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1.
AIM: To study the pathological change in mouse organs immunitied by inactivated SARS-CoV vaccine. METHODS: Inactivated SARS-CoV vaccine was injected into BALB/c and C57BL/6 mice. Anti-SARS antibody was analyzed by ELISA. After 8 weeks, the immunitied mice were killed and those organs were analyzed by pathological methods. RESULTS: Anti-SARS antibody in mice was positive after 8 days. Only minimal injury was observed in a few lungs and livers, but the other organs were not. CONCLUSIONS: Inactivated SARS-CoV vaccine induced mice to create antibody, whereas they did not cause severe injury. This result will be valuable for vaccine into clinical research.  相似文献   

2.
AIM: To investigate the toxicity and reproductive effect of vascular endothelial growth factor (VEGF)/basic fibroblast growth factor (bFGF) complex peptide vaccine (VBP3) on the female-mice. METHODS: The VBP3 was purified with Ni-NTA affinity chromatography. The female BALB/c mice were immunized with the purified VBP3. The antibody titer in the serum was detected by ELISA. The data of the body weight and the organ weight of the parent mice were gathered and analyzed, and the pathological changes of the organs were observed with HE staining to investigate the toxicity of VBP3. To investigate the toxicity of VBP3 in the F1 mice, the parent immunized female mice were mated with the parent non-immunized male mice. After the F1 mice were born, the survival rate was calculated, the change of the body weight and the organ weight of the F1 mice were also determined. The pathological changes of the organs in F1 mice were also observed with HE staining. RESULTS: In the parent mice, high titers of the antibodies were detected against VEGF and bFGF, and no difference of the body weight, the organ weight and the pathological change between the immunized mice and control mice was found. In the F1 mice, a low titer of anti-bFGF antibody was detected compared with blank group. The survival rate in control group was higher than that in immunized group. In the 2 groups of the F1 mice, no obvious difference of the weight of the spleen, kidney, lung and heart was observed, and there was some difference in the weight of liver between the 2 groups. The results of the HE staining in the F1 mice showed some difference in the liver between the 2 groups. CONCLUSION: VEGF/bFGF complex peptide vaccine has no obvious organ toxicity in the parent female mice, but has some side effects on the reproductive and the healthy processes of F1 mice.  相似文献   

3.
AIM: To investigate the effects of sphingosine-1-phosphate receptor 2 (S1PR2) on influenza A virus-induced viral pneumonia.METHODS: The animal model of influenza A virus pneumonia was established by infecting wild-type C57BL/6 mice and S1pr2-/- mice with influenza virus subtype FM1 mouse lung adaptable strain through nose drops. The pathological changes of the lung tissues of wild-type mice (model group), JTE-013 (S1PR2 effective antagonist)-challenged mice and S1pr2-/- mice were observed, and the protein concentration, total cell number, and interleukin (IL)-1β, IL-6 and tumor necrosis factor-α (TNF-α) levels were determined in the bronchoalveolar lavage fluid (BALF) at 4 d and 6 d after virus infection. The phosphorylation levels of AKT and eNOS in the lung tissues were determined by Western blot. RESULTS: Compared with the wild-type mice of control group, the influenza A virus pneumonia in JTE treatment group and S1pr2-/- mice were more serious, and the protein concentration, total cell number and inflammatory cytokines in the BALF were remarkably increased. Moreover, the phosphorylation levels of AKT and eNOS, the downstream targets of PI3K, were significantly increased (P<0.01). CONCLUSION: S1PR2 mediates PI3K/AKT/eNOS signaling transduction pathway to regulate NO generation, and inhibit vascular permeability and inflammatory cytokine release, thus attenuating the viral pneumonia induced by influenza A virus.  相似文献   

4.
AIM: To observe the effects of carvedilol on murine viral myocarditis model. METHODS: A total of 188 inbred male BALB/c mice of 4-6 weeks were divided into 4 groups: myocarditis group (group C, n=60), metoprolol treatment group (group M, n=60), carvedilol treatment group (group K, n=60), control group (group B, n=8). Myocardial histopathololgic changes were observed. The concentrations of cardiac troponin I (cTn-I) were detected by chemiluminescence immunoassay (CLIA). Western blotting was performed to analyze the contents of phosphorylated p38MAPK in myocardium. RESULTS: Metropolol and carvedilol lightened myocardial histopathololgic changes at acute stage, decreased cTn-I concentrations and myocardial phosphorylated p38MAPK value compared with myocarditis group. Treatment with carvedilol was more effective than treated with metropolol on those indexes. CONCLUSION: Carvedilol protects against viral myocarditis by inhibition of p38MAPK signal transduction pathway through blockade of β1 and β2 adrenergic receptors.  相似文献   

5.
AIM: To Investigate the kinetics of pathologic changes in bleomycin-induced pulmonary fibrosis in rats. METHODS: Sixty male SD rats were randomized as a negative control group and pulmonary fibrosis model groups (B3, B7, B14, B28, B56 sub-groups). Except for control group, rats in the other groups were intratracheally administered with bleomycin. Animals in pulmonary fibrosis model groups were sacrificed on day 3, 7, 14, 28 and 56. The sections of the right lung were stained by HE, Masson and sirius red. The left lung was weighed and its hydroxyproline content was assayed. The mRNAs of TGF-β1, MMP-9 and TIMP-1 in the lung homogenate were measured by semi-quantitative RT-PCR. The expressions of TGF-β1, MMP-9 and TIMP-1 in lungs were observed by immunohistochemistry. RESULTS: (1) The content of lung hydroxyproline in pulmonary fibrosis model groups was significantly increased than that in control group (P<0.05). The pulmonary inflammation in pulmonary fibrosis model groups was significantly serious than that in control group, pulmonary fibrosis in B14, B28 and B56 groups was also significantly serious than that in control group. (2) A small quantity of TGF-β1, MMP-9 and TIMP-1mRNA were measured in normal lung, and the expression increased significantly after administration of bleomycin. Different expressions of TGF-β1, MMP-9 and TIMP-1 in different days after bleomycin administration were observed. CONCLUSION: The pathological changes in different days after bleomycin administration are different. TGF-β1, MMP-9 and TIMP-1 may play important roles in the pathogenesis of pulmonary fibrotic process.  相似文献   

6.
AIM: To study the effects of exogenous bone mesenchymal stem cell (BMSC) transplantation on silicosis fibrosis in rats, and to explore the dose-effect relationship. METHODS: BMSCs were isolated and cultured from male 5-week-old SD rats in vitro. Fifty healthy female SD rats were randomly divided into 5 groups: control group, silicosis model group, BMSCs treatment A group (1×109 cells/L), BMSCs treatment B group (3×109 cells/L) and BMSCs treatment C group (5×109 cells/L). The silicosis model was made by one-time infusion of silica dust suspension using the non-exposed tracheal intubation, and different doses of BMSCs were given for intervention therapy. All the rats were sacrificed on the 21st day after the model was established. The morphological changes of the lung tissues were observed by HE staining and Masson staining. The localization and distribution of tumor necrosis factor α (TNF-α) and transforming growth factor β (TGF-β) were determined by the method of immunohistochemistry. The protein levels of TNF-α, TGF-β, collagen type I and collagen type III were detected by Western blotting. The sex-determining region (SRY) protein was searched by an immunofluorescence method to confirm the homing of BMSCs. RESULTS: Compared with control group, the silicosis model group had significant alveolitis changes, silicon nodule formation, collagen deposition and other pathological characteristics. Compared with silicosis model group, the pathological changes in BMSCs treatment A group were improved. The conditions of BMSCs treatment B group were also improved significantly. However,the pathological changes in BMSCs treatment C group were increased obviously. The protein levels of TNF-α, TGF-β, collagen type I and collagen type III in the lung tissues ranked as follows: BMSCs treatment C group > silicosis model group > BMSCs treatment A group > BMSCs treatment B group > control group. The difference between BMSCs treatment C group and silicosis model group was not statistically significant, and the differences between the other groups were statistically significant. The SRY-positive cells were observed in BMSCs treatment B group, but no significant expression in the heart, liver, spleen and kidney tissues was observed. CONCLUSION: The exogenous BMSC transplantation antagonizes the development of silicosis fibrosis in rats, which has dose-effect relationship.  相似文献   

7.
AIM: To study the possible immunologic mechanism of mesenchymal stem cells (MSCs) by which the hematopoiesis of mice with aplastic anemia (AA) is improved. METHODS: The mice model of immuno-mediated aplastic anemia was established. Thirty BALB/c mice were divided into 3 groups: radiation group, AA model group and MSCs group. The mice in radiation group only had processing of 5 Gy ［60Co］γ radiation. The mice in AA model group were intravenously injected with the cell suspension of thymocyte and lymph-node cell mixture (prepared from DBA/2 mice, 1×106 cells) after 5 Gy ［60Co］γ radiation. The animals in MSCs group received the same treatment as the mice in AA model group did, and afterwards was injected with 1×106 MSCs intravenously at 3 days. All the mice in the 3 groups were observed and analyzed the following parameters: peripheral blood cells, pathological features of bone marrow, the relation between the changes of peripheral CD4+, CD8+, CD4+/CD8+, NK cells and the hematopoiesis. RESULTS: After 5 Gy ［60Co］γ radiation, the peripheral blood cells in all groups decreased at 7 days, while at 21 days those in MSCs group and radiation group restored to normal but those in AA model group was still at lower level. At 7 days, the cells of CD4+, CD8+ and CD4+/CD8+ in each group were similar without statistical difference, but the number of NK cells in MSCs group was quite lower than that in the other 2 groups (P<0.05). At 14 days, the CD4+ cells in all groups were obviously decreased, while the CD8+ cells in MSCs group and AA model group were significantly higher than those in radiation group. At 21 days, the CD8+ and NK cells in MSCs group were quite the same as those in radiation group while those in AA model group were obviously higher compared to the other 2 groups. The number of adipose cells observed in the pathological slice of femoral bone in MSCs group and radiation group was no difference while that in AA model group was much higher. CONCLUSION: MSCs transfusion improves the hematopoiesis in mice with aplastic anemia by regulating the functions of immune cells.  相似文献   

8.
A perusal of literature showed that a little is known about the metabolic changes related to senescence in orchid flowers. It was observed that unpollinated flowers of Cymbidium pendulum (Roxb.) Sw. remained fresh for 20 days and senesced within 8 days after pollination (DAP), while that of Cymbidium aloifolium (L.) Sw. took 18 days when unpollinated but showed senescence in 7 DAP. A higher level of electrolyte leakage was recorded in all the floral organs of pollinated flowers in both the species. There was a concomitant increase in levels of malondialdehyde (MDA) and hydrogen peroxide (H2O2); indicators of oxidative damage, in all the organs for both the species. Ascorbic acid, on the other hand, decreased significantly. Higher amount of electrolyte leakage, MDA and H2O2 content were recorded in C. pendulum as compared of the other species while the ascorbic acid, on the other hand, was observed to be decreased and this decrease was more in C. pendulum than C. aloifolium suggesting a higher oxidative damage to the floral organs in the former species than the latter. TIBA, i.e. tri-iodobenzoic acid (an auxin inhibitor; 0.25 μM) and silver nitrate (ethylene inhibitor; 0.25 μM) application to pollinated flowers partially prevented the elevation of oxidative damage and consequently senescence suggesting the involvement of these hormones in governing these changes in orchid flowers. Comparatively, AgNO3 was more effective than TIBA in delaying senescence.  相似文献   

9.
AIM: To explore the effects of Auricularia (A.) auricula-judae extracts on the liver function in septic rats. METHODS: Forty male Wistar rats were randomly divided into control group, model group, A. auricula-judae polysaccharide group and A. auricula-judae crude extract group. Septic model was induced by the procedure of cecal ligation and puncture (CLP). Intragastric administration was performed every 8 h 3 days prior to CLP. The plasma levels of alanine aminotransferase(ALT), aspartate aminotransferase(AST), endotoxin(ET), tumor necrosis factor α(TNF-α), interleukin 6(IL-6) and IL-1β were detected 12 h after CLP. The specimens of the liver were collected to observe the pathological changes. The expression of NF-κB in the liver tissues was detected by the method of immunohistochemistry. RESULTS: Compared with the CLP rats, the intervention of A. auricula-judae polysaccharide and A. auricula-judae crude extract to the septic rats significantly decreased the serum levels of ALT, AST, ET, TNF-α, IL-1β and IL-6 (P<005). The pathological changes of the liver tissues in treatment groups were significantly attenuated compared with CLP group. CONCLUSION: A. auricula-judae polysaccharide and A. auricula-judae crude extract protect liver against sepsis-induced injury by inhibiting the systemic inflammatory response.  相似文献   

10.
AIM: To observe the mRNA expression of urotensin II (UII) and its receptor (G protein-coupled receptor 14,GPR14) in nephridial tissues of rats with acute renal damage. METHODS: Male Wistar rats were divided into 2 groups: the rats in control group (n=10) were administered with normal saline by gavage; the rats in model group (n=30) were administered with Caulis Aristolochiae manshuriensis (CAM) by gavage for 25 d to induce acute renal damage. Every 5 rats in model group were sacrificed on the 3rd, 7th, 15th and 25th days during CAM treatment and all rats in the 2 groups were killed 10 d after withdraw of CAM. The kidneys were collected for pathological observation and the UII and GPR14 mRNA examination.RESULTS: The degeneration, necrosis and disintegration in tubules were observed as major pathological changes in the rat kidneys after 3 d of CAM administration. The pathological changes were aggravated following the duration of in CAM administration, and were remained and even worsen when CAM was withdrawn for 10 d. Compared with control group, the mRNA expression of UII was significantly elevated (P<0.05) at the time point of CAM administration for 15 d,even obviously increased (P<0.01) at the time point of CAM administration for 25 d, and remained at the highest levels to the end of the observation. The mRNA expression of GPR14 was significantly increased (P<0.05) at the time point of CAM administration for 7 d, became higher (P<0.01) on the 15th day, and gradually increased as the experimental time went on. CONCLUSION: The mRNA levels of UII and its receptor are significantly elevated in CAM-induced renal lesion in rats, suggesting that UII plays a pathological role in the development of acute renal damage.  相似文献   

11.
AIM: To investigate the efficacy of microwave ablation (MWA)-coagulated mouse hepatoma tissue in inducing antitumor immune response.METHODS: A model of MWA for s.c. hepatoma in C57L/J mice was established, the anti-tumor effect of MWA-treated mice against Hepa1-6 cells rechallenge and the cytotoxicity of spleen lymphocytes by use of crystal-violet analysis were observed. Mice were immunized with MWA vaccine consisting of MWA-coagulated hepatoma tissue mince, granulocyte-macrophage-colony stimulating factor (GM-CSF) and interleukin-2 (IL-2) slow-release microparticles, the protective anti-tumor immunity induced by MWA vaccine was evaluated.RESULTS: After s.c. challenge of Hepa1-6 cells, hepatoma were observed in 100% mice of control group and 17％ of MWA-treated mice. The tumor volumes of tumor-bearing MWA-treated mice were significantly smaller than those in control group, while MWA-treated mice survived longer than control mice. Spleen lymphocytes deprived from tumor-free MWA-treated mice were specific cytotoxic to Hepa1-6 cells. MWA vaccine protected 50% more mice than that using MWA-coagulated tumor tissue alone, and showed similar anti-tumor effect against hepatoma to formalin-fixed tumor vaccine.CONCLUSION: In situ MWA provides effective tumor antigen for induction of tumor-specific antitumor immune response, and the response is amplified by additional use of cytokines.  相似文献   

12.
AIM: To study the characterization of thyrotropin receptor (TSHR) and its active fragment TSHR aa352-366 as immunogens in BALB/c mice. METHODS: BALB/c mice were injected peritoneally with TSHR aa352-366-KLH (hemocyanin from keyhole limpets) and the mixture of TSHR aa352-366-KLH and guinea pig TSHR every 15 days, respectively. The levels of thyroid hormones and TSHR antibodies and TSHR mRNA were measured, and the pathological changes of thyroid tissue were observed. RESULTS: In the group injected with TSHR aa352-366-KLH, the serum levels of TT3 and TT4 decreased (P<0.01) and levels of TRAb increased (P<0.01), compared with the data in same group on day 0. The thyroid follicles showed some pathological changes like that of hypothyroidism. In the mixture group, the serum levels of TT3 and TT4 decreased (P<0.01) and levels of TRAb (P<0.01), TBAb (P<0.05) and TSAb (P<0.05) increased. The levels of TSHR mRNA went up and herterogeneous pathological changes were observed. CONCLUSION: Both gTSHR and hTSHR aa352-366 have an immunogenic activity because they induce the production of TRAb, TBAb and TSAb in mice.  相似文献   

13.
GUO Xiao-Fang  GU Qin  LIU Ning  YU Sun 《园艺学报》2012,28(11):1971-1975
AIM: To investigate the relationship between renal cell apoptosis induced by ischemia/reperfusion injury and the activation of P53. METHODS: Eighteen mice were randomly divided into 3 groups: sham operation group, acute kidney injury (AKI) group and pifithrin-alpha(PFT-α) treatment group. The AKI model was established by clamping bilateral renal arteries for 45 min and then performing reperfusion. The mice in PFT-α group were intraperitoneally injected with PFT-α at dose of 2.2 mg/kg 5 min before AKI model was established. The changes of serum creatinine and urea nitrogen were determined and renal pathological changes were observed 48 h after AKI. The P53 expression in the kidney was evaluated by Western blotting and immunofluorescence methods. Apoptosis of the renal cells was observed by TUNEL assay. The protein expression of tumor necrosis factor receptor (TNFR), caspase-3 and Bcl-2 was detected by immunohistochemical method. RESULTS: The levels of serum creatinine and urea nitrogen in AKI group and PFT-α group were higher than those in sham operation group. Compared with AKI group, the levels of serum creatinine and urea nitrogen were significantlydecreased in PFT-α group. No pathological change of the kidney was observed in sham operation group. In AKI group, the pathological changes such as shedding of brush border, vacuolus and dropwise degeneration in the renal tissues were observed. These pathological changes were attenuated in PFT-α group as compared with AKI group. The protein was expression level of P53 and the apoptotic cells were much higher in AKI group than those in sham operation group, and P53 protein was mainly expressed in the renal cortex, while those were significantly decreased in PFT-α group as compared with AKI group. Compared with sham operation group, the expression levels of TNFR and caspase-3 were increased and the Bcl-2 levels was decreased. Compared with AKI group, the expression level of TNFR and caspase-3 decreased and Bcl-2 expression was increased. CONCLUSION: P53 protein is mainly expressed in the renal cortex and induces apoptosis by increasing the expression of caspase-3 and regulating the expression of TNFR and Bcl-2 in the kidney following ischemia/reperfusion injury.  相似文献   

14.
Organ fibrosis is a common pathogenetic change of parenchymal organs under chronic conditions, characterized by increased fibrous connective tissues and reduced parenchymal cells. The essence of renal fibrosis is the "repair of scars" after renal tissue damage. It involves a loss of renal parenchyma cells, activation of myofibroblasts, deposition of extracellular matrix, imbalance of metabolism and abnormal interactions with organs. Hepatic fibrosis is a kind of repair response induced by various chronic hepatic diseases, including viral hepatitis and metabolic liver disease, and it is the common pathological basis of end-stage hepatic disease. Pulmonary fibrosis is a progressive and fatal inflammatory interstitial lung disease, characterized by inflammatory destruction and extracellular matrix deposition. Myocardial fibrosis is a process of pathological repair after a variety of injuries caused by hypertension, hypertrophic cardiomyopathy, viral cardiomyopathy, valve disorders, myocardial ischemia, diabetes, obesity and other metabolic abnormalities. Organ fibrosis indicates some common pathogenesis, but the exact mechanisms differ from organs and still need further investigation to identify biomarkers for early diagnosis and to devise drugs specifically for fibrosis. This article comprehensively summarizes the recent developments in organ fibrosis over the last 3 years, including underlying mechanisms and urgent scientific issues remained.  相似文献   

15.
AIM: To study the relationship between the changes of aquaporin 4 (AQP4) expression and the liver functions in the process of hepatic ischemia-reperfusion (I/R) injury in rats. METHODS: Forty-eight Wistar rats were used to establish the animal model of hepatic I/R injury. The rats were subject to ischemia for 30 min and were randomly divided into 4 groups according to the time of reperfusion: 2 h group, 1 day group, 3 days group and 7 days group. The corresponding control animals were also set up. The serum was collected for detecting direct bilirubin (DB), indirect bilirubin (IB) and alanine transaminase (ALT). The pathological changes of the liver tissues were observed under microscope with HE staining. The protein expression of AQP4 was measured by the method of immunohistochemistry and the mRNA expression of AQP4 was detected by RT-PCR. RESULTS: Under microscope, degeneration and necrosis of the hepatic cells were observed in the liver tissues in I/R injury groups. Compared with sham operation group, the concentrations of DB, IB and ALT activity in I/R injury groups increased obviously, peaking on the first day after operation, then declining continuously and restoring to the normal levels on the 7th day after operation. The expression of AQP4 were significantly decreased in I/R injury animals in 2 h group, 1 day group and 3 days group, and reached the minimum level on the first day. The mRNA expression levels of AQP4 were also deceased in hepatic I/R injury rats in 2 h group, 1 day group and 3 days group, and reached the minimum level on the first day after operation, then increased slowly and restored to the normal levels on the 7th day after operation. CONCLUSION: Hepatic ischemia-reperfusion induces a decrease in AQP4 expression and impairs the liver functions, indicating an important role of AQP4 in the pathogenesis of liver ischemia-reperfusion injury.  相似文献   

16.
AIM: To study the pathological features of the dilated cardiomyopathy and the mechanisms involved. METHODS: The left ventricular myocardium specimens were obtained from 8 patients with dilated cardiomyopathy by BATISTA. The morphological changes was examined macropathologically and histopathologically. RESULTS: The dilated cardiomyopathy from 8 patients can be classified into two types macropathology. One of them showed hypertrophy of left ventricular wall and the other showed fatty infiltration on myocardium of the left ventricular. In the first type, swelling of the endothelial cells as well as luminal stenosis even occlusive of small arteries and arterioles were observed in the study. Electronical microscopical examination showed that there were a lot of homogeneous secretory granules in the endothelial cells. CONCLUSION: These results suggested that the secretory granules might be from the damaged myocardial cells and entered into the adjacent endothelial cells. The pathological changes mentioned above could aggravate the ischemia of myocardium. At the same time, the vicious cycle make the pathological changes more serious. Further study should be made to confirm the nature of the secretory granules.  相似文献   

17.
AIM: To establish HCC Hu-PBL-SCID(severe combined immune deficiency) chimeric model,and to observe the antitumor effect of mRNA-dendritic cell vaccine.METHODS: Hu-PBL-SCID chimeric model was established by intraperitoneal injection of human peripheral blood lymphocytes.Human IgG in mouse serum was detected by ELISA to identify the model.After the model was established,the mice were divided into four groups,and were inoculated with mRNA DC vaccine,anti CD4+,CD8++mRNA DC,naive DC,and PBS,respectively.Then the animals were injected subcutaneously with 2×106 HepG-2 cells.Tumorigenecity,latent period,and tumor volume were observed,and antitumor efficacy of CTL was measured.RESULTS: The concentration of human IgG in mouse serum in Hu-PBL- SCID model was detected,indicating that the Hu-PBL-SCID model was established successfully.No significant difference of tumorigenecity among the four groups was observed.However,tumors in mRNA DC vaccine group grew slowly,tumor volumes were significantly smaller than those in anti CD4+,CD8++mRNA DC,PBS and naive DC groups.The spleen cells in mRNA DC vaccine group specifically killed the HepG-2 cells but not SGC-7901 cells.CONCLUSION: mRNA DC vaccine shows anti-tumor immune response in vivo by inducing CD4+,CD8+T lymphocyte immune responses.  相似文献   

18.
AIM:To observe morphological changes in transplanted intracerebral rat gliomas and rat survival time with gliomas under chemotherapy with angiotensin II-induced hypertension. METHODS:C6 glioma cells were cultured, and the effects of carmustine, nimodipine or/and teniposide on gliomas cells was observed. In addition, the brain tumor model was established in Wistar rats by stereotaxic inoculation of C6 glioma cells. The tumor-bearing rats were treated with carmustine, nimodipine lisplatin or/and teniposide during angiotensin II-induced hypertension, the pathological changes in gliomas was also examined. RESULTS:In vitro experiments showed chemotherapy resulted in morphologic changes in glioma cells, including cell enlargement, degeneration. In vivo experiments, the survival time of tumor-bearing rats was longer, the voume of gliomas was smaller in chemotherapy with hypertension group than those in chemotherapy alone, and pathological examination showed necrosis in the gliomas. CONCLUSION:Chemotherapy with angiotensin II-induced hypertension has a better inhibitory effect on rat intracerebral gliomas than chemotherapy alone.  相似文献   

19.
AIM: To investigate the effects and mechanisms of sphingosine-1-phosphate receptor-2 (S1P2R)on lipopolysaccharide (LPS)-induced acute lung injury (ALI). METHODS: ALI model was induced by intratracheal administration of LPS in both wild-type mice and S1P2R -deficient mice. The pathological changes in the lung tissues were observed, and the protein concentration, total cell number, neutrophil ratio, TNF-α level and IL-6 level were determined in the bronchoalveolar lavage fluid (BALF) 24 h after LPS injection. In order to investigate the mechanisms of S1P2R in LPS-induced ALI, 10 min before LPS injection, both wild-type mice and S1P2R -deficient mice were injected with nitric oxide synthase inhibitor by tail vein injection, the pathological changes of the lung tissues were observed, and the protein concentration and total cell number in BALF were determined 12 h after LPS injection. RESULTS: Compared with wild-type mice, S1P2R -deficient mice showed more severe LPS-induced ALI, and the protein concentration, neutrophils and inflammatory cytokines in BALF were significantly increased in S1P2R -deficient mice. Administration of nitric oxide synthase inhibitor Nω-L-nitro-arginine methyl ester protected S1P2R -deficient mice from aggravation of ALI. CONCLUSION: S1P2R mediates the protection from LPS-induced ALI possibly through inhibiting nitric oxide synthase.  相似文献   

20.
AIM: To study the relationship between prostaglandins and acute pulpitis. METHODS: Rat traumatic pulpitis model was established by pulp exposure. The kinetic pathological changes in dental pulpal tissues and changes of PGE2,6-Keto-PGF1α and TXB2 concentration in dental pulp were observed. RESULTS: After pulpal trauma, the dental pulp showed inflammatory changes and the concentrations of PGE2,6-Keto-PGF1α and TXB2 were increased, which peaked at 6 hour post-trauma. CONCLUSION: Prostaglandins play a significant role in the pathogenesis of pulpitis.  相似文献   

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