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1.
AIM:To study the effect of human complement C5b~9 complex on nitric oxide(NO) synthesis of glomerular mesangial cells (MC). METHODS: First, the human complement C5b~9 complexes were isolated and glomerular MC of rats were cultured. Second, the MC were stimulated with C5b~9 complex and changes of metabolism products of NO(NO3- and NO2) in MC culture supernatant at 6,24 and 48 hours after C+5b~9 stimulating were detected. Moreover, cGMP levels in cultured MC were also measured. RESULTS: NO3-／NO2- contents from culture supernatant and cGMP levels in MC were increased parallelly after C5b~9 complex stimulation. Further, NO synthesis was inhibited by L-NG-nitro-arginine-methylester(L-NAME). CONCLUSION: NO synthesis of rat glomerular MC was incerased by human complement C5b~9 stimulation.  相似文献   

2.
AIM: To explore the effect of antiserum against rat complement C5b-9 complexes on nitric oxide synthesis and pathologic changes in renal tissue of rats with mesangioproliferative glomerulonephritis. METHEDS: The rat model of mesangioproliferative glomerulonephritis,namely,anti-thymocyte serum nephritis(ATSN) was established and the rats with ATSN were treated with antiserum against complement C5b-9 complexes. Some parameters related to NO and pathologic changes of the rats were observed.RESULTS: Anti-C5b-9 serum not only reduced the expression of inducible NO synthase(iNOS) mRNA in renal tissue and urinary content of nitrate/nitrite(NO3-/ NO2-) of rats with ATSN, but also reduced renal pathologic changes. L-N G-nitro arginine methylester (L-NAME) also reduced the contents of urinary NO3-/NO2- and the renal pathologic changes of rats with ATSN. CONCLUSION: The antiserum against rat complement C5b-9 complexes inhibited glomerular NO synthesis and glomerular mesangial cell proliferation of rats with ATSN.  相似文献   

3.
AIM: To explore the localization and semi-quantification of the glomerular complement C5b-9 complexes and synthesis of some inflammatory mediators or cytokines such as nitric oxide (NO) and tumor necrosis factor α(TNFα) in the rats with anti-thymocyte serum nephritis(ATSN). METHODS: The animal model of rat ATSN was reproduced by a single intravenous injection of anti-thymocyte serum (ATS). Then, the deposits of glomerular C5b-9 complexes were localized and quantified by immunohistochemical staining and microscopic image scanning separately. And the glomerular mesangial cells (MC) surrounded by C5b-9 complexes were counted under microscope. In addition, the expression of glomerular MC inducible NO synthase(iNOS) mRNA and excretion of urinary NO metabolite (NO-2／NO-3) and TNF α in the rats with ATSN were detected. RESULTS: The MC in the rats with ATSN emerged necrosis followed by a rapid proliferation. In the early time of MC injury, the C5b-9 complexes were mainly seen in glomerular mesangium and MC surface. But with the progression of ATSN, the MC enclosed by C5b-9 appeared gradual decrease. Moreover, the expression of MC iNOS mRNA in early stage of ATSN obviously increased and the excretion of urinary NO-2／NO-3 and TNF α also significantly increased. However, the changes of parameters mentioned above in ATSN proliferative stage (after 7 days) alleviated gradually. CONCLUSION: The secondary lysis of MC has relation to the deposition of C5b-9 complexes and synthesis and release of NO and TNF α in rats with ATSN.  相似文献   

4.
AIM:To observe the changes of iNOS and eNOS in lung tissue and NO in bronchoalveolar lavage fluid (BALF) in smoking rats.METHODS:80 Wistar rats were divided into control, smoking group, L-NIL group and L-NAME group (rats were exposed to smoke and injected (i.p.) with selective iNOS inhibitor L-NIL or NOS inhibitor L-NAME). iNOS and eNOS protein levels in whole lung were detected by immunohistochemical staining, and NOS mRNA was quantified using RT-PCR. In addition, NO2-/NO3- was determined using Griess assay.RESULTS:The expression of iNOS mRNA and protein in smoking rats increased, the expression of eNOS mRNA and eNOS protein decreased, and the total cell count and the level of NO2-/NO3-in BALF increased(P＜0.05). In vivo, L-NIL reduced the total cell count and NO2-/NO3- in BALF (P＜0.05), while L-NAME had no effect on them.CONCLUSION:Cigarette smoke increased expression of iNOS mRNA and protein and decreased expression of eNOS mRNA and protein. The large amount of NO generated by iNOS may amplify inflammation in lung tissue.  相似文献   

5.
AIM:To study the protective effect of Ligustrazini(LGT) on gut barrier function after hemorrhagic shock-reperfusion. METHODS: Thirty white rabbits were divided randomly into 3 groups: control group (A),shock group (B) and LGT group (C). Malondialdehyde(MDA), tumor necrosis factor-α(TNFα), interleukin-1β(IL-1β) and nitric oxide products(NO2-/NO3-) contents were measured in intestinal mucosa at 3 hours following reperfusion,culture of bacteria in blood from rabbits of 3 groups was carried out,the intestinal mucosa was examined under optical and electron microscope. RESULTS: MDA, TNFα, IL-1β and NO2-/NO3- contents of intestinal mucosa remained unchanged in group C,but increased significantly in group B, compared with group A. Incidence of bacterial translocation in group B was markedly higher than that in group A at 30 min following reperfusion,there was not any difference between group A and group C. Under light and electronic microscope,in comparison with A and C groups,intestinal mucosa damage in B group became more severe. CONCLUSION: LGT can protect gut barrier from intestinal ischemia-reperfusion injury induced by hemorrhagic shock through reducing oxygen free radicals,raising nitric oxide and preventing inflammation.  相似文献   

6.
AIM: To study the relationship between the disturbance of nitric oxide/endothelin-1(NO/ET-1) and hepatic ischemia/reperfusion(I/R) injury as well as the regulation of NO/ET-1 system by hepatic ischemic preconditioning(IPC). METHODS: The changes of NO/ET-1 system and their relationship with hepatic I/R injury were compared between I/R group and IPC+I/R group in a rat hepatic I/R model. Two hours after reperfusion, the liver tissues were detected by RT-PCR to see whether there was inducible nitric oxide synthase (iNOS) mRNA expression. RESULTS:In the acute phase of hepatic reperfusion, the ratio of NO/ET-1 was reduced, which was due to a significant reduction of NO2-/NO3- (the metabolic product of NO) and significant elevation of ET-1 in the blood plasma. The content of ALT, AST, LDH and TNF-α in blood plasma, and of MDA in liver tissue were increased but ATP in liver tissue was reduced, the hepatic damage was deteriorated. The protection of the hepatic IPC was concerned with the elevation of the ratio of NO/ET-1 caused by the elevation of NO2-/NO3-, and reduction of ET-1 as well. There was no iNOS mRNA detected in the liver tissues.CONCLUSION: Hepatic I/R injury is related to the disturbance of NO/ET-1. The protection of the hepatic IPC in the acute phase might be conducted by its regulation of NO/ET-1 system. The cNOS rather than the iNOS generated the NO in this situation.  相似文献   

7.
AIM: To study the effect of G-protein-coupled receptor kinase 5 (GRK5) on the activation of astrocytes in the brain cortex of newborn Wistar rats. METHODS: GRK5 gene was silenced in the model of rat brain cortex astrocytes in vitro for 24 h. N-acetylcysteine (NAC), which is a known inhibitor of NF-κB, was added into the culture medium according to gene silencing for 24 h. The expression levels of GFAP and caspase-3 were detected by the method of immunofluorescence, and the mRNA levels of NF-κB, TNF-α, IL-1β and iNOS were determined by real-time PCR. Moreover, the activity of SOD and concentrations of TNF-α and NO were measured. RESULTS: GRK5 gene silencing increased the expression of NF-κB at mRNA and protein levels obviously (P<0.01), and the mRNA levels of IL-1β and iNOS increased synchronously (P<0.01). Furthermore, caspase-3-positive cells in GRK5 siRNA group were increased compared with control siRNA group (P<0.01). Treatment with NAC obviously reduced the activity of NF-κB and weakened the effects induced by GRK5 siRNA (P<0.05). CONCLUSION: GRK5 siRNA increases NF-κB activity and induces the activation of astrocytes.  相似文献   

8.
AIM: To study the up-regulation of inducible nitric oxide synthase (iNOS) in lung of pulmonary fibrosis and its relationship with fibrosis. METHODS: The changes of amount of iNOS positive stain cells and type Ⅰ?Ⅲ collagen were examined on the day 7, 14 and 30 after intratracheal administration of bleomycin A5. The contents of NO2-/NO3- (nitrite/nitrate) in out-flowing pulmonary blood (OPB), hydroxyproline in lung and the histological changes were detected after iNOS was blocked by aminoguanidine (AG). RESULTS: (1) The number of iNOS-positive stain cells increased significantly in BLMA5 7 d, 14 d and 30 d groups compared with that in control group (P<0.01). Furthermore, the increment of the number of iNOS-positive stain cells in BLMA5 7 d, 14 d groups was more than that in BLMA5 30 d group. There was an increment of collagen in BLMA5 14 d group and in BLMA5 30 d group , with an increase in type Ⅲ collagen in BLMA5 14 d group and an increase in type Ⅰcollagen in BLMA5 30 d group. (2) The high level of NO2-/NO3- in OPB and hydroxyproline level in lung could be reversed by AG, a selective inhibitor of iNOS. Large amount of fibroblasts and macrophages were also abated by AG. CONCLUSION: In the development of pulmonary fibrosis, the expression of iNOS is up-regulated, which induces nitric oxide (NO) production and promotes propagation of pulmonary fibrosis.  相似文献   

9.
AIM: To study the role of high level of endogenous nitric oxide (NO) in apoptosis of alveolar epithelial cells in the development of pulmonary fibrosis in rats. METHODS: The content of nitrite/nitrate (NO2-/NO3-) in out-flowing pulmonary blood (OPB) was assayed by nitric acid reduction method. The apoptosis of alveolar epithelial cells was observed by TdT-mediated dUTP nick-end labeling (TUNEL) and electron microscopy, respectively. The above indices were observed on the day 14 and the day 30 after intratracheal administration of BLMA5 alone or along with blockade of iNOS by aminoguanidine (AG) in rats. RESULTS: (1) Both the content of NO2-/NO3- in OPB and the number of apoptotic alveolar epithelial cells in lung were increased in BLMA5 14 d group, compared with normal control group and BLMA5 30 d group, respectively (P<0.05). The high level of NO2-/NO3- in OPB and the apoptosis of alveolar epithelial cells were ameliorated by AG. CONCLUSION: The apoptosis of alveolar epithelial cell is induced by high level of endogenous NO in the development of pulmonary fibrosis.  相似文献   

10.
AIM: To observe free radicals (MDA, NO) and iNOS of patients with severe acute respiratory syndrome (SARS) and to explore its significance. METHODS: MDA, NO2-/NO3- and iNOS were determined in SARS patients during the early, recovery and follow-up stage, front doctors and nurses (contact group) and health people (health control). RESULTS: The level of MDA during first stage was higher than that of recovery stage and the MDA level of recovery stage was higher than that of follow-up stage, contact group, and health control group (P<0.01). The content of NO2-/NO3- during early stage was higher than that of other groups, and the NO2-/NO3- contents of recovery stage, follow-up stage were higher than that of contact group and health control group (P<0.01), respectively. The mean of iNOS during early stage was highest than that of other stages (P<0.01) and the mean of recovery stage was higher than that of contact group (P<0.05), there were no difference in iNOS activity among any other groups (P>0.05). CONCLUSION: The pathological injury in pathogenesis of SARS is related to free radicals.  相似文献   

11.
AIM: To observe the effect of mesenteric lymph duct ligation on free radical and inflammatory mediator in serious hemorrhagic shock rats at different periods, and explore the mechanism of intestinal lymphatic pathway on renal insufficiency. METHODS: 78 male Wistar rats were divided into the sham group, shock group, and ligation group. The model of serious hemorrhagic shock was established in shock group, ligation group, and mesenteric lymph was blocked by ligating mesenteric lymph duct in ligation group after resuscitating. All rats were executed and kidneys were taken out for making homogenate of 10 percent to determine levels of MDA, SOD, NO, NOS, tumor necrosis factor-alpha (TNF-α), interleukin-6 (IL-6) and myeloperoxidase (MPO) at time points after shock 90 min, after transfusion and resuscitate 0 h, 1 h, 3 h, 6 h, 12 h and 24 h. The expression of inducible nitric oxide synthase (iNOS) mRNA in kindey was detected by RT-PCR. RESULTS: The contents of MDA, NO, NOS, TNF-α, IL-6, MPO and iNOS expressions in renal homogenate of shock group were increased after transfusion and resuscitation, and were higher at 6 h and 12 h, and was significantly higher than that in sham group. The acvitity of SOD was significantly lower than that in sham group (P<0.01, P<0.05). The contents of MDA, NO, NOS, TNF-α, IL-6, MPO and iNOS expression in renal homogenate of ligation group after transfusion and resuscitation 6 h, 12 h and 24 h were significantly lower than those in shock group at same points, and the SOD activity was higher (P<0.01, P<0.05). CONCLUSION: The results demonstrate that the ligation of mesenteric lymph duct can antagonise the development of renal failure in serious hemorrhagic shock rats, and its mechanism might relate to reduce the PMN sequestration, decrease the levels of TNF-α and IL-6, inhibit NO production and expression of iNOS mRNA, suppress the release of free radical and consumption of SOD.  相似文献   

12.
AIM:To observe the changes in nitric oxide(NO) and peroxynitrite anion (ONOO- ) in the injuried lung following the ischemia-reperfusion of hind limbs and evaluate the contribution of NO and ONOO- to tissue injury.METHODS:A model of hind limbs ischemia was made by clamping infrarenal aorta with a microvascular clip and lung injury occurring after reperfusion.Lung t issue was obtained from the animals received sham operation(group 1),4 hours ischemia without reperfusion(group2),1 hour reperfusion following 4 hours ischemia(group3)and 4 hours reperfusion fol owing 4 hours ischemia(group4).The contents of MDA,NO2-/NO3- and the activities of SOD in the lung were examined.Immunohistochemical echnique was used to determine the immunoreactivity to iNOS and nitrotyrosine(NT)-a specific "footprint" of peroxynitrite.RESULTS:Compared with group1 and group2,the contents of MDA and NO2-/NO3- increased significantly (P<0.05) and the activities of SOD decreased markedly(P＜0.05) in group3 and group4.Immunohistochemical examination demonstrated intense staining for iNOS and NT throughout the lung in group3 and group4.CONCLUSION:NO and ONOO- are involved in oxidant-mediated lung injury following reperfusion of ischemic hind limbs.  相似文献   

13.
AIM: To observe the kinetic alteration of nitric oxide formation in the lungs in the development of pulmonary fibrosis in the rat. METHODS: The contents of hydroxyproline in the lungs, NO2-/NO3- (nitrite/nitrate) in out-flowing and in-flowing pulmonary blood (OPB, IPB) were assayed on the day 7, 14, 21, 30 and 70 after intratracheal administration of bleomycin A5 . The content of NO2-/NO3- in supernatants of culture of the alveolar macrophages (AMs) and the amount of iNOS positive stain cells in lung tissue section were also observed in the rat on 14th day after-bleomycin A5 administration. RESULTS: The content of lung hydroxyproline had no change on the 7th day, increased on the 14th day (P＜0.05), increased significantly on the 21th day, 30th day and 70th day post-bleomycin A5 compared with control rats. On the 7th day and 14th day, the content of NO- 2 /NO3- increased in OPB and decreased in IPB (P＜0.01). On the 21th day, the content of NO2-/NO3- abated in OPB (P＞0.05) but still decreased in IPB (P＜0.01). On the 30th day and the 70th day, the NO2-/NO3- level recovered both in OPB and IPB. AMs from rats on the 14th day post-bleomycin A5 showed significant elevation (P＜0.01) in NO2-/NO3- level. The amount of iNOS positive stain cells increased in rats on the 14th day post-bleomycin A5. CONCLUSION: The amount of NO in the lungs was high in the initial phase of fibroproliferative reaction induced by bleomycin A5 ,and these might be associated with the enhanced ability of AMs to release NO and the increased amount of iNOS.  相似文献   

14.
AIM: To investigate the relationship between the level of interleukin-2 (IL-2), tumour necrosis factor-α (TNF-α) and nitric oxide (NO) in aqueous humor after intraocular lens implantation. METHODS: New Zealand rabbits were divided randomly into three groups: (1) control group; (2) extracapsular cataract extraction group (ECCE); (3) extracapsular cataract extraction and posterior chamber intraocular lens implantation group (ECCE+IOL). The inflammation in all experimental rabbit eyes was observed via zoom-photo slit-lamp microscope on 1, 3, 7, 14 d and 30 d postoperation. Meanwhile, aqueous humor was drawn for white blood cell (WBC) counting and classifying and for determining IL-2, TNF-α and NO2-/NO3- contents. RESULTS: (1) The level of IL-2 and TNF-α and NO2-/ NO3- in aqueous humor of ECCE+IOL group were higher than that in ECCE and control at 1 to 14 days postoperation, respectively, it increased to peak value at 3 to 7 days postoperation and decreased gradually two weeks postoperation; (2) The changes in IL-2, TNF-α and NO2-/NO3- in each group were basically similer; (3) The changes of IL-2 and TNF-α level were closely related with NO content in aqueous humor (r=0.69, P<0.01 and r=0.98, P<0.01). CONCLUSION: IL-2, TNF-α and NO play an important role in intraocular inflammation intraocular lens implantation.  相似文献   

15.
AIM: To investigate the changes in nNOS and iNOS expression of hippocampal CA3 pyramidal neurons and NO2-/NO3- level of hippocampal homogenate of rats induced by stress, and to explore the effect of phenytoin on them. METHODS: Rats were subjected to forced-swimming stress, phenytoin was administered(ip) at 30 min before stress. Using the immunohistochemistry and the computerized image technique, the expression levels of nNOS and iNOS of rat hippocampal CA3 pyramidal neurons were assayed quantitatively, and the NO2-/NO3- level of hippocampal homogenate was also measured using nitric acid deoxidize enzyme method. RESULTS: The nNOS average grey degree of hippocampal CA3 pyramidal neurons was significantly lower in stress group (155.42±3.77)than that in control group(164.54±4.62)and in stress plus phenytoin group(164.27±2.55)(P<0.01); The iNOS relative sectional area proportion of hippocampal CA3 pyramidal neuron was significantly larger in stress group(5.87%±2.90%) than that in control group (0.90％±0.89%) and in strers plus phenytoin groups (0.90%±0.88%)(P<0.01); The NO2-/NO3- level of hippocampal homogenate was significantly higher in stress group(42.75 umol/L±14.49 umol/L)than that in control group(21.23 umol/L±6.99 umol/L)and in stress plus phenytoin group(18.40 umol/L±8.11 umol/L)(P<0.01). CONCLUSION: It is suggested that the stress could induce nNOS and iNOS expression in CA3 pyramidal neurons and excessive production of NO in hippocampus of rats, which could be inhibited by phenytoin.  相似文献   

16.
AIM:To study the effect of fructose-1, 6-diphosphate (FDP) on adriamycin(ADM)-induced cardiomyocyte apoptosis in rats. METHODS:Twenty-four Wistar rats were randomly divided into three groups: control group, ADM treated group and FDP intervention group. The contents of malondialdehyde (MDA) and NO2-/NO3-, the activities of glutathione peroxidase (GPx) and superoxide dismutase (SOD) were determined by colorimetric method in myocardial tissue, and the cardiomyocyte apoptosis was detected by TUNEL method in myocardial tissue, and the expression of inducible nitric oxide synthase (iNOS) mRNA, Bcl-2 mRNA and Bax mRNA in myocardial tissue were detected by in situ hybridization. RESULTS:The contents of NO2-/NO3- and MDA in myocardial tissue, the expressive levels of iNOS mRNA and Bax mRNA in cardiomyocyes and its apoptotic amounts in FDP intervention group were significantly lower than those in ADM treated group (P＜0.01). However, the activities of SOD and GPx in myocardial tissue, the expressive level of Bcl-2 mRNA of cardiomyocytes in FDP intervention group were significantly higher than those in ADM treated group (P＜0.01). CONCLUSION:FDP antagonized the reduced expression of Bcl-2 mRNA and increased expression of Bax mRNA in myocardial tissue induced by ADM, and in turn inhibited ADM-induced cardiomyocyte apoptosis.  相似文献   

17.
AIM: To validate the anti-inflammatory effect of PYNOD on lipopolysaccharide (LPS)-stimulated BV2 microglial cells.METHODS: A specific GFP and PYNOD fluorescence expression vector pEGFP-C2-PYNOD driven by the promoter of CMV gene was constructed. The anti-inflammatory properties of PYNOD were studied using LPS-stimulated BV2 microglia model. The productions of nitric oxide (NO), inducible NO synthase (iNOS), interleukin-1β (IL-1β) which caspase-1 were evaluated as inflammatory parameters. RESULTS: Pretreatment with pEGFP-C2-PYNOD to BV2 microglia cells stimulated by LPS significantly inhibited the excessive productions of NO and IL-1β, which was associated with down-regulation of iNOS and caspase-1 at mRNA and protein levels. CONCLUSION: PYNOD might be useful for treating the inflammatory and deleterious effects of BV2 microglial cell activation in response to LPS stimulation.  相似文献   

18.
AIM:To investigate the effect of glycine on endotoxin and hypoxia-induced necrotizing exterocolitos (NEC) in rats. METHODS:In glycine+NEC group, twenty anesthetized and artificially ventilated rats received 1g/kg glycine (20%, iv). Five minutes later, the rats were treated with 2 mg/kg lipopolysaccharide (LPS). In control group (NS+NEC), twenty rats were treated with normal saline as a substitute for glycine. In all animals, FiO2 was reduced after 90 min from 21% to 5% and ventilation continued until 180 min or death. At the end of the experiment, the samples of blood and intestine were obtained immediately. Serum TNFα was measured with ELISA, serum NO was determined by nitrate reductase. The histopathology of the necrotic lesions were categoried: grade Ⅰ, focal mild injury confined to villous tips; grade Ⅱ, partial loss of villi; grade Ⅲ, necrosis extending to submucosa; grade Ⅳ, transmural necrosis. RESULTS:The survival time was shorter in the NS+NEC group (P＜0.01). The intestinal injury of the rats in glycine+NEC group was markedly alleviated (P＜0.01). The levels of TNF-α and NO2-/NO3- in serum decreased significantly in animals treated with glycine (P＜0.01, P＜0.05). CONCLUSION:Glycine alleviated LPS-induced NEC by inhibiting excessive production of TNFα and nitric oxide.  相似文献   

19.
AIM: To investigate the effect of NOD8 on lipopolysaccharide (LPS)-induced releases of nitric oxide (NO), tumor necrosis factor α (TNF-α) and interleukin-1β (IL-1β) in RAW264.7 cells. METHODS: The plasmids of pEGFP-C2 and pEGFP-NOD8 were transfected into RAW264.7 cells respectively. The transfected and non-transfected cells were stimulated by LPS for 0, 6, 12 and 24 h. NO production was evaluated by Griess reagent assay, and the levels of IL-1β and TNF-α were measured by ELISA. The protein expression of NOD8 and the nuclear translocation of nuclear factor κB (NF-κB) p65 subunit were detected by Western blotting. The level of activated caspase-1 was determined by fluorimetric method. RESULTS: Compared with pEGFP-C2 group, the protein expression of NOD8 was significantly elevated in pEGFP-NOD8+LPS group. The releases of NO, IL-1β and TNF-α were obviously increased after RAW264.7 cells were treated with LPS for 6 h, 12 h and 24 h, and while the secretion of NO was significantly reduced in the cells transfected with pEGFP-NOD8 and induced by LPS for 12 h and 24 h, and the release of IL-1β was also significantly reduced at 6 h, 12 h and 24 h. However, no significant difference of TNF-α release was observed between pEGFP-C2+LPS group and pEGFP-NOD8+LPS group. The activation of caspase-1 in RAW264.7 cells stimulated with LPS for 6 h, 12 h and 24 h was markedly increased, and the expression of NF-κB p65 subunit in the cytoplasm was significantly decreased, indicating that p65 nuclear translocation was increased. In addition, the activation of caspase-1 and the nuclear translocation of p65 were significantly inhibited in pEGFP-NOD8+LPS group. CONCLUSION: NOD8 suppresses the releases of LPS-induced NO and IL-1β in RAW264.7 cells by inhibiting the activation of caspase-1 and NF-κB.  相似文献   

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