK-2206 treatment to inhibit AKT expression.Cell proliferation was detected by CCK-8 assay.Apoptosis was detected by TUNEL assay.qRT-PCR and western blot assay were used to detect fibrogenic factors as well as activation of the AKT/FOXO3a pathway.The concentrations of inflammatory cytokines were measured by enzyme-linked immunosorbent assay. RESULTS AND CONCLUSION:(1)Uric acid treatment inhibited cell proliferation and promoted cell apoptosis in the HK2+uric acid group compared with the HK2 group.The proliferative ability of cells in the HK2+uric acid+siSLC2A12 group was further decreased and apoptotic cells were further increased compared with the HK2 group.Compared with the HK2+uric acid+siSLC2A12 group,the HK2+uric acid+siSLC2A12+MK-2206 group showed an increase in cell proliferation and a decrease in apoptotic cells.(2)Compared with the HK2 group,the connective tissue growth factor(CTGF),α-smooth muscle actin(α-SMA)and transforming growth factor beta(TGF-β)expressions increased in the HK2+uric acid group;CTGF,α-SMA and TGF-β expression further increased in the HK2+uric acid+siSLC2A12 group.Compared with the HK2+uric acid+siSLC2A12 group,the CTGF,α-SMA and TGF-β expressions decreased.(3)Compared with the HK2 group,the expression of p-AKT,FOXO3a,and p-FOXO3a elevated in the HK2+uric acid group;the expression of p-AKT further increased,while the expression of FOXO3a and p-FOXO3a decreased in the HK2+uric acid+siSLC2A12 group.Compared with the HK2+uric acid+siSLC2A12 group,p-AKT expression decreased;FOXO3a and p-FOXO3a expression increased in the HK2+uric acid+siSLC2A12+MK-2206 group.(4)Compared with the HK2 group,interleukin-6,interleukin-1 β,and tumor necrosis factor α levels increased in the HK2+uric acid group;interleukin-6,interleukin-1 β,and tumor necrosis factor α levels further increased in the HK2+uric acid+siSLC2A12 group.Compared with the HK2+uric acid+siSLC2A12 group,interleukin-6,interleukin-1 β,and tumor necrosis factor α levels diminished in the HK2+uric acid+siSLC2A12+MK-2206 group.(5)These findings indicate that SLC2A12 may protect against hyperuricemia-induced renal injury by counteracting uric acid-induced tubular fibrosis and inflammation through activation of the FOXO3a pathway.