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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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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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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 role of Toll-like receptor 4 (TLR4) and transient receptor potential channel 6 (TRPC6) signaling pathway in lipopolysaccharide (LPS)-induced nuclear factor-κB (NF-κB) P65 expression and nuclear translocation in airway epithelial cells (16HBE) for supplementing the mechanism for airway inflammation. METHODS: After stimulating the 16HBE cells with LPS at 1 mg/L for 0, 0.5, 2, 6, 12 and 24 h, the expression of NF-κB P65 at mRNA and protein levels in the 16HBE cells were determined by RT-PCR and Western blot respectively, and the nuclear translocation of NF-κB P65 was detected by immunocytochemical staining method. The effects of TLR4 inhibitor CLI-095 at 5 μmol/L and TRPC6 agonist Hyp9 at 10 μmol/L on LPS (1 mg/L)-induced NF-κB P65 expression and nuclear translocation in the 16HBE cells were determined by RT-PCR, Western blot and immunocytochemical staining. RESULTS: LPS increased the mRNA and protein expression of NF-κB P65 and nuclear translocation in the 16HBE cells(P<0.05). TLR4 inhibitor CLI-095 reduced the mRNA and protein expression of NF-κB P65 and nuclear translocation induced by LPS, while Hyp9 enhanced the mRNA and protein expression of NF-κB P65 and nuclear translocation induced by LPS in the 16HBE cells(P<0.05). CONCLUSION: LPS induces the expression and nuclear translocation of NF-κB P65 in the 16HBE cells via TLR4-TRPC6 signaling pathway.  相似文献   

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AIM: To study the effect of NF-κB "decoy" oligodeoxynucleotides on TNF-α and IL-6 expression in LPS-induced mouse macrophages. METHODS: Mouse macrophage cell line J774.1 cells were cultured with LPS and liposome-mediated oligodeoxynucleotides, and the levels of TNF-α and IL-6 measured in the different culture supernatant by enzyme linked immunosorbent assay. RNA was extracted from macrophages, and the mRNA expression of TNF-α and IL-6 in macrophages was observed by RT-PCR. RESULTS: NF-κB "decoy" oligodeoxynucleotides decreased the expression of TNF-α and IL-6 in LPS-induced macrophages and inhibited generation of TNF-α and IL-6. The level of TNF-α and IL-6 did not change in control group. CONCLUSIONS: NF-κB "decoy" oligodeoxynucleotides inhibit the expression of TNF-α and IL-6 in LPS-induced macrophages, which is probably due to the specific inhibition of activated NF-κB binding sites .  相似文献   

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AIM: To investigate the role of TLRs/NF-κB pathway in experimental allergic encephalomyelitis (EAE) rats treated with tripterygium glycosides (TG) + dexamethasone (DX). METHODS: Lewis rats were used in the study and divided into control group, EAE model group, therapy 1 group (EAE rats treated with DX) and therapy 2 group (EAE rats treated with DX+TG). The mean clinical score of the rats was determined. The expression of TLR4 and TLR9 at mRNA and protein levels was detected by the methods of real-time quantitative RT-PCR and immunohistochemistry. The protein level of NF-κB p65 was also measured. The levels of TNF-α, IL-1β and IL-6 were assayed by ELISA. RESULTS: The mean clinical scores at 5th, 16th and 20th day were lower in therapy 1 group and therapy 2 group than that in EAE model group. The mean clinical score in therapy 2 group was even lower than that in therapy 1 group. At the 16th day (the peaking period), the mRNA expression of TLR4 and TLR9 in therapy 1 group and therapy 2 group were obviously lower than that in EAE model group. The protein levels of TLR4, TLR9 and NF-κB p65 were also significantly lower in therapy 1 group and therapy 2 group than those in EAE model group at peak stage of EAE. The levels of TNF-α, IL-1β and IL-6 were lower in therapy1 group and therapy2 group than those in EAE model group. The significant differences of the mean clinical score, the mRNA expression of TLR4 and TLR9, the positive ratio of NF-κB p65 and the levels of TNF-α, IL-1β and IL-6 between therapy 1 group and therapy 2 group were found. The result of orthogonal factorial analysis of variance indicated that the difference of therapeutic effect between DX and DX+TG was significant (F=75.749, P<0.01). CONCLUSION: The TLRs/NF-κB pathway takes part in the pathological process of EAE. TG combined with DX alleviates the symptoms of EAE by suppressing inflammatory and immunological reactions of EAE.  相似文献   

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AIM:To study the effect of Toll-like receptor 4 (TLR4) on the secretion of inflammatory factors in the pancreatic acinar AR42J cells induced by lipopolysaccharides (LPS). METHODS:The rat pancreatic acinar AR42J cells were treated with LPS. The expression of TLR4 at mRNA and protein levels was determined by real-time PCR and Western blot. The lentivirus carrying TLR4 small interfering RNA (siRNA) was used to infect the AR42J cells. Under LPS stimulation, the interference efficacy was measured by real-time PCR and Western blot. The cell viability was measured by MTT assay, and the leakage rate of lactate dehydrogenase (LDH) was examined by dinitrophenylhydrazine method. The releases of interleukin-1β (IL-1β) and tumor necrosis factor-α (TNF-α) in the cell culture medium were detected by ELISA, and the malondialdehyed (MDA) content in supernatant was measured by thiobarbituric acid method. The activity of superoxide dismutase (SOD) in the supernatant was determined by xanthine oxidation, and the activity of glutathione peroxidase (GSH-Px) and catalase (CAT) was detected by colorimetry. RESULTS:The expression of TLR4 at mRNA and protein levels in LPS-treated AR42J cells was significantly increased (P<0.05). Infection with TLR4 siRNA-carrying lentivirus significantly inhibited the expression of TLR4 at mRNA and protein levels in the AR42J cells under LPS stimulation(P<0.05). The viability of AR42J cells was decreased after LPS treatment. The leakage rate of LDH was increased, the levels of IL-1β and TNF-α secreted by the AR42J cells were increased, the content of MDA was increased in the supernatant, and the activity of SOD, GSH-Px and CAT was reduced (P<0.05). After knock-down of TLR4 expression, the viability of AR42J cells was increased under LPS stimulation, the LDH leakage rate, secreted levels of IL-1β and TNF-α, and the content of MDA in cell culture medium were decreased, and the SOD, GSH-Px and CAT levels were increased (P<0.05). CONCLUSION:LPS induces the expression of TLR4 in the pancreatic acinar AR42J cells. Knock-down of TLR4 expression reduces the secretion of inflammatory factors IL-1β and TNF-α, and attenuates the oxidative damage in pancreatic acinar AR42J cells induced by LPS.  相似文献   

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AIM: To investigate the expression of calprotectin(CALP) in the rats with renal ischemia-reperfusion injury(IRI). METHODS: Male Sprague-Dawley rats were randomly divided into sham operation and IRI group(n=25 in each group). Blood samples and the kidneys were obtained at 6 h, 12 h, 24 h, 48 h and 72 h after reperfusion. The pathological changes of the kidneys were observed. The serum concentrations of blood urea nitrogen(BUN) and serum creatinine(SCr) were measured. The serum levels of CALP, tumor necrosis factor-α(TNF-α) and interleukin-6(IL-6) were detected by ELISA, and the expression of CALP, Toll-like receptor 4(TLR4) and NF-κB p65 in the renal tissues were determined by the methods of immunohistochemistry and Western blot. RESULTS: Different serial ischemia changes were observed in the renal tissues, mainly in the renal tubular epithelial cells and the mesenchyma, with the infiltration of inflammatory cells. The serum levels of BUN, SCr, CALP, TNF-α and IL-6 in IRI group were markedly increased as compared with sham group(P<0.05). The protein expression of CALP, TLR4 and NF-κB p65 in the renal tubular epithelial cells in IRI group was greatly enhanced in comparison with that in sham group(P<0.05). CONCLUSION: The serum concentrations of CALP, TNF-α and IL-6, and the protein expression levels of CALP, TLR4 and NF-κB p65 in the renal tissue are significantly increased in the rats with IRI, suggesting that calprotectin plays an important role in the inflammation in rats with IRI.  相似文献   

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AIM: To investigate the effects of silent information regulator 1 (SIRT1) on high glucose-induced acetylation of NF-κB p65 subunit and its protective role in rat mesangial cells. METHODS: Rat mesangial cells were cultured in DMEM supplemented with 10% FBS and were divided into control group, mannitol group, high glucose group, resveratrol group and SIRT1 RNAi group. The cell viability was determined by MTT assay. The mRNA expression of SIRT1, monocyte chemoattratant protein 1 (MCP-1), vascular cell adhesion molecule 1 (VCAM-1-1), tumor necrosis factor α (TNF-α), transforming growth factor β1 (TGF-β1) was analyzed by real-time quantitative PCR. The protein expression of SIRT1 and the acetylation of NF-κB p65 subunit were determined by Western blotting. The protein concentrations of MCP-1, VCAM-1, TNF-α, TGF-β1 and malondialdehyde (MDA) were detected by ELISA. RESULTS: The cell viability, superoxide dismutase (SOD) activity, and the expression of SIRT1 at mRNA and protein levels were decreased by high glucose treatment as compared with control group. The acetylation of NF-κB p65 subunit was significantly increased after interfered with high glucose, resulting in the increase in the secretion of MCP-1, VCAM-1, TNF-α and TGF-β1. Resveratrol decreased high glucose-induced acetylation of NF-κB p65 subunit. However, silencing SIRT1 significantly enhanced the acetylation of NF-κB p65 subunit and the expression of MCP-1, VCAM-1, TNF-α and TGF-β1. CONCLUSION: SIRT1 remarkably inhibits the inflammatory reactions by deacetylating NF-κB p65, suggesting that SIRT1 is a possible target for preventing diabetic nephropathy.  相似文献   

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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 investigate the effects of eicosapentaenoic acid(EPA) on the expression of nuclear factor kappa B(NF-κB) and release of vascular endothelial growth factor(VEGF), IL-1α and IL-6 in cultured human umbilical vein endothelial cells(HUVECs) stimulated by lipopolysaccharide(LPS).METHODS: HUVECs were obtained from cell strain and cultured in vitro. HUVECs were divided into 4 groups: control group, LPS group, 0.030 g/L EPA treatment group and 0.050 g/L EPA treatment group. The cells were cultured with LPS alone in LPS group and incubated with EPA for 1 h in the EPA pretreatment groups at the concentrations of 0.030 g/L and 0.050 g/L before LPS stimulation. Twenty-four hours after stimulated by LPS, the protein expression of NF-κB p65 in HUVECs were assessed by Western blotting analysis at different time points. The production of VEGF, IL-1α and IL-6 in cultured HUVECs was evaluated by ELISA. The effects of EPA on the protein expression of NF-κB p65 and the production of VEGF, IL-1α and IL-6 in HUVECs challenged by LPS were also determined.RESULTS: Compared with control group, the protein expression of NF-κB p65 was significantly increased in HUVECs induced by LPS and was inhibited by EPA. Compared with control group, the protein expression of VEGF, IL-1α and IL-6 was dramatically increased in HUVECs induced by LPS and most of the increase was inhibited by EPA.CONCLUSION: LPS enhances the protein expression of NF-κB and the release of VEGF, IL-1α and IL-6. EPA inhibits the protein expression of NF-κB, and the production of VEGF and the inflammatory cytokines in cultured HUVECs stimulated by LPS, indicating that EPA may be useful for preventing and treating neovascular and inflammatory diseases.  相似文献   

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AIM: To investigate whether the opening of ATP-sensitive K+(KATP) channels protects H9c2 cardiac cells against high glucose(HG)-induced injury and inflammation by inhibiting the Toll-like receptor 4(TLR4)/nuclear factor-κB(NF-κB) pathway. METHODS: The protein levels of TLR4 and NF-κB p65 were determined by Western blot. The levels of interleukin-1β(IL-1β) and tumor necrosis factor-α(TNF-α) were detected by ELISA. The cell viability was measured by CCK-8 assay. Mitochondrial membrane potential(MMP) was examined by rhodamine 123(Rh 123) staining followed by photofluorography. The intracellular levels of reactive oxygen species(ROS) were detected by 2', 7'-dichlorfluorescein- diacetate(DCFH-DA) staining followed by photofluorography. The number of apoptotic cells was observed by Hoechst 33258 nuclear staining followed by photofluorography. RESULTS: After the H9c2 cardiac cells were treated with HG(35 mmol/L glucose) for 24 h, the protein levels of TLR4 and phosphorylated NF-κB p65(p-NF-κB p65) were significantly increased. Pretreatment of the cells with 100 μmol/L diazoxide(DZ, a KATP channel opener) for 30 min before exposure to HG considerably blocked the up-regulation of the TLR4 and p-NF-κB protein levels induced by HG. Moreover, co-treatment of the cells with 30 μmol/L TAK-242(an inhibitor of TLR4) obviously inhibited the HG-induced up-regulation of the p-NF-κB p65 protein level. On the other hand, pretreatment of the cells with 100 μmol/L DZ had a clear myocardial protection effect, which attenuated the HG-induced cytotoxicity, inflammatory response, mitochondrial damage, oxidative stress and apoptosis, evidenced by an increase in the cell viability, and decreases in the levels of IL-1β and TNF-α, MMP loss, ROS generation and the number of apoptotic cells. Similarly, co-treatment of H9c2 cardiac cells with 30 μmol/L TAK-242 or 100 μmol/L PDTC(an inhibitor of NF-κB) and HG for 24 h also obviously reduced the above injuries and inflammation induced by HG.CONCLUSION: The opening of KATP channels protects H9c2 cardiac cells against HG-induced injury and inflammation by inhibiting the TLR4/NF-κB pathway.  相似文献   

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AIM: To observe the inhibitory effect of madecassoside on the LPS-stimulated microglia and to investigate its possible mechanism. METHODS: Microglia cells of neonatal Sprague-Dawley (SD) rats were cultured, isolated and purified. Microglia cells were activated with lipopolysaccharide (LPS). The inhibitory effect of madecassoside on microglia was measured by MTT assay. Tumor necrosis factor alpha (TNF-α), interleukin 1β (IL-1β) were detected by ELISA. Cell cycle and apoptotic rate were evaluated by flow cytometry. The expression of TLR4 was detected by Western blotting. The expression of NF-κB was detected by RT-PCR. RESULTS: LPS induced the proliferation of microglia and release inflammatory cytokines significantly. Compared with LPS group, madecassoside inhibited the proliferation of microglia induced by LPS in a dose dependent manner. The IC50 value of madecassoside was 10.97 nmol/L to microglia after incubation for 48 h. Madecassoside also decreased the levels of TNF-α and IL-6, increased the ratios of microglia at the G2 phase and the apoptotic rate, decreased the expression of TLR4 and NF-κB significantly (P<0.05). CONCLUSION: Madecassoside has inhibitory effects on the proliferation of LPS-stimulated microglia, by which the mechanism may be related to inhibition of the expression of TLR4 and NF-κB, change of cell cycle distribution and induction of microglia apoptosis.  相似文献   

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AIM:To analyze the effect of autophagy on inflammatory response regulated by doxycycline in lipopolysaccharide (LPS)-stimulated THP-1 cells and to investigate its molecular mechanism. METHODS:A human monocyte/macrophage cell line THP-1 was stimulated with LPS to establish an cell model of inflammatory response, and the cells were treated with doxycycline. The cytokines, such as tumor necrosis factor-α (TNF-α) and interleukin-8 (IL-8), in cell culture supernatant were measured by ELISA for evaluating the inflammatory levels. For determining the level of autophagy and its effect on inflammatory cell signaling pathways, the protein levels of LC3B, nuclear factor κB (NF-κB) and phosphorylated mammalian target of rapamycin (p-mTOR) were determined by Western blot. 3-Methyladenine (3-MA), an autophagy inhibitor, and rapamycin, an autophagy inducer, were used to study the effect of autophagy on inflammatory response regulated by doxycycline in LPS-stimulated THP-1 cells. RESULTS:The levels of TNF-α and IL-8 were increased rapidly and peaked at 12 h in LPS-stimulated THP-1 cells (P<0.05). Doxycycline significantly inhibited LPS-induced cytokine production in the THP-1 cells. Doxycycline up-regulated LPS-induced autophagy in THP-1 cells and doxycycline itself was an autophagy inducer. The protein levels of p-mTOR was up-regulated by LPS and down-regulated by doxycycline, suggesting that doxycycline induced autophagy via mTOR-dependent pathway while LPS through mTOR-independent pathway. Further studies showed that the combination of LPS, rapamycin and doxycycline inhibited the protein levels of NF-κB, and rapamycin increased the inhibitory effect of doxycycline on cytokine releases. Conversely, 3-MA, the autophagy inhibitor, attenuated the inhibitory effect of doxycycline on NF-κB and cytokine production. CONCLUSION:Autophagy is involved in the process of doxycycline modulating LPS-induced inflammatory response in the THP-1 cells.  相似文献   

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AIM: To investigate the inhibitory effect of ginsenoside Re on intimal hyperplasia induced by balloon-injury and to explore the role of NF-κB p65 signaling pathway in the process. METHODS: SD rats(n=40) were divided into 5 groups randomly: sham operation group, model group, low-dose ginsenoside Re group, middle-dose ginsenoside Re group and high-dose ginsenoside Re group. The carotid artery intima injury model was established by 2F balloon catheters in all groups except the sham operation group. The day after modeling, the animals in model group and sham operation group were administered intragastrically with distilled water, and the rats in low-dose, middle-dose and high-dose ginsenoside Re groups were given ginsenoside Re at doses of 12.5 mg/kg, 25mg/kg and 50 mg/kg, respectively. After 14 continuous days, the morphological changes of the injured arteries were observed by HE staining and the lumen area, intima area and media area as well as the ratio of intimal area/media area were determined. The expression of tumor necrosis factor-α(TNF-α) and interleukin-1β(IL-1β) were detected by real-time PCR. The proliferating cell nuclear antigen(PCNA) and nuclear factor-kappa B(NF-κB) p65 were examined by immunohistochemistry.RESULTS: Compared with sham operation group, the vessel cavity was narrowed(P<0.01), the mRNA levels of TNF-α and IL-1β, and the protein expression of PCNA and NF-κB p65 were increased in model group(P<0.05). Compared with model group, the vascular intimal hyperplasia was alleviated obviously(P<0.05), and the mRNA levels of TNF-α and IL-1β, and protein expression of PCNA and NF-κB p65 were decreased in medium and high-dose ginsenoside Re groups(P<0.05). CONCLUSION: Ginsenoside Re inhibits the vascular neointimal hyperplasia induced by balloon-injury in rats, and the molecular mechanism may be related to the inhibition of NF-κB p65 signaling pathway.  相似文献   

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AIM:To explore the effect of TAK-242 on the learning and memory ability of C57BL/6 mice with sepsis-associated encephalopathy induced by lipopolysaccharide (LPS), to observe the pathological and morphological changes of the mouse brain, and to explore the mechanism of protein pathway associated with the effect of TAK-242. METHODS:Healthy female C57BL/6 mice (n=80), aged 10~12 months, weighing 20~30 g, were randomly divided into 4 groups (n=20):blank control (CON) group, TAK-242 control (TAK) group, sepsis encephalopathy model (LPS) group and TAK-242 pretreatment (T+L) group. Peripheral inflammation in the mice was detected by testing the arterial blood and lung tissues. The behavioral changes of the mice were observed by the open-field test, elevated plus-maze test (EPMT) and Morris water maze test. Immunohistochemistry was performed to observe the changes of microglia-specific marker, ionized calcium-binding adapter molecule-1 (Iba-1), in the hippocampus. Finally, the protein expression levels of NF-κB p65, TLR4, Aβ1-42 and p-tau (S396) were determined by Western blot. RESULTS:Compared with CON group, the mice in other groups didn't showed significant difference in the arterial blood gas analysis and lung tissue HE staining. In the anxiety and fear behavior tests, central active duration and times of crossing central field of the mice in LPS group were significantly decreased compared with CON group (P<0.01). The times of open arm entry and the times of head area entry in the EPMT were significantly less than those in CON group (P<0.05). The escape latency of spatial probe experiments was significantly extended (P<0.05). Microglial activation in the hippocampus was significantly increased (P<0.05) and the protein expression levels of NF-κB p65, TLR4, Aβ1-42 and p-tau (S396) were significantly increased (P<0.01). Conversely, compared with LPS group, the central active duration and times of crossing central field in T+L group were significantly increased (P<0.01). The times of open arm entry and the times of head area entry in the EPMT were significantly increased (P<0.05). The escape latency of spatial probe experiments was significantly shortened (P<0.05). Microglial activation in the hippocampus was significantly decreased and the protein expression levels of NF-κB p65, TLR4, Aβ1-42 and p-tau (S396) were down-regulated (P<0.05). CONCLUSION:TAK-242 obviously improves the ability of learning and memory, and the mechanism may be related to the inhibition of the central microglia activation and down-regulation of protein expression levels of NF-κB p65, TLR4, Aβ1-42 and p-tau (S396).  相似文献   

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AIM: To observe the anti-atherosclerosis effect of paeonal (Pae) on the activation of NF-κB and the expression of cell adhesion molecules in human umbilical vein endothelial cells (HUVECs) induced by hyperlipidemic serum. METHODS: Cultured HUVECs were used as target cells. Hyperlipidemic serum was added to the culture medium to establish the injury mode of HUVECs. Methyl thiazolyl tetrazolium (MTT) method was used to examine the cell viability. The mRNA expression of NF-κB p65 was determined by RT-PCR. The protein levels of IκB-α, intercellular cell adhesion molecule-1 (ICAM-1) and E-selectin were detected by Western blotting. RESULTS: After treated with Pae, the cell viability was increased and the morphological changes of HUVECs injured by hyperlipidemic serum trended to normal. The expression of IκB-α in HUVECs injured by hyperlipidemic serum increased, while the expression of NF-κB p65 mRNA, ICAM-1 and E-selectin protein was decreased. CONCLUSION: The anti-atherosclerosis mechanism of paeonal may be related to the inhibitory effect of the natural compound on the pathway of NF-κB/IκB, thereby reducing the expression of ICAM-1 and E-selectin and attenuating the inflammatory reaction in vascellum.  相似文献   

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