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1.
WANG Li-jun  TONG Lei 《园艺学报》2018,34(2):340-345
AIM: To investigate the anti-inflammatory action of resveratrol (Res) and its correlation with nuclear factor-κB (NF-κB) signaling pathway in a mouse model of inflammatory pain.METHODS: BALB/c mice (n=60) were randomly divided into 6 groups:normal control group, inflammatory pain model group, positive control (dexamethasone, 0.5 mg/kg) group and resveratrol (100, 50 and 25 mg/kg) groups (10 mice in each group). In order to observe the anti-inflammatory pain effects of reseratrol on mice, the paw withdrawal mechanical threshold, paw withdrawal thermal latency and cold withdrawal times were detected. In order to analyze the mechanism of analgesic effect of resveratrol, the expression levels of NF-κB, inhibitor of NF-κB (IκB) α, inhibitor of NF-κB kinase (IKK) β, tumor necrosis factor (TNF)-α and interleukin (IL)-1β in the spinal cord tissues (L4~L6) of the mice were determined by RT-PCR and Western blot.RESULTS: The resveratrol at 100 and 50 mg/kg increased the paw withdrawal mechanical threshold, prolonged the paw withdrawal thermal latency, and decreased the cold withdrawal times in the inflammatory pain mice (P<0.05 or P<0.01). The resveratrol at 100 mg/kg down-regulated the mRNA and protein expression levels of NF-κB, IκBα, IKKβ, TNF-α and IL-1β in the spinal cord tissues (L4~L6) of inflammatory pain mice (P<0.05 or P<0.01).CONCLUSION: Resveratrol ameliorates the inflammatory pain of the mice induced by complete Freund's adjuvant. The mechanism is related to the inhibition of NF-κB signaling pathway.  相似文献   

2.
AIM: The present study was designed to observe the effect of ［D-Arg1, D-Trp7,9, Leu11］-substance P (spantide), a non-selective antagonist of NK receptors, on the up-regulation of nitric oxide synthase (NOS) induced by formalin test. METHODS: Formalin (5%, 0.2 mL) was subcutaneously injected into the plantar side of the right hind paw to produce persistent pain and hyperalgesia. The pain response was determined by spontaneous flinch reflex test. NOS expression was examined using NADPH-d histochemical staining. Spantide was intrathecally injected via L5-L6 intervertebral space 5 min prior to the formalin injection. RESULTS: Injection of formalin resulted in a characteristic behavioral response consisting of vigorous scratching, biting, licking and lifting of the injected hind paw from the box's bottom. Following these behavioral responses, the NOS expression was up-regulated in the pericentral canal region of the L5 segment of the spinal cord. Pre-treatment with spantide depressed the spontaneous flinches of the injected paw in the second phase of the formalin test. At the same time, the up-regulation of NOS was substantially inhibited. CONCLUSION: It might be concluded that substance P played an important role in the up-regulation of NOS in the pericentral canal region of the spinal cord in the formalin test.  相似文献   

3.
AIM: To investigate the effects of silencing of cyclooxygenase-2 (COX-2) gene expression by siRNA on the proliferation, apoptosis, cell cycle and tumorigenicity of human pancreatic cancer Capan-2 cells.METHODS: The gene transfection was performed using Lipofectamine 2000 (Lipo). The proliferation, apoptosis and cell cycle of Capan-2 cells were tested by the methods of cell counting, microscopy and FCM. The mRNA expression of COX-2 was determined by RT-PCR and real-time PCR. The protein level of COX-2 was detected by Western blotting. The tumorigenicity of Capan-2 cells transfected with siRNA-COX-2 was determined using the model of nude mice. RESULTS: Transfection efficiency of 96.47% was obtained under the conditions that the transfection volume was 2 mL, concentration of Lipo was 5 μL and that of siRNA-COX-2 was 50 nmol/L. The best sequence of siRNA-COX-2 for silencing of COX-2 gene expression was siRNA006 with the silencing rate of up to 73% 24 h after tansfection. siRNA-COX-2 slowed down the growth of Capan-2 cells 48 h after transfection (P<0.05). At time points of 48 h and 72 h after transfection, the protein expression of COX-2 was down-regulated to 67% and 61% of the normal level, the proliferation inhibition rate was 35.48% and 56.32%, and the apoptotic rate was 2.03% and 3.27%, respectively. At time points of 24 h, 48 h and 72 h after transfection, the proportion of the cells in G0/G1 phrase was 58.03%, 63.31% and 65.66%, and that of the cells in S phase was 30.27%, 24.87% and 22.2%, respectively. The mean volume and weight of tumor tissues were remarkably decreased due to the transplantation of Capan-2 cells transfected with siRNA-COX-2.CONCLUSION: siRNA-COX-2 effectively silences the expression of COX-2 gene, inhibits the growth and decreases the tumorigenicity of Capan-2 cells.  相似文献   

4.
AIM: To investigate the role of ATP-sensitive potassium (KATP) channels in the inhibitory effect of hydrogen sulfide (H2S) on high glucose(HG)-induced inflammation mediated by necroptosis in H9c2 cardiac cells.METHODS: The expression levels of receptor-interacting protein 3 (RIP3; an indicator of necroptosis) and cyclooxyge-nase-2 (COX-2) were determined by Western blot. The levels of interleukin-1β (IL-1β) and tumor necrosis factor-α (TNF-α) were detected by ELISA.RESULTS: After H9c2 cardiac cells were treated with 35 mmol/L glucose (HG) for 24 h, the expression of RIP3 was significantly increased. Pre-treatment of the cells with 100 μmol/L diazoxide (DZ; a KATP channel opener) or 400 μmol/L NaHS (a donor of H2S) for 30 min considerably blocked the up-regulation of RIP3 induced by HG. Moreover, pre-treatment of the cells with 100 μmol/L 5-hydroxydecanoic acid (5-HD; a KATP channel blocker) attenuated the inhibitory effect of NaHS on HG-induced up-regulation of RIP3. On the other hand, co-treatment of the cells with 100 μmol/L necrostatin-1 (a specific inhibitor of necroptosis) or pre-treatment of the cells with 100 μmol/L DZ or 400 μmol/L NaHS attenuated HG-induced inflammatory responses, evidenced by decreases in the expression of COX-2 and secretion levels of IL-1β and TNF-α. However, pre-treatment of the cells with 100 μmol/L 5-HD significantly attenuated the above anti-inflammatory effects of NaHS.CONCLUSION: KATP channels play an important role in the inhibitory effect of H2S on HG-induced inflammation mediated by necroptosis in H9c2 cardiac cells.  相似文献   

5.
AIM: To investigate the effects of cannabinoids WIN55, 212-2 (WIN) and O-1602 on the expression of heat-shock proteins (HSPs), such as HSP27, HSP60 and HSP70, in the inflammatory tissues of mice with experimental colitis or acute pancreatitis (AP). METHODS: Mouse colitis was induced by feeding the C57/BL with 4% dextran sulfate sodium (DSS) for 7 d, and AP was induced by intraperitoneal injection of ceruline in the mice (50 μg/kg hourly, with a total of 6 times). The mice were intraperitoneally administered with WIN or O-1602 for the therapeutic evaluation by observing the following parameters: pathological changes of the tissues, plasma activity of amylase, plasma levels of IL-6 and cytokine-induced neutrophil chemoattractant-1 (CINC-1), and HSP expression in the colonic and pancreatic tissues. RESULTS: Compared with normal control mice, the colonic tissues from colitis mice and the pancreatic tissues from AP mice appeared obvious signs of inflammation and injury. The plasma levels of IL-6 and CINC-1 significantly increased in colitis mice and AP mice. In DSS group of colitis mice, HSP27 expression increased, but HSP60 and HSP70 were reduced in the colonic tissues. WIN showed anti-inflammatory effects on the pathological changes of colonic tissues and the plasma cytokine levels. WIN also improved the expression of HSP70 (P<0.05). In AP group, the expression of HSP27 and HSP70 in pancreatic tissues increased, and HSP60 decreased. O-1602 also showed some anti-inflammatory effects on the changes of the pathological tissues and the plasma parameters, but had no obvious effects on the HSP expression (P>0.05). CONCLUSION: The experimental colitis and acute pancreatitis in mice were induced by feeding DSS and injection of cerulein, respectively. The changes of HSP expression were different in the inflammatory tissues. WIN and O-1602 show anti-inflammatory effects and increase the expression of several HSPs to some extent.  相似文献   

6.
AIM：To observe how farnesoid X receptor (FXR) functioned in concanavalin A (Con A) -induced hepatitis (CIH) and the regulation of FXR-thyrotropin embryonic factor (TEF) pathway. METHODS：C57BL/6 mice were injected with Con A to induce hepatitis. The expression of FXR and TEF in the liver specimens was determined by qRT-PCR and Western blotting. The concentrations of serum ALT/AST and inflammatory cytokines IFN-γ, TNF-α, IL-4 and IL-2 in the blood samples were tested after Con A injection. RESULTS：FXR was down-regulated in CIH mice. TEF was up-regulated when FXR was activated by chenodeoxycholic acid (CDCA). Activation of FXR reduced the levels of aminotransferases and inflammatory cytokines IFN-γ, TNF-α, IL-4 and IL-2 in the CIH mice induced by Con A injection. CONCLUSION：FXR activation attenuates CIH mouse liver injury and reduces inflammatory cytokines. FXR activation results in TEF up-regulation. The FXR-TEF pathway may play a protective role in autoimmune hepatitis.  相似文献   

7.
AIM：To explore the analgesic effect of active component from cobra venom in Wannan area. METHODS：The active component was purified from crude venom of cobra by cation-exchange chromatography and size-exclusion chromatography. The purity and molecular weight of the active component were determined by SDS-polyacrylamide gel electrophoresis and capillary zone electrophoresis. The analgesic activity was analyzed by hot-plate test and acetic acid writhing test. Normal saline and morphine were used as controls. RESULTS：A single active component was obtained from crude cobra venom. The molecular weight was about 6 500 D. The analgesic effect of the active component persisted from 0.5 h to 8 h after hot-plate test. With intraperitoneal injection of the active component at doses of 0.03 mg/kg, 0.1 mg/kg and 0.3 mg/kg in mice, the writhing inhibition rates were 27%, 50% and 70%, respectively. No statistical difference between 0.3 mg/kg group and morphine group was observed. CONCLUSION：The active component from crude cobra venom has a dose-dependent analgesic effect.  相似文献   

8.
AIM: To test the possibility that TNF-α can induce the display of nociceptive behaviors in rats without any injury. METHODS: The induction of changes in 50% paw withdrawal threshold and paw withdrawal latency by peri-sciatic administration of recombinant rat TNF-α (rrTNF) was determined with the methods of behavioral tests. PDTC (a NF-κB inhibitor) was also intrathecally delivered before or after the administration of rrTNF. RESULTS: We found that peri-sciatic administration of rrTNF at the concentrations of 10, 100, and 1 000 ng/L (daily for 2 d) induced mechanical allodynia and thermal hyperalgesia in bilateral hindpaws, lasting for around 20 d. Intrathecal administration of PDTC 30 min before each peri-scitic administration of rrTNF completely prevented the decrease in bilateral thresholds, and delayed the decrease of paw withdrawal latencies. In contrast, the same dose of PDTC had no effect on mechanical allodynia when applied intrathecally 6 d after the first administration of rrTNF, while inhibited thermal hyperalgesia for about 7 d. CONCLUSION: Without any nerve injury, peri-sciatic administration of recombinant rat TNF-α at low doses produces mechanical allodynia and thermal hyperalgesia in bilateral hindpaws. NF-κB pathway may play different roles in mechanical allodynia and thermal hyperalgesia.  相似文献   

9.
AIM: To study the role of autophagy-related gene 5 (Atg5) in cerebral ischemia and reperfusion injury in mice. METHODS: BALB/c male mice (weighing 18~22 g) were randomly divided into sham group, ischemia/reperfusion (I/R) group, Atg5 siRNA group and control siRNA group. Focal cerebral ischemia was performed using the method of middle cerebral artery occlusion (MCAO) for 60 min and reperfusion for 24 h. In siRNA group and control group, 5 μL Atg5 siRNA or scrambled siRNA was administered by intracerebroventricular injection 24 h before MCAO. The expression of Atg5 at mRNA and protein levels in ischemic cortex at 24 h after reperfusion was determined by real-time PCR and Western blot. The infarct volume and edema were evaluated by TTC staining, and motor deficits were evaluated by neurological scoring. RESULTS: The expression of Atg5 at mRNA and protein levels was significantly increased 24 h after reperfusion in I/R group compared with sham group. Atg5 siRNA obviously decreased the expression of Atg5 at mRNA and protein levels induced by I/R. Inhibition of Atg5 exacerbated the infarct volume and ameliorated the neurological symptoms. CONCLUSION: Atg5 has neuroprotective effect on focal cerebral ischemia and reperfusion injury.  相似文献   

10.
AIM: To investigate the dynamic influence of zanthoxylum seed oilA2 (ZSOA2) on NF-кB signaling pathway and inflammatory factor in pulmonary tissue of asthmatic mice. METHODS: The suspensoid (0.2 mL containing 20% albumin hydroxide and 10% ovalbumin) was administered by intraperitoneal injection to sensitize the BALB/c mice on day 1, then 0.4% ovalbumin solution (50 μL in phosphate buffer fluid) was dripped into the respiratory tract through nasal cavity to establish the asthmatic mouse model. After dripped ovalbumin for 24 h, 48 h, 3 d, 7 d and 14 d, the mice were killed at specified time points. The contents of interleukin-4 (IL-4), interleukin-5 (IL-5) and interferon-γ (IFN-γ) in bronchoalveolar lavage fluid (BALF) were determined by ELISA. The pathological changes of the lung tissues were observed with HE staining. The inflammatory cell counts were conducted by Eosin staining. The protein levels of adhesion molecule and the molecules of NF-κB signaling pathway in lung tissues were determined by Western blotting. RESULTS: In ZSOA2 treated mice, the pathological injury of the lung was significantly attenuated as compared to the model mice, the counts of eosinophils and lymphocytes were reduced obviously in lung bronchial area of asthmatic mice at all observed time points (P<0.05). The levels of IL-5 and IL-4 decreased and IFN-γ increased in BALF. The results of Western blotting showed that ZSOA2 down-regulated the protein levels of intercellular adhesion molecule-1, vascular cell adhesion molecule-1, I kappa B kinase alpha-α and phosphorylation inhibitory-κB. ZSOA2 also up-regulated the protein levels of tumor necrosis factor receptor 1 and phosphorylation nuclear factor-kappaB in lung tissue at all observed time points. CONCLUSION: ZSOA2 has therapeutic effect on asthma by down-regulating the protein expression of IκB-β and p-IκB, inhibiting the releases of cytokines and chemotactic factors, and attenuating the infiltration of inflammatory cells in the lungs of ovalbumin challenged asthma mice.  相似文献   

11.
AIM To investigate the role of mast cells in the pain of adjuvant arthritis (AA) in mice induced by complete Freund's adjuvant (CFA). METHODS The animals were divided into 4 groups: normal control group (control group), AA model group (model group) and AA model + cromolyn sodium (CS) group (CS group), AA model + mast cell lacking group (W-4Bao group), with 6 mice in each group. The animals in the first 3 groups were C57BL/6 mice, while those in W-4Bao group were KitW-4Bao mice lacking of mast cells. The pain model of chronic AA was induced by intraplantar injection of CFA into the right hind paws of the mice, while the mice in control group was injected with saline. One day after CFA injection, the mice in CS group were intraperitoneally injected with CS (20 mg/kg), and those in other groups received an equal volume of saline once a day for 14 d. The paw edema, paw withdrawal threshold (PWT) and paw withdrawal latency (PWL) were evaluated at 0, 1, 3, 7, 10 and 14 d after CFA injection. The mouse right ankle joint was harvested after 14 d for HE and toluidine blue staining, and the concentrations of histamine, tryptase, substance P (SP), calcitonin gene-related peptide (CGRP) were detected by ELISA. RESULTS One day after CFA injection, the inflammation of the right hind paw in model group was more serious compared with control group, and the PWT and PWL were notably decreased (P<0.05). In addition, the numbers of mast cells and degranulated mast cells were increased obviously, and the concentrations of histamine, tryptase, SP and CGRP were increased (P<0.05). However, compared with model group, hyperalgia and the release of neuropeptides in CS group and W-4Bao group were significantly decreased (P<0.05). CONCLUSION The activation of mast cells promotes the pain of AA in mice, and its mechanism may be associated with the release of neuropeptides and relevant inflammatory factors.  相似文献   

12.
AIM:To investigate the role of Chinese medical herb Radix Puerariae extract puerarin in a rat model of radicular pain caused by lumbar disc herniation (RAPLDH) and to explore the possible mechanism involving spinal glial cell activation and inflammatory response. METHODS:The rat model of RAPLDH was induced by autologous nucleus pulposus (NP) implantation. The rats in sham group received the same operation procedure except NP implantation. Puerarin injection at different doses (50, 100 and 150 mg/kg) was delivered intraperitoneally 1 h before surgery, and once daily for 7 d. Mechanical paw withdrawal threshold (PWT) test was employed for assessing pain behaviors. Spinal microglia and astrocyte activation was evaluated by immunofluorescence staining of relevant specific markers. The expression of pro-and anti-inflammatory cytokines in spinal dorsal horn was measured by ELISA. RESULTS:The rats with NP implantation showed long-lasting pain behaviors, characterized by decrease in PWT from day 3 to day 14 after surgery. Compared with vehicle group, puerarin at doses of 100 mg/kg and 150 mg/kg significantly increased PWT of the rats with NP implantation. Puerarin significantly reduced the expression of spinal microglia marker ionized calcium-binding adaptor molecule 1 and astrocyte marker glial fibrillary acidic protein (P<0.01). Puerarin also decreased spinal expression of pro-inflammatory cytokines tumor necrosis factor-α, interleukin-1β and interleukin-6, and increased anti-inflammatory cytokine interleukin-10 (P<0.01). CONCLUSION:Puerarin alleviate RAPLDH by inhibiting spinal glial cell activation and inflammatory response.  相似文献   

13.
AIM: To investigate the role of peroxisome proliferator-activated receptors (PPARs)-inflammation signaling pathways in diabetic hepatopathy. METHODS: Diabetic mouse model was established by feeding the mice with a high-energy diet for 4 weeks combined with intraperitoneal injection of streptozotocin (STZ; 40 mg·kg-1·d-1 for 5 d). The hepatopathy model was confirmed by histopathological observation and the indexes of liver function, such as alanine aminotransferase (ALT), aspartate aminotransferase (AST) and alkaline phosphatase (ALP), after another 4 weeks. Moreover, fasting blood glucose (FBG), and serum levels of total cholesterol (TC), triglyceride (TG) and insulin were measured, and the HOMA insulin resistance index (HOMA-IR) was calculated. The mRNA and protein expression levels of PPARs and inflammation-related factors were measured by qPCR and Western blot, respectively. RESULTS: After treatment with STZ for 7 d, the FBG of mice exceeded 11.1 mmol/L, suggesting that the diabetic model was established. After 4 weeks, the structural deformation of the hepatocytes (including hepatocytes containing abundant fat vacuoles, and inflammatory cell infiltration), and the increases in the serum levels of insulin, HOMA-IR, TC, TG, ALT, AST and ALP were observed (P<0.01), indicating the occurrence and progression of hepatopathy in diabetic mice. Meanwhile, compared with the control group, the mRNA and protein expression of PPARα, PPARβ and PPARγ decreased, but the expression of nuclear factor-κB (NF-κB), cyclooxygenase 2 (COX-2) and inducible nitric oxide synthase (iNOS) significantly increased in the diabetic hepatopathy mice (P<0.01). CONCLUSION: Down-regulation of PPARα, PPARβ and PPARγ and activation of NF-κB-COX-2/iNOS signaling pathways may be involved in the diabetic hepatopathy in mice induced by long-term high-energy diet feeding combined with intraperitoneal injection of STZ.  相似文献   

14.
AIM：To investigate whether celecoxib,a cyclooxygenase-2 (COX-2) inhibitor,potentiates the anti-leukemia activity of STI571 in K562 cells.METHODS：K562 cells were treated with STI571,celecoxib or combination of both at different concentrations in suspension culture.Cell proliferation was documented by MTT assay,and cell apoptosis was determined by flow cytometry and morphology.Meanwhile,RT-PCR was applied to analyze the probable mechanism underlying the effects of the drugs.RESULTS：The combination of STI571 and celecoxib dramatically suppressed the proliferation of K562 cells,in which 0.25 μmol/L STI571 and 40.0 μmol/L celecoxib enhanced the inhibiting rate to 76.1%±1.6%.Furthermore,the combining administration of drugs significantly promoted the apoptosis induced by STI571，which showed characteristic changes of morphologic features and increase in sub-G1 cells.By using RT-PCR technique,the expression of COX-2 had no decline by single administration of celecoxib or STI571.However,a progressive down-regulation was caused by coadministration of two drugs.In contrast with COX-2,the expression of VEGF had no changes at any time.CONCLUSION：The administration of celecoxib alone only inhibits the proliferation of K562 cells.Combination treatment with STI571 and celecoxib promotes the apoptosis induced by STI571.  相似文献   

15.
AIM: To explore the effects of lipoxin A4 on the expression of cyclooxygenase 2 (COX-2) in human bronchial epithelial cells (HBECs). METHODS: HBECs were incubated with various concentrations (0.1, 1 and 10 mg/L) of lipopolysaccharide(LPS) for 9 h, or 1 mg/L LPS for different time (3 h, 6 h and 9 h). The levels of COX-2 mRNA in HBECs and prostaglandin E2 (PGE2) in the culture supernatant were measured. In addition, the HBECs were exposed to lipoxin A4 at concentration of 0, 100 and 400 μmol/L after stimulated with LPS at concentration of 1 mg/L for 9 h, and the supernatant of the culture cells was collected for determining the content of PGE2 by ELISA. The cells were also harvested, and the mRNA and protein levels of COX-2 were analyzed by RT-PCR and Western blotting, respectively. RESULTS: LPS increased the mRNA expression of COX-2 and production of PGE2 in a dose and time dependent manners in HBECs. Induction of COX-2 mRNA and protein by LPS were inhibited by lipoxin A4 in a dose-dependent manner. Lipoxin A4 also significantly decreased LPS-induced production of PGE2. CONCLUSION: Lipoxin A4 down-regulates LPS-induced expression of COX-2 and consequently inhibits the production of PGE2 in HBECs.  相似文献   

16.
AIM：To evaluate the immune state in rats with chronic Clonorchis sinesis (Cs) infestation by investigating the effects of Cs on macrophage polarization and inflammatory reactions. METHODS：Sprague-Dawley rats were used in the study. Chronic Cs infestation model was reproduced by intragastric perfusion with Cs eggs. Twenty rats were randomly divided into normal group (n=10) and Cs infestation group (n=10). The serum levels of interleukin (IL-4) and IL-10, tumor necrosis factor α(TNF-α) and interferon γ (IFN-γ) were detected by ELISA. The macrophages were harvested by peritoneal lavage. The differentiation proportion of M1 and M2 macrophages were detected by flow cytometry. The macrophages were divided into control group, normal group and chronic Cs infestation group according to the sources of macrophages. The levels of TNF-α and IL-10 in the culture supernatants were detected by ELISA at 0, 2, 12 and 24 h after lipopolysaccharide (LPS, 10 μg/L) stimulation in vitro. RESULTS：Compared with normal group, chronic Cs infestation increased the serum levels of TNF-α, IFN-γ, IL-4 and IL-10. The differentiation proportion of M1 detected by flow cytometry was 92.1% in normal group and that of M2 macrophages was 93.8% in Cs infestation group. The levels TNF-α and IL-10 in culture supernatants were increased at 2~24 h after LPS stimulation both in normal group and Cs infestation group, but the levels of TNF-α were lower in chronic Cs infestation group than that in normal group at 2 h,12 h and 24 h after LPS stimulation. The level of anti-inflammatory cytokine IL-10 was higher in Cs infestation group than that in normal group at 2 h, 12 h and 24 h after LPS stimulation. CONCLUSION：Chronic Cs infestation increases the serum levels of both pro-inflammatory cytokines and anti-inflammatory cytokines, thus inducing the polarization of M2 macrophages. The macrophages derived from chronic Cs-infected rats produce tolerance in the inflammatory process against LPS in vitro.  相似文献   

17.
AIM：To investigate the effects of dexmedetomidine-ulinastatin combination on acute lung injury induced by lipopolysaccharide (LPS) in rats. METHODS：Male Wistar rats were randomly divided into 5 groups: saline control group (NS group) was given saline (5 mL/kg, iv) alone; LPS group (L group) was given LPS (10 mg/kg, over 10 min); dexmedetomidine+LPS group (L+D group) was treated with the additional administration of dexmedetomidine (1 μg·kg -1·h -1) immediately after LPS injection; ulinastatin+LPS group (L+U group) was treated with the addi-tional administration of ulinastatin (50 000 U/kg, ip) immediately after LPS injection; dexmedetomidine+ulinastatin+LPS group (L+D+U group) received dexmedetomidine (1 μg·kg -1·h -1) and ulinastatin (50 000 U/kg) immediately after LPS injection. The animals were sacrificed at 6 h after LPS or NS administration. Partial pressure of arterial oxygen (PaO 2), pH and base excess (BE) were measured, and the lungs were removed for evaluation of histological characteristics and determining the concentrations of TNF-α, IL-1β, macrophage inflammatory protein 2 (MIP-2), malondialdehyde (MDA), nitric oxide (NO), prostaglandin E 2 (PGE 2) and myeloperoxidase (MPO) in lung tissues, lung wet/dry weight ratio (W/D), and albumin in brochoalveolar lavage fluid (BLAF). The pulmonary expression of nuclear factor kappa B (NF-κB) p65 was evaluated by Western blotting. RESULTS：Compared with NS group, PaO 2, pH and BE was lower in L group, which was increased by treatment with dexmedetomidine-ulinastatin combination but not by dexmedetomidine or ulinastatin alone. Compared with NS group, LPS induced marked lung histological injury, which was less pronounced in the animals treated with dexmedetomidine-ulinastatin combination but not dexmedetomidine or ulinastatin alone. The levels of IL-1β, IL-6, MIP-2, MDA, NO and PGE 2 in the lung tissues increased in L group compared with NS group, which were reduced by dexmedetomidine-ulinastatin combination but not by dexmedetomidine or ulinastatin alone. The MPO activity, MDA level and W/D increased in the lung tissues in L group compared with NS group, which was reduced by dexmedetomidine-ulinastatin combination but not by dexmedetomidine or ulinastatin alone. Compared with NS group, the albumin concentration in the BLAF increased, which was reduced by dexmedetomidine-ulinastatin combination but not by dexmedetomidine or ulinastatin alone. Compared with NS group, the expression of NF-κB p65 increased in L group, which was reduced by dexmedetomidine-ulinastatin combination but not by dexmedetomidine or ulinastatin alone.CONCLUSION：Dexmedetomidine-ulinastatin combination has a protective effect on LPS-induced acute lung injury in the rats.  相似文献   

18.
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   

19.
AIM: To investigate the effect of high glucose on the expression of an endoplasmic reticulum stress marker glucose-regulated protein 78 (GRP78), and explore its underlying mechanism. METHODS: (1) Human umbilical vein endothelial cells (HUVECs) were exposed to normal glucose (5.5 mmol/L) and high glucose (30 mmol/L) for 24 h, 36 h or 48 h. Cell viability was determined by MTT method. Cell apoptosis was detected by flow cytometry analysis. The expression of proteins was evaluated by Western blotting analysis. RESULTS: After treated with high glucose for 24-48 h, the expression of GRP78 increased early but decreased at 48 h of incubation, while cyclooxygenase-2 (COX-2) expression increased in a time-dependent manner. COX-2 selective inhibitor nimesulide inhibited high glucose induced changes of GRP78 expression and also inhibited high glucose induced cell apoptosis. CONCLUSION: Prolonged high glucose exposure changes the expression of GRP78 in a COX-2 dependent manner in HUVECs.  相似文献   

20.
AIM：To investigate the effects of pioglitazone, a peroxisome proliferator-activated receptor γ (PPARγ) agonist, on the cognitive impairments and inflammatory cytokine production induced by isoflurane in aged mice. METHODS：Male C57BL/6J mice (11-month-old, n=136) were assigned randomly into 5 groups: control group (Con), isoflurane group (Iso), 10 mg/kg pioglitazone + isoflurane group (Pi10+Iso), 20 mg/kg pioglitazone + isoflurane group (Pi20+Iso) and 20 mg/kg pioglitazone alone group (Pi20). The mice in all isoflurane-treated groups were exposed to oxygen mixed with 1.4% isoflurane for 2 h. The mice in Con group and in Pi20 group were exposed to oxygen only for 2 h. Pioglitazone was suspended in 1% carboxymethyl cellulose (CMC). Pioglitazone (10 mg/kg or 20 mg/kg) was gavaged 2 h prior to the exposure of isoflurane or oxygen alone. The same volume of 1% CMC was gavaged in Con group and in Iso group. Fear conditioning tests were performed to determine the learning and memory abilities 48 h after isoflurane exposure. Fresh cerebral cortice and hippocampi were dissected to measure the protein expression of PPARγ by Western blotting, and the contents of IL-1β and TNF-α were analyzed by ELISA 6 h after isoflurane exposure. RESULTS：Compared with Con group, the response of freezing behavior decreased (P<0.05) and IL-1β content in the hippocampus increased (P<0.05) in Iso group. Compared with Iso group, the response of freezing behavior and PPARγ protein expression level had no significant change (P>0.05) in Pi10+Iso group, but the response of freezing behavior and PPARγ protein expression level increased significantly (P<0.05) and IL-1β content in the hippocampus decreased (P<0.05) in Pi20+Iso group. IL-1β content in the cerebral cortex and TNF-α levels both in the cerebral cortex and the hippocampus showed no significant difference among all groups (P>0.05). CONCLUSION：Pioglitazone attenuates cognitive impairments and the elevates the level of IL-1β in the hippocampus induced by isoflurane in aged mice.  相似文献   

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