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81.
AIM:To study the role of endothelin-1 (ET-1) in portal hypertension (PHT) induced by endotoxin. METHODS:Collagenase in situ perfusion was adopted to separate hepatic stellate cells (HSCs). HSCs was cultured on concretized collagen. ET-1 anti-sense oligonucleotide was added into the culture medium and then LPS was also added up to the concentration of 1 000 μg/L. The diameters of the concretized collagen were measured. Sense and mis-sense oligonucleotide were applied as control. ET-1 in the culture medium was detected by radioimmunoassay and ET-1 mRNA in HSCs was detected by RT-PCR. β-actin of HSCs was detected by Western blotting. RESULTS:The diameter of concretized collagen on which HSCs pretreated with ET-1 anti-sense oligonucleotide was 93.3%±3.8% the size of the primary. The diameter of concretized collagen of the control groups were 70.1%±4.8% and 70.5%±3.9% (P<0.05). ET-1 was (49.8±7.4)ng/L in the culture medium of HSCs pretreated with ET-1 anti-sense oligonucleotide and (329.8±34.9), (339.1±43.7)ng/L in the control medium (P<0.05). β-actin and ETI mRNA presented in HSCs pretreated with ET-1 anti-sense oligonucleotide was much less than that in the controls. CONCLUSION:ET-1 anti-sense oligonucleotide inactivated HSCs by counteracting the expression of ET-1, which may be helpful to control PHT induced by LPS. 相似文献
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AIM: To investigate the changes and significance of hydrogen sulfide (H2S) in both plasma and various tissues, including liver, kidney, heart, lung and arteriae aorta, in rats with LPS-induced shock. METHODS: A rat model of shock induced by injection of lipopolysaccharide (LPS) was developed. Male Wistar rats were divided into four groups: control group, LPS group, LPS+NaHS (H2S donor) group and LPS+ propargylglycine (PPG, metabolic enzyme inhibitor of H2S) group. The mean arterial pressure (MAP) of rats within 240 min was observed，and H2S contents were determined. The structures of various tissues were observed. RESULTS: Administration of LPS to male Wistar rats caused a sustained fall in MAP, various tissue injuries and a significant increase in H2S contents in plasma as well as liver, kidney, heart, lung and arteriae aorta within 240 min（all P<0.05）. Treatment with metabolic enzyme inhibitor of H2S, propargylglycine, was shown to reduce H2S content elevation in plasma as well as liver, kidney, heart, lung, and arteriae aorta, and ameliorate the hypotension and tissue injuries caused by LPS（all P<0.05）. However, treatment with H2S donor-NaHS was shown to increase H2S content elevation in plasma as well as liver, kidney, heart, lung and arteriae aorta, and aggravate the hypotension and tissue injuries caused by LPS（all P<0.05）. Endogenous H2S contents in both plasma and various tissues were negatively correlated with MAP（all P<0.05）.CONCLUSION: H2S may be a new endogenous mediator and play a role in the pathogenesis of endotoxic shock. 相似文献
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AIM:To investigate the effect of LPS on phagocytosis of Kupffer cells in vitro. METHODS:Isolated Kupffer cells were treated with LPS in vitro. The phagocytosis, microfilament, microtubules and apoptosis of Kupffer cells were determined by the beads phagocytosis test, fluorescence staining, fluorometry and flow cytometric analysis.RESULTS:LPS enhances the phagocytosis, actin content, microtubules fluorescence density of Kupffer cells in vitro, while at a large dose or for a long time, it lessened the phagocytosis increasing or phagocytosis, inhibites the microfilament and microtubules expression, and induced apoptosis.CONCLUSION:LPS enhances the phagocytosis of Kupffer cells in vitro, but in large amount, it inhibites the phagocytosis of Kupffer cells, which is probably related to LPS -induced microfilament, microtubules expression changes and apoptosis in Kupffer cells. 相似文献
85.
AIM: To investigate the roles of Notch signaling in lipopolysaccharide (LPS)-induced proliferation and secretion of interleukin-6 (IL-6) and chemokine CXCL1 in bone marrow mesenchymal stem cells (BMSCs).METHODS: BMSCs were isolated by whole bone marrow culture. The expression levels of Notch signaling pathway receptors and ligands in the BMSCs treated with LPS were measured by qPCR and Western blot. The proliferation of BMSCs was analyzed by MTT assay and viable cell counting. The secretion levels of IL-6 and CXCL1 induced by LPS were measured by ELISA.RESULTS: Treatment with LPS at 1 mg/L effectively induced the proliferation of BMSCs and the secretion of IL-6. Obvious expression of Notch receptors and ligands in the BMSCs was observed, and LPS had little effect on the mRNA and protein levels of Notch receptors and ligands, but LPS increased the protein levels of Hes1 and Hey1, the target genes of Notch signaling. LPS at 1 mg/L increased the proliferation of BMSCs, whereas DAPT (Notch signal inhibitor) reduced the basal and LPS-induced proliferation of BMSCs (P<0.01). LPS treatment robustly increased the secretion of IL-6 and CXCL1 as assessed by ELISA. However, inhibition of Notch signaling almost completely abolished LPS-induced secretion of IL-6 and CXCL1 (P<0.05).CONCLUSION: Inhibition of Notch signaling reduced not only the proliferation of BMSCs but also IL-6 and CXCL1 secretion induced by LPS. 相似文献
86.
AIM: To investigate the protective effect of mucin 2 (MUC2) on intestinal mucosa of colitis model mice, and to explore the correlation between the expression of anti-CBir1 flagellin antibody and MUC2. METHODS: The mice were randomly divided into normal control group, 2,4,6-trinitrobenzenesulfonic acid (TNBS) group, lipopolysaccharide (LPS)+ovalalbumin (OVA)+TNBS group and ketotifen+TNBS group. The expression of MUC2 in colon tissue was determined by PAS staining and immunohistochemistry, and the anti-CBir1 antibody level in the serum of mice in each group was measured by ELISA. RESULTS: The scores of disease activity index and histological index in TNBS group were higher than those in normal control group (P<0.05). The scores in LPS+OVA+TNBS group were much higher than those in TNBS group (P<0.05). However, the values in ketotifen+TNBS group were lower than those in TNBS group (P<0.05). PAS staining showed a decrease in goblet cells in TNBS group. Compared with TNBS group, the colonic mucosa integrity in LPS+OVA+TNBS group was destroyed, and the number of goblet cells in ketotifen+TNBS group increased significantly. Immunohistochemical staining showed that the expression of MUC2 in the intestinal tract of each mo-del group was basically consistent with the results of PAS staining. The serum anti-CBir1 antibody level in TNBS group was higher than that in normal control group (P<0.05), and that in LPS+OVA+TNBS group was significantly higher than that in TNBS group (P<0.05), whereas that in ketotifen+TNBS group was decreased slightly (P<0.05). CONCLUSION: MUC2 plays a protective role in the pathogenesis of colitis in mice, and there is a negative correlation between the expression of MUC2 and the bacterial flagellin in the intestinal mucosa of mice with colitis. 相似文献
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AIM: To observe the changes of endogenous hydrogen sulfide/cystathionine-γ-lyase (H2S/CSE) system while acute lung injury induced by LPS in rats. METHODS: Eighty rats were randomly divided into six groups (n=8): Ⅰ, control group;Ⅱ, LPS 1 h group; Ⅲ, LPS 3 h group; Ⅳ, LPS 6 h group; Ⅴ, LPS 9 h group; Ⅵ, LPS 12 h group. The ALI model of rats was prepared with LPS. The rats were respectively killed at 1, 3, 6, 9 or 12 h after administration of LPS. The morphological changes of lung tissues were observed by light and electron microscope. The lung coefficient and the wet-to-dry weight ratio were measured. The contents of IL-1β and IL-10 in serum, the H2S level in plasma and the CSE activity in lung tissue were respectively detected. RESULTS: ⑴ In LPS 1 h group, the morphology, the lung coefficient, the wet-to-dry weight ratio, the H2S level and the CSE activity showed no changes compared with the control group. The contents of IL-1β and IL-10 were increased compared with the control group (IL-1β, P<0.05;IL-10, P<0.01). ⑵ In LPS 3 h, 6 h, 9 h and 12 h groups, compared with the control group, the lung tissues were significantly damaged, the lung coefficient and the wet-to-dry weight ratio were significantly increased respectively (LPS 3 h, P<0.05; LPS 6 h, 9 h, 12 h, P<0.01). The contents of IL-1β and IL-10 in serum were markedly increased (P<0.01). The H2S level in plasma and the CSE activity in lung tissue were significantly decreased (P<0.01).CONCLUSION: The changes of inflammatory cytokines may be the pathological foundation of the ALI induced by LPS and the endogenous hydrogen sulfide/cystathionine-γ-lyase system is possibly involved in the formation of the ALI. 相似文献
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CHEN Chu-tian LU Da-xiang QI Ren-bin WANG Hua-dong FU Yong-mei WANG Yan-ping 《园艺学报》2008,24(5):843-848
AIM: To investigate the effects of lipopolysaccharide, hypoxia/reoxygenation,isoproterenol and high concentration of glucose on glycine receptor α1 subunit mRNA expression in the neonatal rat cardiomyocytes. METHODS: Isolation of cardiomyocytes from Sprague-Dawley rats aging 1～3 d were performed. Cardiomyocytes （1×105～5×105 cells·L-1）were cultured in DMEM medium containing 15% fetal bovine serum at 37 ℃ in 5%CO2 atmosphere for 72 h. Then, cultured rat cardiomyocytes were treated with lipopolysaccharide, isoproterenol or high concentration of glucose for 24 h, respectively, or were exposed to hypoxia for 3 h followed by reoxygenation for 3 h. Subsequently, the cell survival rate was measured using CCK-8 reactant and RT-PCR was applied to monitor the expression of glycine receptor α1 subunit mRNA. RESULTS: Compared with the control group, no significant difference in the cell survival rate was observed （P＞0.05）. The expression of glycine receptor α1 subunit mRNA was increased （P＜0.01） in lipopolysaccharide（5,10,20,40,80 mg/L）,isoproterenol（20,100,500 μmol/L） or hypoxia/reoxygenation, hypoxia groups, but decreased（P＜0.01）in the group treated with high concentration of glucose（25, 50 mmol/L）. CONCLUSION: Lipopolysaccharide, isoproterenol, hypoxia/reoxygenation or hypoxia upregulates the expression of glycine receptor α1 subunit mRNA,but high concentration of glucose down-regulates the expression of glycine receptor α1 subunit mRNA in cultured neonatal rat cardiomyocytes. 相似文献
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AIM: To investigate the effects of nitric oxide (NO) and NO synthase (NOS) inhibitor NG-nitro-L arginine (L-NA) on LPS induced-lung injury in rats. METHODS: Forty healthy male SD rats, weighing 300±20 g, were used. The animals were anesthetized with 20% urethane 1 g·kg-1. Common carotid artery (CAA) and jugular vein were exposed through a median incision in the neck. Mean arterial pressure (MAP) was measured through a pressure transducer connected with intubation of CAA. The animals were randomly divided into five groups: group 1: control; group 2: LPS (5 mg·kg-1, iv); group 3: high dose L-NA (20 mg·kg-1 intraperitoneal injection, ip); gropu 4: middle dose L-NA (10 mg·kg-1, ip); group 5: low dose L-NA (5 mg·kg-1, ip). Group1 : 0.9% saline solution was given and the animals were killed 6 h after the saline solution. Gruop 2: saline solution was given 3 h after LPS and the animals were killed 3 h after administration. Group 3, 4 and 5: L-NA was given 3 h after LPS iv and the animals were killed 3 h after administration, respectively. The pulmonary was removed immediately. The pulmonary coefficient and water content in pulmonary tissue were calculated (%). The NO2-/NO3- content in plasma, MDA content and NOS, SOD activity in the pulmonary tissue were measured. RESULTS: L-NA significantly decreased pulmonary coefficient and water content in pulmonary tissue and ameliorated LPS induced lung injury. The effect in high dose group was better than that in low dose group. L-NA significantly decreased NO2-/NO3- content in plasm, decreased MDA content and inhibited NOS activity and enhanced SOD activity in the pulmonary tissue. CONCLUSION: It may be concluded that L-NA has a beneficial effect on lung injury induced by LPS. 相似文献