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1.
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   

2.
AIM: To observe the effects of TNF-α/nuclear factor-κB(NF-κB)/matrix metalloproteinase-2(MMP-2) pathway on the expression of MMP-2 in the mice with viral myocarditis. METHODS: Six-week-old inbred male mice were randomly assigned to control and myocarditis group. The mice in myocarditis group and control group were intraperitoneally inoculated with 0.1 mL 10-5.69 TCID50/mL coxsackievirus B3 and vehicle (PBS), respectively. Ten mice were sacrificed at the 4th and 10th days after injection. The blood and heart specimens were harvested. The serum content of TNF-α was measured by ELISA. The myocardial levels of MMP-2, NF-κB p65 and IκBα were determined by Western blot. RESULTS: Compared with control group, the protein expression of MMP-2 and NF-κB p65 in the myocardium and the serum content of TNF-α were significantly increased in myocarditis group (P<0.05). The protein expression of IκBα was lower in myocarditis group than that in control group (P<0.05).CONCLUSION: TNF-α, NF-κB p65 and MMP-2 were higher in the mice with acute viral myocarditis. The increased expression of them might be involved in the pathogenesis of viral myocarditis.  相似文献   

3.
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   

4.
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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6.
AIM: To investigate the serum levels of inflammatory factors and adiponectin in type 2 diabetic retinopathy (DR) patients.METHODS: One hundred and ten cases of type 2 diabetic patients were divided into 3 groups: no diabetic retinopathy group (DM, n=35), non-proliferative diabetic retinopathy group (NPDR, n=45), and proliferative diabetic retinopathy group (PDR, n=30). Other 40 normal persons served as controls (NC group). The physical examinated was performed for each patient. Serum levels of fasting plasma glucose (FPG), glycated hemoglobin A1c (HbA1c), 2 h postprandial plasma glucose (2hPG), fasting insulin (FINS), total cholesterol (TC), triglyceride (TG), low-density lipoprotein cholesterol (LDL-C), high-density lipoprotein cholesterol (HDL-C), adiponectin, intercellular adhesion molecule-1(ICAM-1), tumor necrosis factor-α (TNF-α) and high-sensitivity C-reactive protein (hs-CRP) were measured. Insulin resistance index (HOMA-IR) was also calculated.RESULTS: The systolic blood pressure, body-mass index, waist-hip ratio, serum levels of TG, LDL-C, FPG, 2hPG, HbA1c, ICAM-1, TNF-α, hs-CRP and HOMA-IR were significantly higher in DM group, NPDR group and PDR group than those in NC group (P<0.05). The systolic blood pressure, serum levels of ICAM-1, TNF-α, hs-CRP and HOMA-IR were higher in NPDR group and PDR group than those in DM group (P<0.05). The serum concentration of adiponectin was lower in DM group, NPDR group and PDR group than that in NC group (P<0.05), and that was also lower in NPDR group and PDR group than that in DM group (P<0.05). The negative correlations between adiponectin and ICAM-1 (r=-0.735,P<0.01), TNF-α (r=-0.781,P<0.01), hs-CRP (r=-0.768, P<0.01) or HOMA-IR (r=-0.752, P<0.01) were observed. The relationships between HOMA-IR and ICAM-1 (r=0.857,P<0.01), TNF-α (r=-0.906, P<0.01) or hs-CRP (r=-0.888,P<0.01) were positive.CONCLUSION: The results suggest that inflammatory refactors and adiponectin play important roles in the pathophysiology and progression of DR. The protective effects of adiponectin on DR may be related with its anti-inflammatory reactions to improve insulin resistant.  相似文献   

7.
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   

8.
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   

9.
AIM：To investigate whether hydrogen sulfide (H2S) attenuates doxorubicin (DOX)-induced inflammation and cytotoxicity in rat cardiomyocytes (H9c2 cells) by modulating nuclear factor κB (NF-κB) pathway. METHODS：The expression of NF-κB p65 was measured by western blotting. The secretion levels of interleukin (IL)-1β, IL-6 and tumor necrosis factor α (TNF-α) were tested by enzyme-linked immunosorbent assay (ELISA). Cell viability was detected by Cell Counting Kit-8 (CCK-8) assay. Hoechst 33258 nuclear staining was used to detect the morphological changes and number of apoptotic cells. RESULTS：Treatment of H9c2 cells with 5 μmol/L DOX significantly up-regulated the expression level of phosphorylated NF-κB p65 (p-p65), and induced inflammation and cytotoxicity, as evidenced by increases in secretion levels of IL-1β, IL-6 and TNF-α and number of apoptotic cells as well as a decrease in cell viability. Pretreatment of H9c2 cells with 400 μmol/L NaHS (a donor of H2S) for 30 min markedly depressed the up-regulation of p-p65 expression induced by DOX. In addition, NaHS pretreatment also reduced DOX-induced inflammatory response and injury, leading to decreases in IL-1β, IL-6 and TNF-α secretion and number of apoptotic cells as well as an increase in cell viability. Similar to the effect of NaHS, pretreatment with 100 μmol/L pyrrolidine dithiocarbamate (PDTC), an inhibitor of NF-κB, also blocked DOX-induced cardiac inflammation and cytotoxicity. Co-administration of IL-1 receptor antagonist (IL-1Ra) and DOX reduced DOX-induced activation of NF-κB and cytotoxicity in H9c2 cells. CONCLUSION：During the DOX-induced cardiomyocyte inflammation, there is positive interaction between NF-κB pathway and IL-1β. H2S may protect cardiomyocytes against DOX-induced inflammatory response and cytotoxicity by inhibiting NF-κB pathway.  相似文献   

10.
AIM：To observe the expression of tumor necrosis factor α (TNF-α) and nuclear factor κB (NF-κB) in the renal tissue of the rats with contrast-induced nephropathy (CIN). METHODS：Male Sprague-Dawley rats (n=96) were randomly divided into control group (n=48) and CIN group (n=48). The model rats in CIN group were intravenously injected with iodinated contrast media (76% compound diatrizoate injection,10 mL/kg), while the rats in control group were injected with the same volume of saline. Six rats in each group were sacrificed at 6 h, 12 h, 24 h, 48 h, 72 h, 5 d, 10 d and 15 d after intravenous injection, respectively, and the blood and kidney samples of the rats were obtained. The renal tubular injury was assessed by histological examination (HE staining). The expression of kidney injury molecule-1 (KIM-1), TNF-α and NF-κB at mRNA and protein levels in the renal tissues were semiquantitatively measured by the methods of RT-PCR and immunohistochemistry, respectively. The correlations between the expression of TNF-α, NF-κB and tubular injury score, KIM-1 expression in renal tissue of CIN group were analyzed. RESULTS：The levels of serum creatinine (SCr) and blood urea nitrogen (BUN) in control group were not changed between different time points (P>0.05). The levels of SCr and BUN in CIN group displayed significant increases at different time points (except 15 d) compared with control group (P<0.05). The renal tubular injury score in CIN group was significantly higher at all time points than that in control group (P<0.05). The expression of KIM-1, TNF-α and NF-κB at mRNA and protein levels up-regulated significantly at 6 h and the peaking of KIM-1 expression was at 24 h, while the peaking of TNF-α and NF-κB expression was at 48 h in CIN group. The expression of KIM-1,TNF-α and NF-κB was significantly increased in CIN group compared with control group except at 15 d (P<0.05). The expression of TNF-α and NF-κB at mRNA and protein levels showed close correlations with renal tubular injury score (r=0.843, 0.758, 0.743 and 0.707, P<0.05). The expression of TNF-α and NF-κB at mRNA and protein levels was also positively correlated with KIM-1 expression (r=0.863, 0.807, 0.839 and 0.855, P<0.05). CONCLUSION：The expression of TNF-α and NF-κB at mRNA and protein levels in the renal tissues of CIN group is up-regulated and is closely related with renal tubular injury, indicating that the inflammatory response is involved in the pathogenesis of CIN.  相似文献   

11.
AIM: To investigate the ameliorative effect of salvianolic acid B on vasodilatory function in diabetic rats and the possible mechanisms. METHODS: SD rats (n=40) were fed on high-sugar and high-fat diet for 4 weeks, followed by a single intraperitoneal injection of streptozotocin (40 mg/kg). The rats with random blood glucose level over 16.7 mmol/L were considered diabetic and randomly allocated to 3 groups, namely model group, low dose (80 mg·kg-1·d-1) of salvianolic acid B group and high dose (160 mg·kg-1·d-1) of salvianolic acid B group. The rats in salvianolic acid B groups were intragastrically administered with corresponding doses of salvianolic acid B for 6 weeks. Vasodilatory function was measured as endothelium-dependent and-independent vasodilation of the aortic rings. The primary histopathological changes of aorta were observed by HE staining. Serum levels of interleukin-6 (IL-6), tumor necrosis factor-α (TNF-α) and C-reactive protein (CRP) were measured by ELISA. The levels of total antioxidant capacity, malondialdehyde (MDA) and nitric oxide (NO) in aortic tissues were evaluated by colorimetric assays. The protein levels of intercellular adhesion molecule-1 (ICAM-1) and monocyte chemotactic protein-1 (MCP-1), and the activation of nuclear factor-κB (NF-κB) were determined by Western blot. RESULTS: Treatment with salvianolic acid B evidently ameliorated endothelium-dependent diastolic function and pathological changes of aorta in diabetic rats (P<0.05 or P<0.01). Supplementation with salvianolic acid B resulted in significant increases in NO content and total antioxidant capacity in aortic tissues, accompanied by marked decreases in the level of MDA in aorta tissues and the serum levels of IL-6, TNF-α and CRP (P<0.05 or P<0.01). Salvianolic acid B markedly down-regulated NF-κB p65 nuclear translocation and protein expression of ICAM-1 and MCP-1 in aorta tissues (P<0.05 or P<0.01). CONCLUSION: Salvianolic acid B effectively ameliorates endothelium-dependent diastolic function of aorta in diabetic rats, which might be attributed to suppression of NF-κB activation and subsequent expression of inflammatory cytokines. The beneficial effect of salvianolic acid B on vascular endothelium might be derived from its antioxidant capacity.  相似文献   

12.
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   

13.
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   

14.
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   

15.
AIM:To investigate the protective effect of ethanol extract from Cortex Albiziae on acute liver injury, and to explore its possible mechanism. METHODS:Acute liver injury in mice was induced by single intraperitoneal injection of 25% carbon tetrachloride (olive oil solubilization). The effective parts of ethanol extract from Cortex Albizziae against acute liver injury were screened. The pathological changes of the liver tissues were examined by pathological sections with HE staining. The activity of total superoxide dismutase (T-SOD) and the content of malondialdehyde (MDA) of the liver tissues were detected, the serum levels of interleukin-6 (IL-6) and tumor necrosis factor-α (TNF-α) were mea-sured by ELISA, and the protein expression levels of NF-κB p65, Bcl-2 and Bax in the liver cells of the mice in each group were determined by Western blot. RESULTS:Compared with model group, the serum levels of AST and ALT in low-dose n-butanol phase of ethanol extract from Cortex Albiziae (AB-L, 4 mg·kg-1·d-1) group and high-dose n-butanol phase of ethanol extract from Cortex Albiziae (AB-H, 8 mg·kg-1·d-1) group were significantly decreased. The necrosis extent and degree of the hepatocytes and infiltration of inflammatory cells were significantly lower than that in model group. Compared with model group, the serum levels of TNF-α and IL-6 in AB-H group and AB-L group were significantly decreased (P<0.05). The protein level of NF-κB p65 in the nuclei of mouse liver cells in AB-H group and AB-L group were also decreased significantly (P<0.05). Compared with model group, the protein expression of Bax was decreased, the protein expression of Bcl-2 was increased, and the Bcl-2/Bax ratio was increased in AB-L group and AB-H group. CONCLUSION:The n-butanol phase of ethanol extract from Cortex Albiziae may protect the liver by reducing the activation of NF-κB p65, inhibiting the excessive release of inflammatory cytokines IL-6 and TNF-α, and decreasing hepatocyte apoptosis via regulating Bcl-2 and Bax expression.  相似文献   

16.
AIM: To study the role of 4-hydroxynonenal (4-HNE) in hepatocyte death induced by tumor necrosis factor α (TNF-α).METHODS: Human liver cell line HepG2 and primary mouse hepatocytes were used to establish the cell model. The effect of 4-HNE on TNF-α-induced cell death was determined by lactate dehydrogenase (LDH) release and MTT assays. The intracellular levels of 4-HNE-protein adducts were determined by Western blotting. The intranuclear NF-κB (p65) and its DNA binding activity were detected by Western blotting and ELISA, respectively. Long-term intake of alcohol in C57BL/6 mice was performed to establish the animal model. The histological changes of mouse hepatic tissues and the apoptosis of hepatocytes were observed by HE staining and TUNEL assay, respectively. The hepatic levels of triglyceride (TG), TNF-α and 4-HNE-protein adducts, and the plasma activity of alanine aminotransferase (ALT) were also detected.RESULTS: (1) 4-HNE significantly increased the sensitivity of HepG2 cells and primary mouse hepatocytes to the killing effect of TNF-α. (2) 4-HNE significantly increased the intracellular levels of 4-HNE-protein adducts. (3) 4-HNE inhibited TNF-α-mediated NF-κB (p65) activation in HepG2 cells. (4) Long-term intake of alcohol in mice resulted in high hepatic levels of 4-HNE and TNF-α, accompanied with the increases in hepatic TG content, plasma ALT activity and hepatocyte death.CONCLUSION: Long-term intake of alcohol induces oxidative stress and produces 4-HNE as a hepatocyte-sensitizing factor, which inhibits TNF-α-mediated NF-κB anti-apoptotic signaling pathway in hepatocytes, thus inducing alcoholic liver damage.  相似文献   

17.
AIM： To investigate the role of damaged mitochondria in dendritic cell (DC) apoptosis induced by Vibrio vulnificus (Vv) and its possible mechanism. METHODS：DC2.4 cells were co-cultured with Vv 1.1758 strain. Fluorescent probes DCFH-DA and Fluo-8-AM were used to detect reactive oxygen species (ROS) and intracellular Ca2+ concentration in the invaded cells, respectively. The cellular apoptotic rates and mitochondrial membrane potential (Δψm) were measured by flow cytometry. The expression of nuclear factor-kappa B p65 (NF-κB p65) and tumor necrosis factor-alpha (TNF-α) was detected by Western blotting. RESULTS： Vv 1.1758 induced DC2.4 cell apoptosis. Vv 1.1758 bacteria invaded into the DC2.4 cells by binding with cellular membrane though the end of the body. In the invaded DC2.4 cells, the visible mitochondrial damage, elevated ROS and intracellular Ca2+ levels, and declined Δψm were presented. After 1 h of co-culture, NF-κB p65 began to rise and reached the peak at 5 h, and then slightly decreased at 6 h. The TNF-α level increased after 2 h of co-culture and reached the peak at 6 h. CONCLUSION： The damaged mitochondria play an important role in DC apoptosis induced by Vv, and its possible mechanism may associate with the elevation of ROS and intracellular Ca2+ level, and the declined Δψm. Meanwhile, NF-κB p65 and TNF-α are potential critical signaling molecules in the process of apoptosis.  相似文献   

18.
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19.
LU Bang-chao  ZOU Da-jin 《园艺学报》2011,27(9):1832-1835
AIM: To investigate the effect of p38 MAPK signal pathway on cerulein-treated pancreatic acinar AR42J cells.METHODS: AR42J cells were divided into control group, cerulein group (treated with 10-8 mol/L of cerulein), and SB203580 group (treated with 10 μmol/L of SB203580 and 10-8mol/L of cerulein).The cells were harvested 3 h after treatment.Secretion rate of amylase was measured.The translocation of p-p38 MAPK to nuclei was imaged by immunofluorescence.The protein expression levels of p-p38 MAPK and TNF-α were detected by Western blotting.The activation of NF-κB was measured by electrophoretic mobility assay.RESULTS: Compared with control group, cerulein resulted in increases in the secretion rate of amylase and protein level of TNF-α (P<0.01), as well as the expression levels of p-p38 MAPK and NF-κB (P<0.01).Cerulein induced nuclear translocation of p-p38 MAPK.Compared with cerulein group, the secretion rate of amylase and protein level of TNF-α in SB203580 group decreased significantly (P<0.01).The expression of p-p38 MAPK and NF-κB also decreased greatly (P<0.05).Nuclear translocation of p-p38 MAPK was inhibited by SB203580.CONCLUSION: The p38 MAPK pathway involves in cerulein-induced pancreatic inflammatory response via regulating NF-κB.  相似文献   

20.
DU Xiao-gang  GAN Hua  XIAO Gang 《园艺学报》2004,20(7):1204-1207
AIM: To study the action of NF-κB p65 in tubule-interstitium in rats with active Heymann nephritis(AHN). METHODS: Twenty female Wistar rats in 6-8 weeks of age were divided into two groups. The nephritis was induced with Fx1A/CFA by subcutaneous injection and with CFA as control. After rats were killed, the activation of NF-κB p65 in renal tissue was observed by immune histochemistry. RESULTS: The lesion score of renal interstitium and activation of NF-κB p65 of renal tubule in rats with AHN was higher than those of control group(P<0.01). A positive correlation was found between the positive rate of NF-κB p65 in renal tubule and the lesion score of renal interstitium, the levels of urinary protein (r=0.7138 and 0.6376, P<0.05).CONCLUSION: The activation of NF-κB p65 participates in the damage of pathophysiological functions of tubule-interstitium in AHN.  相似文献   

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