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AIM: To investigate NF-κB p65 activation and IκB-α expression in keloid fibroblasts (KFB) and normal skin fibroblasts (NSF) stimulated with TNF-α and to explore the underlying molecular pathogenesis of keloid formation. METHODS: Primary KFB was cultured. The location of NF-κB p65 and IκB-α in KFB and NSF at quiescent condition and the nuclear translocation of NF-κB p65 after TNF-α stimulation were observed by immunofluorescence technique. NF-κB p65 DNA binding activity was detected with TransAMTM NF-κB p65 kit. The IκB-α protein level was determined by means of Western blotting technique. RESULTS: After stimulated with TNF-α, NF-κB p65 translocated into the nucleus. NF-κB p65 DNA binding activity increased to its maximum at 1 h and was dropped to normal at 4 h. TNF-α induced most degradation of IκB-α at 15 min and became detectable in cytoplasm after 4 h. KFB showed more sensitive ability to TNF-α stimulation than NSF. CONCLUSION: NF-κB may play a role in keloid pathogenesis.  相似文献   

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AIM: To investigate the expression, distribution and significance of nuclear factor κB (NF-κB) in experimental hepatic fibrosis.METHODS: Wistar rats were randomly divided into normal control group, hepatic fibrisis model group and the pyrrolidine-1-dithiocarboxylic acid ammonium sail (PDTC) group. The PDTC group was treated with subcutaneous injection of carboan tetrachloride, and treated with PDTC by oral administration. The content of hydroxyproline was measured. Endotoxin was determined with a Limulus amebocyte lysate test kit. The alanine aminotransferase (ALT) in plasma was measured by laishi method. The content of malondialdehyde (MDA) in liver tissue was detected by means of TBA method. The expression of NF-κB was determined by immunohistochemistry. The expression of connective tissue growth factor (CTGF) was measured by Western blotting.RESULTS: In control group, just a small amount of NF-κB p65 was expressed in the cytoplasm of a few hepatocytes around central veins. In model group, the positive staining of NF-κB p65 was expressed in cytoplasm and nucleus, mainly in fibrous stepta, hepatic sinusoid and partial vascular endothelial cells, part of proliferating ductular epithelial cells and impaired hepatocytes. The positive staining began to increase from the first week. The expression of NF-κB in the liver tissues in PDTC group was lower than that in model control group (P<0.05). The ET levels and expression of NF-κB and CTGF began to increase significantly in liver fibrosis group. The levels of plasma ET and expression of NF-κB and CTGF were correlated positively with each other. In PDTC group, ET content in plasma increased significantly at first, then began to decline at the end of the test. The expression of NF-κB and CTGF in liver tissues in PDTC groups was lower than that in model group. Furthermore, the expression of NF-κB in liver tissues in PDTC group was correlated positively with CTGF. The levels of plasma ET were not correlated with the expression of NF-κB and CTGF.CONCLUSION: ET may up-regulate the expression of CTGF by activating NF-κB.  相似文献   

4.
AIM:To investigate the role of NF-κB in pentetrazole-induced repeated seizure in developing rats with the inhibitor of NF-κB pyrrolidine dithiocarbamate (PDTC). METHODS:10-day-old Wistar rats (n=72) were prepared for epilepsy model and divided into three groups at random: the PTZ group, the PDTC+PTZ group and the control group. The behavioral changes, the cells morphology and neurons counts in hippocampus, the expression of NF-κB, BrdU (5-bromo, 2-deoxyuridine) immunoreactive cells in hippocampus and the mossy fiber sprouting were observed.RESULTS:(1) The NF-κB expressed in PTZ group was significantly higher than that in PDTC+PTZ group and control group (P<0.01). (2) The dentate gyrus granule cell count in PTZ group was significantly higher than that in control group (P<0.05). In PDTC+PTZ group cell counts in CA1, CA3 and hilar region were significantly lower than those in PTZ group (P<0.05). (3) The BrdU-immunoreactive cells counts in dentate gyrus in PTZ group and PDTC+PTZ group were significantly higher than those in control group (P<0.01), but in PDTC+PTZ group BrdU-immunoreactive cell count was significantly lower than that in PTZ group (P<0.01). Correlate analyzes between NF-κB expression and BrdU-immunoreactive cell counts/granule cell counts showed positive correlation (P<0.01). (4) The mossy fiber sprouting in both PTZ and PDTC+PTZ group was observed. However, the degrees of sprouting showed no significant differences between two groups. CONCLUSION:NF-κB plays a crucial role in epilepsy of developing rats. It encourages neurogenesis and protects neurons in hippocampus, but has no significant effect on mossy fiber sprouting.  相似文献   

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AIM: To investigate the effects and molecular mechanism of 1-O-acetylbritannilatone (ABL) on LPS-induced inflammatory responses in aorta in vitro.METHODS: The aorta loops pretreated with ABL were stimulated with LPS for different times. The protein extracts from the aorta were used to detect the expression of inflammatory factors by Western blotting. RESULTS: ABL inhibited the activation of NF-κB and the expression of inflammatory factors iNOS, COX-2, ICAM-1 and VCAM-1, and increased the level of anti-inflammatory factor IκBα via blocking the phosphorylation activation of IKK and the degradation of IκBα induced by LPS. CONCLUSION: ABL abolishes the vascular inflammatory response to LPS stimulation through modulating NF-κB activity.  相似文献   

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AIM: To investigate the expression of nuclear factor-κB (NF-κB), inducable nitric oxide synthase (iNOS) and cyclooxygenase-2 (COX-2) in diabetic myocardium. METHODS: Thirty SD rats were randomly divided into control and experimental groups. Diabetes was induced by a single intraperitoneal injection of STZ. The weight, blood glucose level and heart weight index (HWI) were measured 24 weeks after injection. The myocardial NF-κB, iNOS and COX-2 were stained at the same time. Furthermore, NF-κB activation in myocardium was investigated by electrophoretic mobility shift assay (EMSA).RESULTS: (1) Compared to the normal rats, the NF-κB-positive cells in the myocardium in diabetic rats significantly increased. (2) NF-κB activation in myocardium by EMSA was significantly higher in the diabetic rats than that in the normal rats. (3) The iNOS was not expressed in normal rat myocardium and was significantly expressed in the diabetic rat myocardium. (4) The COX-2 was rarely expressed in normal rat myocardium and was significantly expressed in the diabetic rat myocardium.CONCLUSION: The expressions of NF-κB, iNOS and COX-2 are significantly enhanced in the diabetic myocardium.  相似文献   

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AIM: To investigate the effects of erigeron breviscapine on nuclear factor-κB (NF-κB) expression following lung ischemia-reperfusion (I/R) injury in rats. METHODS: Thirty-two male Sprague-Dawley rats were randomized into four groups with 8 animals in each group: sham operation group (I), I/R group (II), erigeron 25 mg/kg group (III) and erigeron 50 mg/kg group (IV). A lung I/R injury rat model was established in situ. I/R injury consisted of 45 min of lung cross-clamping followed by 2 h of reperfusion; sham operation animals had a thoracotomy only. The wet-to-dry weight ratio (W /D), myeloperoxidase (MPO) of lung tissue, the content of nuclear NF-κB p65 were detected by immunohistochemical staining and Western blotting. The histopathological changes of lung tissue were observed under light microscopy. Electron microscopic evaluation was done on randomly selected lungs of two rats in each group at the end of the experiment. RESULTS: Compared to sham operation group, W /D and MPO in the I/R group increased significantly after reperfusion, and the expression of NF-κB in nucleus was up-regulated. As compared with I/R group, the level of NF-κB decreased in group III and IV. Also the changes of W /D and MPO were ameliorated as compared with group II. There was significant difference between group III and IV. CONCLUSION: Erigeron breviscapine reduced I/R lung injury through suppressing the activation of NF-κB and subsequent neutrophils accumulation.  相似文献   

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AIM To investigate the effects of simvastatin （SIM） on the proliferation of esophageal cancer Eca109 cells through NF-κB p65 pathway. METHODS Esophageal cancer Eca109 cells were cultured in vitro and treated with SIM at different concentrations （2 , 4, 8, 16 and 32 μmol/L）. The proliferation of Eca109 cells was measured by MTT assay and plate colony formation assay. The proliferation-related protein levels of cyclin D1, c-Myc, NF-κB p65 （p65） and IκB-α in the esophageal cancer Eca109 cells were determined by Western blot. ELISA was used to detect the levels of tumor necrosis factor α （TNF-α） and interleukin-6 （IL-6） in the culture supernatant of Eca109 cells. RESULTS Compared with control group, the inhibitory effects of SIM at 2 , 4 , 8 and 16 μmol/L on the viability of Eca109 cells were increased in a concentration-dependent and time-dependent manners （P<0.05）. Simultaneously, the inhibitory rates of SIM at 16 and 32 μmol/L on the viability of Eca109 cells showed no significant difference （P>0.05）. The inhibitory rates of SIM at 16 μmol/L on the viability of esophageal cancer cells was 50.61% at 48 h, which was closed to half of the inhibitory dose IC50, and it was used as the optimum concentration and time for follow-up experiments. Compared with control group, the plate colony formation rate of Eca109 cells, the protein levels of cyclinD1, c-Myc, nuclear p65, TNF-α and IL-6 in 8 and 16 μmol/L groups were decreased, while the levels of cytosolic p65 and IκB-α proteins were increased （P<0.05）. No significant difference of plate colony formation rate in Eca109 cells, and the protein levels of cyclin D1, c-Myc, nuclear and cytoplasmic p65, IκB-α, TNF-α and IL-6 between 16 μmol/L SIM group and 32 μmol/L SIM group was observed （P>0.05）. CONCLUSION Simvastatin inhibits the proliferation of esophageal cancer Eca109 cells, and its mechanism may be related to up-regulation of IκB-α, down-regulation of cyclinD1 and c-myc, inhibition of p65 nuclear translocation, and the expression of TNF-α and IL-6 downstream of NF-κB p65 pathway.  相似文献   

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AIMTo investigate the effects of cucurbitacin E on airway inflammation and the signaling pathways of MAPKs and NF-κB in asthmatic mice. METHODSHealthy mice (n=40) were randomly divided into control group, model group, low-dose cucurbitacin E group, high-dose cucurbitacin E group and dexamethasone group. Ovalbumin sensitization was used to induce asthma in the mice. The protein levels of p-JNK, p-ERK1/2, p-p38 MAPK and p-p65 in the lung tissues were determined by Western blot. RESULTSCompared with control group, the numbers of inflammatory cells, such as eosinophils, lymphocytes and neutrophils, were significantly increased in model group, and the activity of MAPKs and NF-κB signaling pathway-related proteins was significantly enhanced. Cucurbitin E at high dose attenuated airway inflammation in asthmatic mice, and significantly inhibited the activity of MAPKs and NF-κB signaling pathway-related proteins. Histopathological results showed proliferation of goblet cells and bronchial mucosal epithelial cells, infiltration of inflammatory cells in the alveoli, and narrow alveolar cavity in model group, while the pathological changes were significantly alleviated in cucurbitin E treatment groups. CONCLUSION Cucurbitin E improves airway inflammation in asthmatic mice, and its mechanism may be related to the inhibition of MAPKs and NF-κB signaling pathways.  相似文献   

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AIM: The present study was undertaken to investigate the effect of angiotensin II (AngⅡ) on expression of MMP-9 in THP-1 macrophages. METHODS: Macrophages converted from THP-1 monocytes by incubating with PMA (0.1 μmol/L) for 48 h were divided into PMA group; PMA+AngⅡ group (10-7mol/L, 1 h); PMA+AngⅡ+PDTC group (10 μmol/L, 30 min) and PDTC group. Western blotting was used to detect the MMP-9 and phosphorylation of NF-κB p65, and the expression of MMP-9 mRNA in THP-1 macrophages was measured by RT-PCR.RESULTS: Compared to control group, the expression of MMP-9 (1.06±0.11, P<0.05) and phosphorylation of NF-κB p65 (1.02±0.10, P<0.05) in THP-1 macrophages were expressed when treated with AngⅡ (10-7mol/L); and the expression of MMP-9 mRNA were upregulated (1.22±0.08, P<0.05). However, NF-κB inhibitor PDTC reduced the NF-κB p65 (0.99±0.12, P<0.01) and MMP-9 (1.04±0.14, P<0.01) expressions and decreased the expression of MMP-9 mRNA (0.90±0.06,P<0.01). CONCLUSION: NF-κB signaling pathway contributes to the expression of MMP-9 in THP-1 macrophage induced by AngⅡ.  相似文献   

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AIM To investigate the effects of geniposide （Gen） on Toll like receptor 4/nuclear factor-κB （TLR4/NF-κB） signaling pathway and cognitive dysfunction in sleep deprived rats. METHODS Wistar rats （n=120） were randomly divided into normal control （NC） group, model （M） group, low-dose （5 g·kg-1·d-1） Gen （Gen-L） group, medium-dose （10 g·kg-1·d-1） Gen （Gen-M） group, high-dose （20 g·kg-1·d-1） Gen （Gen-H） group and Gen-H+LPS （0.4 mg·kg-1·d-1, tail vein injection） group. After 7 days of intervention, the sleep deprivation model of rats in M group, Gen-L, Gen-M, Gen-H and Gen-H+LPS group was established by improved small platform water environment. The escape latency of Morris water maze experiment and the behavior correct rate of Y maze experiment were measured. The serum levels of S100B and neuron-specific enolase （NSE）, and the levels of interleukin-1β （IL-1β）, IL-6 and tumor necrosis factor-α （TNF-α） in hippocampus were detected by ELISA. The mRNA levels of TLR4 and NF-κB p65 were detected by RT-qPCR, and the protein levels of TLR4 and NF-κB p65 were determined by Western blot. RESULTS Compared with NC group, the escape latency, the serum levels of S100B and NSE, the hippocampal levels of IL-1β, IL-6 and TNF-α, and the mRNA and protein expression of TLR4 and NF-κB p65 were increased significantly in M group （P<0.01）, and the behavior correct rate was decreased significantly （P<0.01）. Compared with M group, the escape latency, the hippocampal levels of IL-1β, IL-6 and TNF-α, and the expression of TLR4 and NF-κB p65 at mRNA and protein levels were decreased significantly in Gen-L, Gen-M and Gen-H groups （P<0.01）, and the behavior correct rate was increased in turn （P<0.01）. Compared with Gen-H group, the escape latency, the serum levels of S100B and NSE, the hippocampal levels of IL-1β, IL-6 and TNF-α, and the expression of TLR4 and NF-κB p65 at mRNA and protein levels were increased significantly in Gen-H+LPS group （P<0.01）, and the behavior correct rate was decreased significantly （P<0.01）. CONCLUSION Geniposide may inhibit the TLR4/NF-κB p65 signaling pathway to effectively improve cognitive function in sleep-deprived rats and reduce hippocampus inflammation.  相似文献   

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B2B介绍     
正B2B(也有写成BTB,是Business-to-Business的缩写)是指企业与企业之间通过专用网络或Internet,进行数据信息的交换、传递,开展交易活动的商业模式。它将企业内部网和企业的产品及服务,通过B2B网站或移动客户端与客户紧密结合起来,通过网络的快速反应,为客户提供更好的服务,从而促进企业的业务发展。含  相似文献   

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AIM: To explore the role of transforming growth factor-β1 (TGF-β1)/TGF-β-activated kinase (TAK)-nuclear factor-κB (NF-κB) signaling pathway in chronic pancreatitis (CP) mice and the effect of baicalin on pancreatic fibrosis in the mice. METHODS: Kunming mice (n=58) were randomly divided into 3 groups, including control group, CP group and baicalin group. The mice in CP group and baicalin group were intraperitoneally injected with 20% L-arginine. After 2 weeks of CP, the mice in baicalin group were intraperitoneally injected with baicalin (100 mg/kg, once a day). At 2 weeks, 4 weeks and 6 weeks after modeling, the mice were anesthetized and sacrificed. The morphological changes of the pancreas were observed by HE and Masson staining. The serum level of TGF-β1 was analyzed by ELISA. The expression of fibronectin (FN) and NF-κB in the pancreas was observed by immunohistochemistry staining. The protein levels of transforming growth factor-β receptor type Ⅰ (TGF-βRⅠ), phosphorylated TAK1 (p-TAK1) and NF-κB in the pancreas were determined by Western blot. The mRNA expression of matrix metalloproteinase-1 (MMP-1) and tissue inhibitor of metalloprotease-1 (TIMP-1) was detected by real-time PCR. RESULTS: At 2 weeks, 4 weeks and 6 weeks after intraperitoneal injection of L-arginine, the pancreatic tissues were obviously injured and exhibited different degrees of fibrosis, and FN expression was significantly increased. After treatment with baicalin, the degrees of pancreatic injury and fibrosis were significantly attenuated and the expression of FN was reduced (P<0.01). Compared with control group, the protein levels of TGF-β1, TGF-βRⅠ, p-TAK1, NF-κB and TIMP-1 in the pancreas of CP group were significantly increased, and the expression of MMP-1 was decreased at each time point. In baicalin group, the protein levels of TGF-β1, TGF-βRⅠ, p-TAK1, NF-κB and TIMP-1 were significantly decreased, and the expression of MMP-1 was markedly increased at the corresponding time points compared with CP group (P<0.01). CONCLUSION: Baicalin effectively atte-nuates pancreatic fibrosis by inhibiting the activation of TGF-β1/TAK-NF-κB signaling pathway and regulating the balance of MMP-1/TIMP-1.  相似文献   

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AIM: To investigate the relationship of p38 mitogen-activated protein kinases (p38MAPK), nuclear factor-kappa B (NF-κB) and heme oxygenase-1 (HO-1) in acute lung injury (ALI) in rats.METHODS: Forty male Wistar rats were divided into 5 groups (n=8) at random: control group or normal saline group (NS group), lipopolysaccharide group (LPS group), Hemin (inducer of HO-1)+LPS group, ZnPPIX (inhibitor of HO-1)+LPS group and SB203580 (inhibitor of p38MAPK)+LPS group (SB+LPS group). Six hours after endotracheal instillation of LPS or NS, the ratio of neutrophils and the protein contents in bronchoalveolar lavage fluid (BALF) of right lung, the ratio of wet/dry weight (W/D) of the superior lobe of right lung, and arterial blood gas analysis (ABG) were examined. The protein levels of p38MAPK and NF-κB in the lower lobe of right lung were detected by Western blotting. The protein expression of HO-1 in the middle lobe of right lung was measured by the method of immunohistochemisty. The structure of the lung was evaluated under light microscope. RESULTS: Compared with NS group, the ratio of neutrophils and protein contents in BALF, the ratio of W/D, the protein levels of HO-1, p38MAPK and NF-κB were obviously higher, and arterial oxygen pressure (PaO2), partial pressure of carbon dioxide in artery (PaCO2) and bicarbonate content (HCO-3) were significantly lower in LPS group, Hemin+LPS group, ZnPPIX+LPS group and SB+LPS group (P<0.05 or P<0.01). The ratio of neutrophils and proteins in BALF, the ratio of W/D, the protein levels of p38MAPK and NF-κB were significantly lower, the protein level of HO-1 was obviously higher in Hemin+LPS group and SB+LPS group than those in LPS group (P<0.05), while the changes of the parameters in ZnPPIX+LPS group were in a contrary manner (P<0.05). No significant difference of the parameters between Hemin+LPS group and SB+LPS group (P>0.05) was found. The structures of the lung tissues in LPS group were severely damaged and even severer damages were observed in ZnPPIX+LPS group. The structural changes of the lung tissues in Hemin+LPS group and SB+LPS group were slighter. CONCLUSION: p38MAPK/NF-κB and HO-1 are inhibited by each other and the effects of them are independent on the acute lung injury.  相似文献   

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AIM To investigate the inhibitory effect of protocadherin 10 （PCDH10） on proliferation of human breast cancer cells and its possible mechanism. METHODS RT-PCR was used to measure the mRNA expression levels of PCDH10 in 4 human breast cancer cell lines and normal mammary epithelial MCF-10A cells. The breast cancer cell line MDA-MB-231 with stable PCDH10 overexpression was constructed by recombinant lentivirus （pLV-PCDH10） infection, and blank control （blank） group and negative control （pLV-NC） group were also set up. The cell proliferation ability was detected using methyl thiazolyl tetrazolium （MTT） and colony formation experiments. The cell cycle was detected by flow cytometry. Western blot was used to determine the expression of cyclin D1, cyclin-dependent kinase 4 （CDK4）, nucear factor-κB p65 subunit （NF-κB p65） and NF-κB inhibitor α （IκBα）. RESULTS The mRNA expression levels of PCDH10 in 4 breast cancer cell lines were lower than that in normal mammary epithelial MCF-10A cells （P<0.05）. A breast cancer cell line MDA-MB-231 with stable PCDH10 overexpression was constructed successfully. Compared with negative control group, PCDH10 overexpression significantly inhibited cell proliferation, induced cell cycle arrest at G1 phase, down-regulated the expression of cyclin D1 and CDK4, and decreased phosphorylation of NF-κB p65 and IκBα（P<0.05）. CONCLUSION PCDH10 inhibits the proliferation and blocks cell cycle progression of breast cancer cells by targeting NF-κB/cyclin D1 signaling pathway.  相似文献   

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AIM: To investigate the effects of metformin on nuclear factor-κB (NF-κB),its inhibitor IκB,and the level of serum high sensitivity C-reactive protein (hs-CRP) in rabbits.METHODS: 24 New Zealand male rabbits were randomly divided into control group,atherosclerosis (AS) group and metformin (Met) group.AS group and Met group were made as models by cholesterolenriched diets feeding and vascular intimal immunologic injury.The AS model was confirmed by high frequency ultrasound.Met group were given metformin 150 mg·kg-1·d-1 for 8 weeks.At the end of experiment,serum hs-CRP and serum lipids in all three groups were detected.Immunohistochemistry and Western blotting technique were applied to detect the expression of nucleus NF-κB p65 and cytoplasma IκBα in aorta in all three groups.RESULTS: Compared to normal control group,the level of serum hs-CRP was elevated (1.27±0.43 vs 3.96±0.63,P<0.01),the expression of nucleus NF-κB p65 increased significantly (P<0.01) while the expression of IκBα reduced significantly (P<0.01).Compared to AS group,metformin significantly reduced the level of serum hs-CRP (2.79±0.40 vs 3.96±0.63,P<0.05) and the expression of nucleus NF-κB p65 (P<0.01),and increased the expression of IκBα (P<0.05).CONCLUSION: Metformin inhibits the activation of NF-κB p65 and the degradation of IκBα,and decreases the levels of serum hs-CRP in AS rabbits.These results suggest that metformin exerts direct vascular anti-inflammatory effects.It may be one important mechanism of metformins antiatherogenic properties.  相似文献   

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AIM: To investigate the time course of nuclear factor-κB (NF-κB) and the effects of 3-aminobenzamide (3-AB) on the expressions of NF-κB, interleukin-1β (IL-1β) and cyclooxygenase-2 (COX-2) in hippocampus after seizures. METHODS: Epilepsy were induced by kainic acid through cerebral ventricular injection. Western blotting was used to detect NF-κB p65 expression in nucleus at various experiment groups. Moreover, mRNA and protein expressions of IL-1β and COX-2 in different experiment groups were determined by RT-PCR and Western blotting analysis. RESULTS: NF-κB p65 immunoreactivity began to increase in the nuclear fraction at 2 h (P<0.05), kept rising at 12 h (P<0.05) and returned to control level at 24 h after epilepsy seizures. Furthermore, 3-AB sharply decreased the accumulation of NF-κB p65 in nucleus (P<0.05). In addition, 3-AB significantly decreased the mRNA and protein expressions of IL-1β and COX-2 which obviously increased in hippocampus at 6 h after epilepsy seizures (P<0.05). CONCLUSION: Seizures triggers NF-κB nucleus translocation and promotes the expressions of IL-1β and COX-2 in hippocampus. In addition, poly (adenosine diphosphate-ribose) polymerase inhibition by 3-AB suppresses NF-κB associated inflammatory pathway in epileptic rat hippocampus.  相似文献   

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AIM: To investigate the effect of ischemic postconditioning (I-postC) on the expression of nuclear factor-κB (NF-κB) and intercellular adhesion molecule-1 (ICAM-1) in the lungs following intestinal ischemia reperfusion(II/R) in rats, and to explore the possible mechanism of I-postC in attenuating lung injury induced by II/R. METHODS: Thirty-two male Wistar rats were randomly divided into sham, II/R, intestinal ischemic postconditioning (II-postC) and limb ischemic postconditioning (LI-postC) groups. The model of intestinal I/R injury was established by clamping the super mesenteric artery for 45 min followed by 120 min of reperfusion in rats. At the end of the experiment, the changes of arterial blood gas and lung index were measured, and the morphological changes of the lung tissues were observed under light microscope. The content of malondialdehyde (MDA), the activities of superoxide dismutase (SOD) and myeloperoxidase (MPO) in the lung tissues were also detected. The contents of NF-κB p65 and ICAM-1 in lung tissue were determined by immunohistochemical staining and Western blotting. RESULTS: (1) Compared to those in II/R group, II-postC and LI-postC improved the respiratory functions of the lung, characterized by the increase in PaO2 and decrease in PaCO2 (P<0.05 vs II/R group). The lung index was decreased (P<0.01) and the pathologic lesion of the lung tissues was alleviated significantly by II-postC and LI-postC. (2) Both II-postC and LI-postC markedly inhibited the decrease in SOD activity, the increase in the content of MDA and the activity of MPO in the lung tissues (P<0.05 or P<0.01) induced by intestinal I/R. In addition, the over-expression of NF-κB p65 and ICAM-1 in the lung tissues was inhibited markedly by II-postC and LI-postC (P<0.05 or P<0.01 vs II/R group). CONCLUSION: I-postC attenuates lung injury induced by intestinal I/R in rats due to suppressing the activation of NF-κB and subsequent accumulation of neutrophils mediated by ICAM-1.  相似文献   

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