共查询到20条相似文献，搜索用时 31 毫秒
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LU Yang ZHAO Guang-ju HONG Guang-liang QIU Qiao-meng LI Dong LU Zhong-qiu 《园艺学报》2014,30(10):1748-1752
AIM:To investigate the effect of capsaicin on lipopolysaccharide (LPS)-induced activation of cultured endothelial cells of mouse aorta in vitro. METHODS:The endothelial cells were isolated from mouse aorta and cultured in vitro, and the specific cell markers of the cells were identified by immunofluorescence staining. The cells were stimulated with LPS (100 μg/L) combined with or without capsaicin, and the cells and supernatant were collected at 12 h, 24 h and 48 h. The levels of soluble intercellular adhesion molecule 1 (sICAM-1), soluble vascular cell adhesion molecule 1 (sVCAM-1) and soluble P-selectin (sP-selectin) in the supernatant were measured by ELISA. The levels of nuclear NF-κB p65 and cytopasmic p-IκBα and IκBα were detected by Western blotting. RESULTS:Compared with control group, the levels of sP-selectin, sICAM-1 and sVCAM-1 in LPS group were significantly increased (P<0.05), and LPS promoted the expression of sICAM-1 and sVCAM-1 in a time-dependent manner. Compared with LPS group at the same time point, capsaicin inhibited the expression of sP-selectin, sICAM-1 and sVCAM-1 in a dose-dependent manner. Compared with control group, the protein levels of NF-κB p65 and p-IκBα in LPS group at 24 h were significantly increased (P<0.05), while the protein level of IκBα in LPS group at 24 h were significantly decreased (P<0.05). Compared with LPS group, capsaicin decreased the protein levels of NF-κB p65 and p-IκBα and increased the protein level of IκBα in a dose-dependent manner. CONCLUSION: Capsaicin has a protective effect on LPS-induced vascular endothelial cell activation, which potentially contributes to the suppression of IκBα degradation and NF-κB p65 nuclear translocation. 相似文献
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AIM: To study the protective effect of anti-aging Klotho protein on human umbilical vein endothelial cells (HUVECs) treated with high glucose (HG).METHODS: HUVECs were cultured in vitro, and divided into PBS control group, 5.5 mmol/L glucose group, 33.3 mmol/L glucose group, 0.1 μmol/L Klotho+33.3 mmol/L glucose group, 1 μmol/L Klotho+33.3 mmol/L glucose group, and 10 μmol/L Klotho+33.3 mmol/L glucose group. The viability of the HUVECs was measured by MTT assay. The content of malondialdehyde (MDA), and the activities of lactate dehydrogenase (LDH), superoxide dismutase (SOD) and glutathione (GSH) in cell culture supernatants were observed. The production of reactive oxygen species (ROS) in HUVECs was analyzed by flow cytometry. The levels of nitric oxide (NO), endothelin (ET-1), intercellular adhesion molecule-1 (ICAM-1) in HUVEC culture medium were detected by ELISA. The protein expression of nuclear factor-kappa B (NF-κB) in the HUVECs was determined by Western blot. RESULTS: Compared with PBS control group, 33.3 mmol/L glucose significantly decreased the HUVEC viability, increased ROS, LDH and MDA levels, reduced the activities of SOD and GSH, decreased the NO secretion, and induced the ET-1 and ICAM-1 secretion and the protein expression of NF-κB in HUVECs. When HUVECs were treated with Klotho protein at different concentrations combined with 33.3 mmol/L glucose, the cell viability was increased significantly, the ROS, LDH and MDA levels were decreased significantly, the antioxidant SOD and GSH activities were significantly increased, the secretion of NO was increased, but ET-1 and ICAM-1 releases and protein expression of NF-κB were significantly reduced.CONCLUSION: Anti-aging Klotho protein promotes the viability of HUVECs treated with HG, reduces the oxidative damage and ROS production, and restores the normal secretory function of HUVECs, thus playing a protective role in vascular endothelial cells through reducing the protein expression of NF-κB. 相似文献
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AIM: To investigate the effect of NOD8 on lipopolysaccharide (LPS)-induced releases of nitric oxide (NO), tumor necrosis factor α (TNF-α) and interleukin-1β (IL-1β) in RAW264.7 cells. METHODS: The plasmids of pEGFP-C2 and pEGFP-NOD8 were transfected into RAW264.7 cells respectively. The transfected and non-transfected cells were stimulated by LPS for 0, 6, 12 and 24 h. NO production was evaluated by Griess reagent assay, and the levels of IL-1β and TNF-α were measured by ELISA. The protein expression of NOD8 and the nuclear translocation of nuclear factor κB (NF-κB) p65 subunit were detected by Western blotting. The level of activated caspase-1 was determined by fluorimetric method. RESULTS: Compared with pEGFP-C2 group, the protein expression of NOD8 was significantly elevated in pEGFP-NOD8+LPS group. The releases of NO, IL-1β and TNF-α were obviously increased after RAW264.7 cells were treated with LPS for 6 h, 12 h and 24 h, and while the secretion of NO was significantly reduced in the cells transfected with pEGFP-NOD8 and induced by LPS for 12 h and 24 h, and the release of IL-1β was also significantly reduced at 6 h, 12 h and 24 h. However, no significant difference of TNF-α release was observed between pEGFP-C2+LPS group and pEGFP-NOD8+LPS group. The activation of caspase-1 in RAW264.7 cells stimulated with LPS for 6 h, 12 h and 24 h was markedly increased, and the expression of NF-κB p65 subunit in the cytoplasm was significantly decreased, indicating that p65 nuclear translocation was increased. In addition, the activation of caspase-1 and the nuclear translocation of p65 were significantly inhibited in pEGFP-NOD8+LPS group. CONCLUSION: NOD8 suppresses the releases of LPS-induced NO and IL-1β in RAW264.7 cells by inhibiting the activation of caspase-1 and NF-κB. 相似文献
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AIM: To investigate the effect of artemisinin on lipopolysaccharide(LPS)-induced intestinal epithelial barrier damage in IEC-6 cells and its molecular mechanism. METHODS: Cultured IEC-6 cells were divided to 5 groups: control group, LPS(100 mg/L) group and LPS+Artemisinin(30, 50 and 100 μmol/L) groups. The cytotoxicity was detected by MTT assay. The releases of TNF-α, IL-1β and IL-6 in the IEC-6 cells were measured by ELISA. The transepithelial electrical resistance(TER) was detected by electrical resistance tester, and the horseradish peroxidase(HRP) flux permeability were analyzed by a microplate reader. The expression of tight junction proteins, ZO-1, claudin-1 and occludin, and the expression of TLR4/MyD88/NF-κB at mRNA and protein levels were determined by RT-qPCR and Western blot. RESULTS: Artemisinin alone(up to 100 μmol/L) or in combination with LPS(100 mg/L) was not toxic to IEC-6 cells. Compared with control group, the releases of TNF-α, IL-1β and IL-6 in the culture supernatant of IEC-6 cells significantly increased after treatment with LPS. The expression of TLR4/MyD88/NF-κB was activated by LPS. LPS down-regulated the protein expression of ZO-1, claudin-1 and occludin. However, artemisinin treatment decreased the releases of TNF-α, IL-1β and IL-6 in the culture supernatant of IEC-6 cells. The expression of TLR4/MyD88/NF-κB at mRNA and protein levels was gradually reduced after treatment with artemisinin. In addition, artemisinin upregulated the protein expression of ZO-1, claudin-1 and occludin significantly(P<0.01) in a dose-dependent manner. CONCLUSION: Artemisinin attenuates LPS-induced intestinal epithelial barrier damage by inhibiting TLR4/MyD88/NF-κB activation in the IEC-6 cells. 相似文献
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SHI Jing CUI Jing-jing YANG Hai-ping LIU Wei WAN Jun-li WANG Zhi-tie QIU Gui-xia LI Qiu 《园艺学报》2013,29(7):1230-1234
AIM：To investigate the molecular mechanism that interleukin-1 beta (IL-1β) exacerbates lipid-induced endoplasmic reticulum stress (ERS) and the injury of human mesangial cells (HMCs). METHODS：HMCs were cultured and divided into control group, low-density lipoprotein (LDL) group, IL-1β+LDL group and 4-phenyl butyric acid (4-PBA)+IL-1β+LDL group. Oil red O staining was used to evaluate the accumulation of lipid droplet in the cells. The mRNA levels of glucose-regulated protein 78(GRP78), protein kinase R-like endoplasmic reticulum kinase (PERK) and α-smooth muscle actin (α-SMA) were examined by real-time PCR. Immunocytochemistry was used to observe GRP78 expression. The protein level of NF-κB p65 was measured by Western blotting. The releases of IL-6 and TGF-β1 in the culture supernatants of HMCs were detected by ELISA. RESULTS：Compared with LDL group, the intracellular lipid accumulation, the mRNA levels of GRP78 and PERK, the protein expression of GRP78 and NF-κB p65, and the release of IL-6 were significantly increased in IL-1β+LDL group. Dramatically reduced intracellular lipid accumulation, down-regulated GRP78 and PERK mRNA expression, decreased protein levels of GRP78 and NF-κB p65, and suppressed IL-6 release were observed in 4-PBA+IL-1β+LDL group as compared with IL-1β+LDL group. The mRNA level of α-SMA was higher in IL-1β+LDL group than that in LDL group, and that in 4-PBA+IL-1β+LDL group was significantly depressed. CONCLUSION：IL-1β exacerbates lipid-induced ERS, thus promoting the injury of HMCs. 相似文献
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AIM: To investigate the mechanism that dl-3-n-butylphthalide (NBP) protects cells from the induced by oxygen-glucose deprivation (OGD).METHODS: Human umbilical vein endothelial cells (HUVECs) were exposed to OGD to induce endothelial damage. Endothelial injury was assessed by measuring the changes of chromatin morphology and MTT method. The protein levels of vascular endothelial growth factor (VEGF) and hypoxia inducible factor-1 alpha (HIF-1α) were determined by immunofluorescence and quantitatively analyzed with the software IPP. Western blotting was applied to verify the results.RESULTS: NBP at the concentrations of 0.01 to 100 μmol/L dose-dependently protected against OGD-induced cell damage. Compared with OGD group, NBP enhanced OGD-induced the expression of VEGF and HIF-1α, and the difference was statistically significant. The expression of VEGF and HIF-1α reached to the peak at the time points of 6 h and 8 h after OGD, respectively.CONCLUSION: Under the condition of OGD, NBP enhances the expression of HIF-1α in HUVECs, subsequently promotes the expression of downstream VEGF, and eventually elevates the survival of the cells. 相似文献
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LI Yan MA Ming-ming ZHANG Xiao-qiang PAN Wen-fei LIU Xiang-yong WANG Xiao-zhi 《园艺学报》2013,29(11):2088-2091
AIM:To observe the effects of angiopoietin 4 (Ang-4) on lipopolysaccharide (LPS)-induced injury of human umbilical vein endothelial cells (HUVECs). METHODS:The EnVision immunohistochemical method was used to identify the HUVECs. After pre-treated with different doses of Ang-4 for 0.5 h, HUVECs was exposed to LPS at concentration of 10 mg/L for 24 h. The cell viability was evaluated by MTT assay. The content of tumor necrosis factor-alpha (TNF-α) in the supernatant and the concentrations of intracellular and supernatant von Willebrand factor (vWF) were detected by ELISA. The mRNA levels of Toll-like receptor 4 (TLR4), NF-κB p65 and TNF-α were determined by real-time PCR. RESULTS:Factor Ⅷ in the cytoplasm was positive in the HUVECs.Compared with normal group, LPS reduced the cell viability (P<0.01), and significantly increased the secretion of TNF-α and vWF (P<0.01). The mRNA expression of TLR4, NF-κB p65 and TNF-α also increased (P<0.01). Ang-4 at concentration of 100 μg/L enhanced the cell viability (P<0.01), reduced the content of vWF and TNF-α, and inhibited the LPS-induced increases in the mRNA levels of TLR4, NF-κB p65 and TNF-α (P<0.01). CONCLUSION: Ang-4 antagonizes LPS-induced damage in HUVECs by inhibiting TLR4-NF-κB p65-TNF-α signaling pathways. 相似文献
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WANG Wen-xiang ZHANG Niu-niu ZENG Xian-yan LI Ting-rui JI Ye-nan HE Zhong-mei 《园艺学报》2018,34(7):1201-1205
AIM:To investigate the role of hypoxia-inducible factor-1α (HIF-1α) stable expression in myocardial inflammatory injury induced by ischemia and reperfusion (I/R) in rats. METHODS:Male Wistar rats were randomly divided into 4 groups:sham operation (sham) group, I/R group, HIF-1α stabilizer dimethyloxalyl glycine (DMOG)+I/R group and HIF-1α inhibitor YC-1+I/R group. The protein expression of myocardial Toll-like receptor 4 (TLR4) and nuclear factor-κB (NF-κB) was determined by Western blot. The mRNA levels of interleukin (IL)-1β, tumor necrosis factor-α (TNF-α), IL-6, TLR4 and NF-κB were detected by real-time PCR. The myeloperoxidase (MPO) activity in the myocardial tissues was measured. HE staining was used to observe the infiltration of inflammatory cells. RESULTS:HIF-1α decreased the infiltration of inflammatory cells, the MPO activity, and the mRNA levels of inflammatory factors IL-1β, IL-6 and TNF-α in the myocardial tissues. HIF-1α also reduced the expression of TLR4 and NF-κB at mRNA and protein levels (P<0.05). CONCLUSION:The stable expression of HIF-1α has an anti-inflammatory effect on the myocardial tissues after I/R injury in rats. The mechanism may be related to the inhibition of TLR4/NF-κB signaling pathway. 相似文献
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AIM:To investigate the effect of platelet inhibitor from Agkistrodon halys venom (AHV-PI) on lipopolysaccharide (LPS) induced human umbilical vein endothelial cells (HUVECs) injury in vitro, and to explore its mechanism. METHODS:Cultured HUVECs were induced inflammatory injury by LPS (1 mg/L). The experiment was divided into blank control group, LPS group, AHV-PI group and AHV-PI+LPS group. The viability of HUVECs was measured by MTT assay. The morphological changes of HUVECs were observed under inverted microscope. The optimum concentration of AHV-PI at 5 mg/L was selected. Flow cytometry was used to detect apoptosis of HUVECs. Immunohistochemical method was used to observe the expression of tissue type plasminogen activator (t-PA) and plasminogen activator indhibitor-1 (PAI-1) of HUVECs. ELISA was used to detect the concentrations of intercellular adhesion molecule-1 (ICAM-1) and tissue factor (TF) in the supernatant. The activation and translocation of NF-κB subunit p65 were observed by immunofluorescence staining. RESULTS:The HUVECs were spindle shaped, the ratio of length to width was increased, the cells were fibroblast-like, and granular substance appeared in the cytoplasm in LPS group. The viability and morphological changes of HUVECs were not significantly affected as treated with AHV-PI at concentration of 0~5 mg/L, but the viability of HUVECs induced by LPS was inhibited and the morphological changes were alleviated. Compared with the blank control group, the levels of TF and ICAM-1 in the supernatant increased, and the expression of t-PA and PAI-1 in the HUVECs was decreased in LPS group. Compared with the LPS group, the contents of TF and ICAM-1 in the supernatant were significantly decreased, the expression of t-PA and PAI-1 in the HUVECs was increased and the expression of nucleus NF-κB p65 was decreased in AHV-PI+LPS group (P<0.05). CONCLUSION:AHV-PI reduces HUVECs damage. The protective mechanism is related to the inhibition of cytokine secretion and NF-κB activation. 相似文献
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AIM:To investigate the effect of oxidized α1-antitrypsin (Ox-AT) on interleukin 8 (IL-8) and monocyte chemotactic protein 1(MCP-1) production in cultured human bronchial epithelial (HBE) cells. METHODS:Plasma native α1-antitrypsin (N-AT) was purified from human plasma by 50% and 75% ammonium sulfate fractionation followed by glutathione and anion exchange chromatography. Ox-AT was prepared by incubating N-AT (0.5 g/L) with N-chlorosuccinimide in a 25-fold molar excess to N-AT in PBS at room temperature for 30 min. HBE cells were cultured in the presence of Ox-AT (0.5 g/L) for 4 h, 10 h and 24 h, and the levels of IL-8 and MCP-1 in the supernatant were assayed using respective DuoSet kits. The effect of NF-κB inhibitor Bay11-7082 on the inflammatory cytokine release induced by Ox-AT was also evaluated. RESULTS:Ox-AT concentration-dependently and time-dependently increased the production of IL-8 and MCP-1 in HBE cells. The concentrations of IL-8 and MCP-1 in HBE cells induced by 0.5 g/L Ox-AT at 4 h, 10 h and 24 h were significantly higher than those in blank control and N-AT groups. Ox-AT increased the activity of NF-κB in a dose-dependent manner. The proinflammatory effect of by Ox-AT was inhibited by NF-κB inhibitor Bay11-7082. CONCLUSION: Ox-AT is a strong proinflammatory factor for HBE cells. The mechanism is related to NF-κB signaling pathway activation. 相似文献
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AIM: To investigate the effects of taurine on lipopolysaccharide (LPS)-induced myocardial damage in rats. METHODS: Healthy male SD rats (n=30) were randomly divided into control group (CON), LPS model group (LPS) and taurine treatment group (TAU). The rats in CON group and LPS group were intravenously injected with normal saline, and the rats in TAU group were injected with taurine (100 mg/kg). After 2 h, the rats in LPS group and TAU group were intraperitoneally injected with LPS at 10 mg/kg, and the rats in CON group were injected with normal saline. Six hours after injection of LPS, the blood samples were collected for determination of superoxide dismutase (SOD) activity, malondialdehyde (MDA) content, and tumor necrosis factor α (TNF-α) and interleukin-6 (IL-6) levels. The myocardial tissues were processed for histological examination and the analysis of Western blot. RESULTS: Compared with CON group, LPS significantly reduced SOD activity in the serum and heme oxygenase 1 (HO-1) protein expression in the myocardial tissues, increased the serum content of MDA and levels of TNF-α and IL-6. LPS also significantly elevated the levels of TNF-α and IL-6, and up-regulated the cyclooxygenase-2 (COX-2) expression and phosphorylation of nuclear factor kappa B (NF-κB) in the myocardial tissues. Taurine pretreatment significantly elevated SOD activity and HO-1 protein expression level, decreased the levels of COX-2, TNF-α, IL-6 and phosphorylated NF-κB. Histological observation showed that taurine reduced inflammatory response in the myocardial tissue. CONCLUSION: Taurine attenuates LPS-induced myocardial damage in rats. The beneficial effects of taurine may be associated with its reduction of p-NF-κB/COX-2 signaling by activation of HO-1/CO. 相似文献
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AIM:To study the induction of IL-8 expression by bypass-activated complement in human umbilical vein endothelial cells (HUVECs) and regulatory effect of nuclear factor-kappa B on the expression of IL-8. METHODS:In vitro, zymosan-activated human serum(ZAHS) directly challenged the HUVECs monolayers. Following techniques were used in the experiment: ① RIA for measurement of IL-8,ISH for measurement of their mRNA.② EMSA for measurement of nuclear factor-kappa B(NF-κB). RESULTS:①After HUVECs monolayers were stimulated with ZAHS, the level of IL-8 increased significantly at 4 h. ②The NF-κB activity began upregulated within 30 min after ZAHS stimulation, maximal NF-κB activity was observed at 120 min. Pretreatment of endothelial monolayers with PDTC (20 μmol/L) significantly inhibited the secretion of IL-8 (P＜0.05). CONCLUSION:Bypass-activated complement directly challenged HUVECs to secret IL-8. Cytoplasma to nuclear translocation of NF-κB was necessary for this response. 相似文献
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AIM：To study the effects of autoantibodies against α1-adrenergic receptor (α1-AAs) isolated from the hypertensive patients, which showed the agonist-like activity similar to norepinephrine, on the signal mechanism of vascular smooth muscle cells (VSMCs) isolated from rat thoracic aorta. METHODS：Rat VSMCs were cultured and identified. The serum of hypertensive patients was purified by immunoaffinity chromatography. The autoantibodies were detected by ELISA and used to activate the cells with the titer of 1∶80. The total protein was extracted and the expression of NF-κB in different treatment groups was detected by Western blotting. Meanwhile, the activation of NF-κB in the nucleus was analyzed by immunofluorescence method. RESULTS：The expression of NF-κB in VSMCs was obviously higher in α1-AAs group than that in control group. Meanwhile, the expression of NF-κB was inhibited by prasozin and PDTC. The autoantibodies caused a significant increase in NF-κB expression in the nucleus. The fluorescence intensity in α1-AAs group was high than that in control group and α1-AAs+prasozin group (P<0.01). CONCLUSION:The α1-AAs from hypertensive patients increase NF-κB expression in rat VSMCs. 相似文献
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AIM: To investigate the effects of advanced glycation end products (AGEs) on protein and mRNA expression of macrophage inflammatory protein-1α (MIP-1α) in cultured human umbilical vein endothelial cells(HUVECs). METHODS: HUVECs were cultured with AGEs at different concentrations for 24 h and at a concentration of 400 mg/L for different time.The levels of mRNA and protein expression of MIP-1α in cultured HUVEC were detected by in situ hybridization and Western blot, respectively. RESULTS: In situ hybridization showed that after exposure of HUVECs to AGEs at different concentrations (100 mg/L, 200 mg/L, 400 mg/L) for 24 h, the average integrated optical density values (18.76±3.17, 26.58±1.61, 34.23±2.25) of MIP-1α mRNA expression in HUVECs were higher than that in control group (13.83±1.24, P0.05). After exposure of HUVECs to AGEs at a concentration of 400 mg/L for 12 h, 24 h and 36 h, the average integrated optical density values of MIP-1α mRNA expression in HUVECs were 22.67±1.46, 34.23±2.25 and 42.28±3.14, higher than that in 0 h group (12.56±1.24, P0.05). Western Blot showed that exposure of HUVECs to AGEs at different concentrations(100 mg/L, 200 mg/L, 400 mg/L) for 24 h resulted in a 1.34-fold, 1.87-fold and 2.46-fold increase in the expression of MIP-1α protein in HUVECs compared with BSA control group (P<0.05). Meanwhile, exposure of HUVECs to AGEs at a concentration of 400 mg/L for 12 h, 24 h and 36 h resulted in a 1.82-fold, 2.71-fold and 3.34-fold increase in MIP-1α protein expression in HUVECs compared with 0 h group (P<0.05). CONCLUSION:These data suggest that AGEs could induce a high expression of MIP-1αmRNA and protein in cultured HUVECs in a dose-dependent and time-dependent manner. 相似文献
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AIM: To evaluate the effects of renal denervation (RDN) on the expression of tumor necrosis factor-α (TNF-α), interleukin-1α (IL-1α) and interleukin-6 (IL-6) in a rabbit model of early atherosclerosis. METHODS: New Zealand male rabbits were divided into control group, RDN+ high-fat diet (HFD) group (RDN group), sham+HFD group (sham group) and HFD group. The rabbits in later 3 groups were fed with 2% cholesterol for 8 weeks to establish an early atherosclerosis model. The blood samples were collected to test the levels of lipids, norepinephrine (NE), TNF-α, IL-1α and IL-6. The protein expression of angiotensin Ⅱ (Ang Ⅱ) was detected by the method of immunohistochemistry. The levels of nuclear factor-κB (NF-κB) and Ang II 1 type receptor (AT1R) were evaluated by Western blot. The mRNA expression of TNF-α, IL-1α and IL-6 was determined by real-time PCR. RESULTS: After 1 d of RDN procedure, the NE level was lower in RDN group than that in sham group (P<0.01). After 8 weeks, the NE level was lower in RDN group than that in sham group and HFD group (P<0.05), and triglyceride (TG) was lower in RDN group than that in HFD group (P<0.05). The protein expression of Ang II was decreased in RDN group compared with sham group and HFD group (P<0.01). The protein expression of NF-κB was lower in RDN group than that in sham group (P<0.05). The plasma levels of TNF-α and IL-1α were reduced in RDN group compared with sham group and HFD group (P<0.05). The mRNA expression of TNF-α, IL-1α and IL-6 was reduced in RDN group compared with sham group (P<0.05). CONCLUSION: RDN inhibits sympathetic activity, decreases the plasma level of TG, and alleviates inflammatory reactions in the rabbits with atherosclerosis. 相似文献
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AIM: To explore the effect of recombinamt rat CC16 protein (rCC16) on LPS-induced expression of tumor necrosis factor-alpha (TNF-α), interleukin-6 (IL-6) and IL-8 in the rat tracheal epithelial (RTE) cells.METHODS: The RTE cells were incubated with rCC16 at concentrations of 0.5, 1.0 and 2.0 mg/L in serum-free media for 2 h prior to LPS (0.1 mg/L) treatment for further 24 h. The cells were harvested for assessing the mRNA levels of TNF-α, IL-6 and IL-8 by RT-qPCR. The cell culture supernatants were collected for analyzing the protein levels of TNF-α, IL-6 and IL-8 by ELISA. In addition, the nuclear translocation of nuclear factor-κB (NF-κB) p65 was tested by Western blot.RESULTS: rCC16 inhibited LPS-induced IL-6 and IL-8 expression at both mRNA and protein levels in the RTE cells in a concentration-dependent (0~2 mg/L) manner, as demonstrated by RT-qPCR and ELISA. However, no concentration-dependent manner between the dose of rCC16 and TNF-α expression was observed, and rCC16 inhibited LPS-induced TNF-α expression at lower concentration (0.5 mg/L). rCC16 concentration-dependently inhibited the effects of LPS on the level of nuclear translocation of NF-κB p65.CONCLUSION: rCC16 suppresses LPS-mediated TNF-α, IL-6 and IL-8 production through inactivation of NF-κB activity in RTE cells.[KEY WORDS] CC16 protein; Airway inflammation; LPS; Inflammatory mediators; Nuclear factor-κB 相似文献
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XU Han-shi YE Ren-gao YANG Qiong-qiong SUN Lin YANG Nian-sheng LI You-ji ZENG Li-xia 《园艺学报》2001,17(5):428-430
AIM:To investigate the regulatory role of nuclear factor κB (NF-κB) in the expression of interleukin-6 in mesangial cells (MC) induced by interleukin-1β.METHODS:Activation of NF-κB was measured by electrophoresis mobility shift assay (EMSA). RT/PCR and ELISA were used to detect IL-6 mRNA expression and IL-6 production, respectively.RESULTS:rhIL-1β could rapidly stimulate the activation of NF-κB in MC, and increase the expression of IL-6 mRNA and protein. PDTC, one of the inhibitor of NF-κB, could inhibit the expression of IL-6 in mRNA and protein in MC stimulated by rhIL-1β.CONCLUSION:IL-6 expression induced by IL-1β may be regulated by NF-κB in MC, NF-κB may modulate the immune-inflammatory reaction in glomerular disease. 相似文献