ABSTRACT
Objective:To investigate the effect of PLTP gene on CSE-induced IL-8 production in human alveolar Type Ⅱcells ( Adenocarcinomic human alveolar epithelial cells , A549 ) .Methods: The different concentrations of CSE co-cultured with human alveolar epithelial cell line ( A549 ) for 24 hours.MTT assay was performed to study the effect of CSE on human alveolar epithelial cell line(A549) growth.Expression levels of PLTP mRNA and IL-8 mRNA were examined by RT-PCR,protein of PLTP were examined by Western blot ,and protein of IL-8 was examined by ELISA .Results: MTT assay showed that the proliferation of A 549 cell line were stimulated by the 0.125%CSE,while the proliferation of A549 cell tends to decrease at high concentrations of CSE (2.0% CSE and 4.0%CSE),and in this middle concentrations of CSE (0.25%CSE ,0.5%CSE and 1.0%CSE),the proliferation of A549 cell was not significantly affected .Our studys suggested that PLTP and IL-8 release were induced by CSE in a concentration-dependent and time-dependent manner ,and expression levels of IL-8 obviously increased after silence PLTP gene .Conclusion:PLTP siRNA can increased CSE-induced IL-8 production in human alveolar epithelial cells (A549).
ABSTRACT
Objective:To investigate the effect of PLTP gene on CSE-induced IL-8 production in human bronchial epithelial cell line (HBECs). Methods:Wistar rats were exposed to air or cigarette smoke for 6 hours/day on 3 consecutive days,then the lungs were sectioned and examined. The number of total white blood cell and differential white blood cells in BALF were counted. The different concentrations of CSE co-cultured with HBECs for 24 hours. Cells growth was detected by MTT assay. Expression levels of PLTP mRNA and IL-8 mRNA were examined by RT-PCR,protein of PLTP was investigated by Western blot,and production of IL-8 ex-amined by ELISA. Results:The number of white blood cells in BALF was significantly increased compared with controls. Enhanced ex-pression level of PLTP and IL-8 were observed in CS-exposure group. Proliferation of HBECs tends to decrease at high concentrations of CSE(2. 0% CSE and 4. 0% CSE). The results suggested that the production of IL-8 induced by CSE in a time- and concentration-dependent manner,while the expression of PLTP induced by CSE in a dose-dependent manner. Furthermore,expression levels of IL-8 significantly increased after silence PLTP gene. Conclusion:PLTP siRNA could increase CSE-induced IL-8 production in HBECs.
ABSTRACT
Aim To observe the effects of the total fla-vonoids of scutellaria barbataon ( TFSB ) on high-fat feeding ApoE gene deficiency mice in early atheroscle-rosis ( AS ) and its underlying mechanisms. Methods 40 ApoE-/ -male mice were divided into five groups:model group, SIM group and L-TFSB, M-TFSB, H-TFSB group, 5 C57BL/6J mice were selected as nor-mal control group. All mice in experimental group were fed with high-lipid diet for 4 weeks and all mice were killed after 8 weeks. H&E staining was used to observe morphology of aorta. Blood rheometer was used to ex-amine plasm viscosity and whole blood viscosity. Fully automatic biochemical analyser was used to detect the serum levels of TG, TC, LDL-C and HDL-C. The ex-pression levels of PLTP and VE in serum were meas-ured by ELISA. The expression levels of PLTP and FXR in liver were examined by Western blot. Results The model was established successfully. TFSB groups could improve the aorta AS morphology of model mice and significantly reduce the serum levels of TG, TC and LDL-C, while increase the level of HDL-C ( P hematocrit value, plasma viscosity and whole blood vis-cosity of AS model mice significantly and had statistical significance when compared with model group ( P <0. 01 ) . The expression levels of PLTP of serum were reduced significantly when compared with model group ( P <0. 01 ) . We also found that the expression of PLTP was in negative correlation with VE ( r = -0. 675,P<0. 01). M-TFSB and H-TFSB group could decrease the expressions of PLTP and FXR of liver when compared with model group ( P <0. 01 ) . Con-clusion TFSB may exert its anti-AS effect partly through inhibiting the levels of FXR and PLTP of ApoE-/ -mice, increasing the level of VE, regulating blood lipids, improving blood rheology and reducing the damage of AS in mice.