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1.
AIM:To investigate the effects of protein C activator (PCA) from Agkistrondon acutusvenom (AAV) on the tension of thoracic aorta rings isolated from the rats with sepsis. METHODS:The model of sepsis was established by intraperitoneal injection of lipopolysaccharide (LPS). SD rats were randomly divided to 6 groups (n=6): sham group, LPS group, PCA intervention group (LPS+PCA, PCA at doses of 0.1 mg/kg, 0.3 mg/kg and 0.6 mg/kg) and LPS+ polymyxin B (at dose of 0.2 mg/kg) group. Using perfusion experiment in vitro, the tension of the aortic rings was measured by biological signal analytical system. RESULTS:The values of MABP, HR, LVDP and ±dp/dtmax were significantly lower in LPS group than those in sham group and LPS+PCA groups. Compared with sham group, the relaxation response to acetylcholine (ACh) and the contractile response of aorta rings induced by phenylephrine (Phe) were significantly decreased in LPS group, which were increased significantly in PCA intervention group (especially at dose of 0.6 mg/kg) compared with LPS group. The dose-response curve of aorta contraction with denuded endothelium induced by Phe shifted down significantly in LPS group compared with sham group, and no significant difference between LPS group and PCA intervention group was observed. Also no statistical difference was found in non-endothelium dependent relaxation of aortic rings induced by sodium nitroprusside among the groups. Pretreatment of N-nitro-L-arginine methl ester and methylene blue increased the contraction amplitude of aortic rings induced by Phe. CONCLUSION: PCA from AAV effectively reverses the hypoergia of the vessels in rats with sepsis through protecting vascular endothelium, the mechanism of which may be mediated by inhibiting NO-GC-cGMP signal transduction pathway.  相似文献   

2.
AIM:To investigate the effects of propofol (P) on the inflammatory response of microglia induced by lipopolysaccharide (LPS) and the mechanisms. METHODS:Mouse microglia BV2 cells were treated with LPS at 100 μg/L to establish a neuroinflammatory injury model. The BV2 cells were divided into 4 groups:control group (C group), model group (L group), L+P group and LPS+AMG517 group (L+A group). The level of tumor necrosis factor-α (TNF-α) in the cell culture supernatant was measured by ELISA. The mRNA expression of transient receptor potential cation channel subfamily V member 1 (TRPV1) was detected by real-time PCR. The protein levels of TRPV1, TNF-α, interleukin-1β (IL-1β), interleukin-6 (IL-6) and phosphorylated calcium/calmodulin-dependent protein kinase Ⅱ (p-CaMKⅡ) were determined by Western blot. The content of free Ca2+ in the microglia BV2 cells was detected by Fluo-3 AM assay. RESULTS:Compared with C group, the level of TNF-α was significantly increased in L group (P<0.01), but that in P group was not changed. Compared with L group, the level of TNF-α was significantly lower than that in L+P group within 4 h (P<0.01). Compared with C group, the mRNA expression of TRPV1 was significantly increased in L group (P<0.01). Compared with L group, the mRNA expression of TRPV1 was significantly down-regulated in L+P group (P<0.01).Compared with L group, the protein levels of TNF-α, IL-1β, IL-6 and p-CaMKⅡ and intracellular Ca2+ concentration were significantly lower than those in L+P group and L+A group (P<0.01). CONCLUSION:Propofol inhibits the inflammatory response of microglia by reducing the expression of TNF-α, IL-1 and IL-6, which may be related to the down-regulation of TRPV1 and p-CaMKⅡ and the reduction of intracellular Ca2+ concentration.  相似文献   

3.
AIM: To study the effects of estrogen on the inflammatory response and vascular remodeling of intracranial artery in rats.METHODS: Thirty-two female spontaneous hypertensive rats (SHR) were randomized into 4 groups: spontaneous hypertensive group(sham-operated), ovariectomized group, ovariectomized+17 beta-estradial group and ovariectomized+vehicle group (8 rats in each group).On day 14, estradiol was detected by radioimmunoassay.The pathological changes were observed under light microscope.The protein expression of tumor necrosis factor alpha (TNF-α) and matrix metalloproteinase-9 (MMP-9) in vascular wall of Willis circle was detected by Western blotting.RESULTS: The estrogen level was lower in ovariectomized group than that in sham-operated group (P<0.01).The estrogen level was higher in ovariectomized rats treated with 17 beta-estradial than that in ovariectomized rats treated with vehicle (P<0.01).Advanced aneurysm was not found in all groups.Early aneurysmal change was not found in sham-operated group.Early aneurysmal changes in some rats were observed in ovariectomized group (2 rats), ovariectomized+vehicle group (3 rats) and ovariectomized+17 beta-estradial group (1 rat).The protein levels of TNF-α and MMP-9 in the vascular wall of Willis circle in sham-operated group were lower than that in ovariectomized group (P<0.01).Additionally, the protein levels of TNF-α and MMP-9 in the vascular wall of Willis circle of ovariectomized rats treated with 17 beta-estradial were lower than those of ovariectomized rats treated with the vehicle (P<0.01).CONCLUSION: Estrogen can influence the vascular remodeling of intracranial artery by inhibiting the inflammatory response and degradating MMP-9 in the vascular wall.  相似文献   

4.
AIM: To investigate the effect of traditional Chinese medicine tetramethylpyrazine on neurocognitive impairment and functional imaging changes induced by lipopolysaccharide (LPS). METHODS: Sprague-Dawley (SD) rats (〖WTBX〗n=36) were randomly divided into 6 treatment groups (n=6 for each group):control group, sham operation group, LPS group, and low dose, medium dose and high dose of tetramethylpyrazine groups. The rats in LPS group and tetramethylpyrazine groups were intracerebroventricularly injected with LPS (150 μg per rat, dissolved in cerebrospinal fluid), whereas the rats in sham operation group were administered the same volume of cerebrospinal fluid in a similar manner. The rats in low dose group, medium dose group and high dose group were intraperitoneally injected with tetra-methylpyrazine at 50 mg/kg, 100 mg/kg and 200 mg/kg, respectively. The neurocognitive impairment was accessed using Morris water maze. The protein levels of interleukin-1β (IL-1β) and tumor necrosis factor-α (TNF-α) were measured by ELISA. The functional imaging changes induced by LPS, including the diffusion motion component of the imaging pure water molecule and the blood perfusion-related diffusion movement, were determined using the imaging IVIM D and IVIM D* functional sequence. RESULTS: In Morris water maze, LPS significantly increased the escape latency, and decreased the number of crossing platform and the time in the target quadrant compared with sham operation group (P<0.05). In addition, low dose of tetramethylpyrazine treatment obviously shortened the escape latency, and increased the number of cros-sing platform and the time in the target quadrant compared with LPS group (P<0.05), but no significant difference between LPS group and medium dose or high dose group was observed. LPS exposure significantly increased IL-1β and TNF-α levels in the cortex and hippocampus compared with sham operation group (P<0.05), while low dose of tetrame-thylpyrazine treatment obviously attenuated the elevated IL-1β and TNF-α levels in the cortex and hippocampus induced by LPS (P<0.05). The imaging results showed that LPS exposure significantly decreased the IVIM D, IVIM D*, and f va-lues of the cortex and hippocampus compared with sham operation group (P<0.05), whereas low dose of tetrame-thylpyrazine treatment obviously inhibited the decreases in IVIM D, IVIM D*, and f values induced by LPS (P<0.05). However, no significant difference of the IVIM D, IVIM D*, and f values between LPS group and midium dose or high dose group was found. CONCLUSION: Tetramethylprazine attenuates neurocognitive impairment induced by LPS in the rats. The mechanism may be related to the inhibition of inflammatory response through the increases in the water molecule diffusion and the perfusion of cerebral blood flow in the brain.  相似文献   

5.
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   

6.
AIM：To explore the effect of mesenteric lymph duct ligation against actue lung injury (ALI) in rats.METHODS：45 Wistar rats were divided into three groups：the ligation group,the non-ligation group and sham operated group,and the two-hit model was established by hemorrhage and LPS injection.Mesenteric lymph was diverted by ligating mesenteric lymph duct in ligation group.All rats facilitated blood withdrawal for blood sample to arterial gas analysis after 24 hours.Then the WBC,NO,NOS,MDA,SOD and lung permeability index (LPI) were determined in bronchoalveolar lavage fluid (BALF),the MPO and ATPase activity were determined in lung homogenate.The ultrastructure was also observed.RESULTS：After two-hit,the PaCO2,the total cells and PMN,the NO2-/NO3-,NOS and MDA content in BALF and MPO activity in lung homogenate and LPI in non-ligation group were significantly increased than those in sham operated group.PaO2 and pH in arterial blood,SOD in BALF and the ATPase in lung homogenate were significantly lower (P<0.01 or P<0.05).The total cells and PMN,MDA,NO2-/NO3- in BALF,LPI in ligation group were significantly increased than those in sham operated group,and SOD in BALF was significantly lower (P<0.01 or P<0.05).The pH and PaO2 in arterial blood,the ATPase in lung homogenate in ligation group were significantly increased than those in non-ligation group,and the PaCO2,the total cells,PMN,NO2-/NO3-,NOS,MDA in BALF,LPI,and MPO in lung homogenate in ligation group were significantly lower than those in non-ligation group (P<0.01 or P<0.05).The injury of pulmonary vascular endothelium in ligation group was lighter than that in non-ligation group.CONCLUSION：The ligation of mesenteric lymph duct attenuates the ALI of rats.Mesenteric lymph might play an important role in the pathogenesis of ALI.  相似文献   

7.
AIM: To investigate the effect of resveratrol on the lipids(CHOL, TG, LDL-C and HDL-C), nitric oxide(NO), peroxynitrite anion(ONOO-) and the expression of inducible nitric oxide synthase(iNOS) in the artery of the mice with ovariotomy(OVX).METHODS: The lipid levels and NO level in the serum were measured. The changes of atherosclerosis were evaluated with Oil Red O staining. The expression of iNOS was measured by DAB staining and Western blot. The ONOO- production was measured by DAB staining.RESULTS: Compared with sham group, the levels of the lipids and NO production in OVX+ high fat(HF) group were increased(P<0.05). Compared with OVX+HF group, the levels of the lipids and NO production in resveratrol group were decreased(P<0.05). Fourteen weeks later, the atherosclerosis model was successfully established. Compared with OVX+HF group, the iNOS expression and the ONOO- production in resveratrol group were decreased(P<0.05), while those in sham group were increased(P<0.05).CONCLUSION: Resveratrol prevents and treats atherosclerosis by inhibiting the iNOS expression in C57BL/6J mice.  相似文献   

8.
AIM: To evaluate the effects of renal denervation (RDN) on the expression of tumor necrosis factor-α (TNF-α), interleukin-1α (IL-1α) and interleukin-6 (IL-6) in a rabbit model of early atherosclerosis. METHODS: New Zealand male rabbits were divided into control group, RDN+ high-fat diet (HFD) group (RDN group), sham+HFD group (sham group) and HFD group. The rabbits in later 3 groups were fed with 2% cholesterol for 8 weeks to establish an early atherosclerosis model. The blood samples were collected to test the levels of lipids, norepinephrine (NE), TNF-α, IL-1α and IL-6. The protein expression of angiotensin Ⅱ (Ang Ⅱ) was detected by the method of immunohistochemistry. The levels of nuclear factor-κB (NF-κB) and Ang II 1 type receptor (AT1R) were evaluated by Western blot. The mRNA expression of TNF-α, IL-1α and IL-6 was determined by real-time PCR. RESULTS: After 1 d of RDN procedure, the NE level was lower in RDN group than that in sham group (P<0.01). After 8 weeks, the NE level was lower in RDN group than that in sham group and HFD group (P<0.05), and triglyceride (TG) was lower in RDN group than that in HFD group (P<0.05). The protein expression of Ang II was decreased in RDN group compared with sham group and HFD group (P<0.01). The protein expression of NF-κB was lower in RDN group than that in sham group (P<0.05). The plasma levels of TNF-α and IL-1α were reduced in RDN group compared with sham group and HFD group (P<0.05). The mRNA expression of TNF-α, IL-1α and IL-6 was reduced in RDN group compared with sham group (P<0.05). CONCLUSION: RDN inhibits sympathetic activity, decreases the plasma level of TG, and alleviates inflammatory reactions in the rabbits with atherosclerosis.  相似文献   

9.
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   

10.
YANG Hong  SI Qin  SUN Ren-yu 《园艺学报》2000,16(9):831-834
AIM: Effect of endothelial cell on the development of acute lung injury and the prevention of dexamethasone in acute lung injury were observed.METHODS:Rats were divided into three groups:1.Control group.2.LPS group:Venous injection with LPS(5mg/kg body weight),execute respectively at 1 h,2 h,6 h and 24 h after LPS injection. 3.dexamethasone group:intraperitoneal injection with dexamethasone ,1 h before LPS injection,execute after 2 hours after LPS injection.RESULTS: Serum NO,TNF-α levels,lung iNOS activity and lung ICAM-1mRNA expression were increased( P <0.05, P <0.01, vs control group),but serum ACE was decreased( P <0.01).Dexamethasone could improve all the changes above mentioned.CONCLUSION:Endothelial cell played a vital role in the development of acute lung injury and dexamethasone could prevent acute lung injury.  相似文献   

11.
AIM: To investigate the inhibitory effect of ginsenoside Re on intimal hyperplasia induced by balloon-injury and to explore the role of NF-κB p65 signaling pathway in the process. METHODS: SD rats(n=40) were divided into 5 groups randomly: sham operation group, model group, low-dose ginsenoside Re group, middle-dose ginsenoside Re group and high-dose ginsenoside Re group. The carotid artery intima injury model was established by 2F balloon catheters in all groups except the sham operation group. The day after modeling, the animals in model group and sham operation group were administered intragastrically with distilled water, and the rats in low-dose, middle-dose and high-dose ginsenoside Re groups were given ginsenoside Re at doses of 12.5 mg/kg, 25mg/kg and 50 mg/kg, respectively. After 14 continuous days, the morphological changes of the injured arteries were observed by HE staining and the lumen area, intima area and media area as well as the ratio of intimal area/media area were determined. The expression of tumor necrosis factor-α(TNF-α) and interleukin-1β(IL-1β) were detected by real-time PCR. The proliferating cell nuclear antigen(PCNA) and nuclear factor-kappa B(NF-κB) p65 were examined by immunohistochemistry.RESULTS: Compared with sham operation group, the vessel cavity was narrowed(P<0.01), the mRNA levels of TNF-α and IL-1β, and the protein expression of PCNA and NF-κB p65 were increased in model group(P<0.05). Compared with model group, the vascular intimal hyperplasia was alleviated obviously(P<0.05), and the mRNA levels of TNF-α and IL-1β, and protein expression of PCNA and NF-κB p65 were decreased in medium and high-dose ginsenoside Re groups(P<0.05). CONCLUSION: Ginsenoside Re inhibits the vascular neointimal hyperplasia induced by balloon-injury in rats, and the molecular mechanism may be related to the inhibition of NF-κB p65 signaling pathway.  相似文献   

12.
AIM:To investigate the effect and potential mechanism of fucoidan on intestinal ischemia-reperfusion (I/R) injury in rats. METHODS:Adult male Wistar rats were randomly divided into 3 groups:sham group, I/R group and Fucoidan+I/R group. Fucoidan at 160 mg/kg was intraperitoneally injected in rats of Fucoidan+I/R group 7 d prior to operation, and the equal volume of saline was intraperitoneally injected in rats of sham group and I/R group. The rats in I/R group and Fucoidan+I/R group underwent superior mesenteric artery occlusion for 1 h and then reperfusion for 2 h. Following reperfusion, the histomorphological changes of the ileum were examined by HE staining. The levels of diamine oxidase (DAO), D-lactic acid (D-LA), tumor necrosis factor-α (TNF-α), interleukin-6 (IL-6) and IL-1β were detected in the blood samples, the levels of malondialdehyde (MDA) and glutathione (GSH), the activity of superoxide dismutase (SOD) and myeloperoxidase (MPO), and the protein levels of Bax, cleaved caspase-3 and Bcl-2 were analyzed in intestinal tissue samples. RESULTS:Compared with sham group and Fucoidan+I/R group, the serum levels of DAO, D-LA, TNF-α, IL-6 and IL-1β were significantly increased in I/R group (P<0.05), Chiu's score of intestinal tissue, MDA content, MPO activity, the levels of Bax and cleaved caspase-3 protein in the intestinal tissues were also significantly increased (P<0.05), while the tissue GSH content, SOD activity, and Bcl-2 protein levels were significantly decreased (P<0.05). CONCLUSION:Fucoidan attenuates intestinal tissue damage caused by I/R, which may be related to anti-oxidation, anti-inflammatory and anti-apoptotic effects.  相似文献   

13.
AIM: To study the effects of cholecystokinin octapeptide (CCK-8) on cerebral cortex injury during endotoxic shock (ES) and its mechanisms. METHODS: Rabbits were injected intravenously with lipopolysaccharide (LPS, 8 mg/kg) to establish ES model. Rabbits (n=32, 8 in each group) were randomly assigned to receive one of four treatments intravenously: normal saline (as control), LPS, CCK-8 pretreatment 30 min before LPS, proglumide (Pro, nonspecific antagonist of CCK receptors) pretreatment 30 min before LPS. The changes of mean arterial pressure (MAP) were measured. The morphologic changes in cerebral cortex were observed through light microscope (LM) and transmission electron microscope (TEM). The alterations of activities of nitric oxide synthase (NOS) and superoxide dismutase (SOD), contents of nitric oxide (NO) and malondialdehyde (MDA) in cerebral cortex were assayed. The expressions of protein of inducible NOS (iNOS) and neuronal NOS (nNOS) were detected by immunohistochemistry staining in cerebral cortex in 4 groups of Sprague-Dawley (SD) rats (n=12, 3 in each group) which were grouped as that of the rabbits. RESULTS: LPS administration resulted in lower MAP than that in control group (P<0.01). Hydropic degeneration of neurons and severe injuries to capillaries were observed in cerebral cortex of ES rabbits. LPS administration induced the expression of iNOS protein in the cytoplasm of neurocytes, and lead to stronger positive signals of nNOS than that in control group. NOS activity, NO2ˉ/NO3ˉ level and MDA content were higher (P<0.05, P<0.01 and P<0.01), while SOD activity was lower in cerebral cortex of ES rabbits than those in control group (P<0.01). CCK-8 pre-administration alleviated the changes induced by LPS, while Pro pre-administration aggravated those alterations. CONCLUSION: CCK-8 protects brain tissues against the injury induced by LPS, which may be associated with its effects of suppressing the overproduction of NO and free radicals.  相似文献   

14.
AIM:To observe the effects of taurine-zinc (TZC) on the learning and memory abilities of vascular dementia (VD) mice and to investigate the related mechanism. METHODS:The mice were randomly divided into model group, sham group, and TZC at 50 mg/kg, 100 mg/kg and 200 mg/kg groups. The mice in drug groups were given TZC by gavage at 10 mL/kg once daily. The mice in sham group and model group were given equal volume of distilled water. VD mice were established by intercepting both common carotid arteries and bleeding at caudal vein after 14 d of gavage. The levels of tumor necrosis factor-α (TNF-α) and interleukin-1β (IL-1β) were detected by ELISA. The levels of inducible nitric oxide synthase (iNOS) and nitric oxide (NO) were measured via spectrophotometer. Step-down test and Morris water maze test were used to examine the abilities of learning and memory in the mice. RESULTS:TZC at 50 mg/kg, 100 mg/kg and 200 mg/kg reduced the levels of TNF-α, IL-1β, iNOS and NO in the brain tissues. In the water maze test, TZC at 100 mg/kg and 200 mg/kg significantly decreased the error times and latency compared with model group. In the step-down test, the escape latency was prolonged and error times were lowered significantly by treatment with TZC at 50 mg/kg, 100 mg/kg and 200 mg/kg as compared with model group. CONCLUSION:TZC improves the abilities of learning and memory, which might be related to the reduction of TNF-α, IL-1β, iNOS and NO levels in VD mice.  相似文献   

15.
AIM: To explore the expression level of tristetraprolin (TTP) in rats after subarachnoid hemorrhage (SAH) as well as the potential role of TTP in the early brain injury (EBI) after SAH in rats.METHODS: In the first experiment setting, total 56 adult male SD rats were randomly divided into sham group and SAH group. The SAH model was performed by endovascular perforation. The brain tissues were taken out after SAH at 5 different time points (0, 12, 24, 48, 72 h and 1 week). The expression of TTP in the brain tissues was detected by Western blot. In the second experiment, a total of 60 SD rats were divided into 4 groups:sham group, SAH group, SAH+vector group and SAH+TPP group. Neurological score, brain water content and blood-brain barrier were evaluated at 48 h after SAH. TUNEL staining was performed to detect cell apoptosis in the rat brain tissue. ELISA method was used for quantitative detection of interleukin-6 (IL-6) and tumor necrosis factor-α (TNF-α). The protein levels of TTP, Bax, Bcl-2 and cleaved caspase-3 in the rat brain tissue were detected by Western blot.RESULTS: The protein expression of TTP in the brain was downregulated markedly from 12 h after SAH, reached the lowest level at 48 h, and then had an upward trend. After modeling for 48 h, Garcia neurological score was significantly reduced, and brain water content and Evans blue (EB) content of the brain tissue of the rats in SAH group were significantly higher than those in sham group (P<0.05). SAH induced significant increases in IL-6 and TNF-α levels in the brain tissue (P<0.05). The number of TUNEL-stained cells was increased in the subcortical brain region after SAH compared with sham group. In addition, a lower level of Bcl-2 and higher levels of Bax and cleaved caspase-3 in the rat brains were observed at 48 h after SAH. However, the neurological deficit score was significantly increased, and the brain water content and EB content in the rat brains were significantly reduced in SAH+TTP group in comparison with SAH+vector group (P<0.05). Over-expression of TTP dramatically suppressed the levels of IL-6 and TNF-α in the rat brains, and reduced the number of TUNEL positive cells. Furthermore, upregulation of TTP significantly decreased the levels of cleaved caspase-3 and Bax, and evidently enhanced the expression of Bcl-2 (P<0.01).CONCLUSION: The expression of TTP is significantly decreased in early period after SAH, and enhancing the level of TTP effectively inhibits EBI following SAH in rats.  相似文献   

16.
AIM:To observe the effects of angiopoietin 4 (Ang-4) on lipopolysaccharide (LPS)-induced injury of human umbilical vein endothelial cells (HUVECs). METHODS:The EnVision immunohistochemical method was used to identify the HUVECs. After pre-treated with different doses of Ang-4 for 0.5 h, HUVECs was exposed to LPS at concentration of 10 mg/L for 24 h. The cell viability was evaluated by MTT assay. The content of tumor necrosis factor-alpha (TNF-α) in the supernatant and the concentrations of intracellular and supernatant von Willebrand factor (vWF) were detected by ELISA. The mRNA levels of Toll-like receptor 4 (TLR4), NF-κB p65 and TNF-α were determined by real-time PCR. RESULTS:Factor Ⅷ in the cytoplasm was positive in the HUVECs.Compared with normal group, LPS reduced the cell viability (P<0.01), and significantly increased the secretion of TNF-α and vWF (P<0.01). The mRNA expression of TLR4, NF-κB p65 and TNF-α also increased (P<0.01). Ang-4 at concentration of 100 μg/L enhanced the cell viability (P<0.01), reduced the content of vWF and TNF-α, and inhibited the LPS-induced increases in the mRNA levels of TLR4, NF-κB p65 and TNF-α (P<0.01). CONCLUSION: Ang-4 antagonizes LPS-induced damage in HUVECs by inhibiting TLR4-NF-κB p65-TNF-α signaling pathways.  相似文献   

17.
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   

18.
AIM:To explore the therapeutic effect of Qishen-Yiqi dripping pills (QS) on atherosclerosis (AS) and the mechanism. METHODS:AS rat model was established by high-fat diet, and SD rats were randomly divided into normal control group, AS model group, low-dose, middle-dose and high-dose QS groups, and positive group (n=6 each). After administration for 12 weeks, serum samples were collected to detect the serum lipid and Ca2+ levels. HE staining was used evaluated the histopathological changes of arterial tissue. The serum levels of interleukin-1β (IL-1β), IL-6 and tumor necrosis factor-α (TNF-α) were measured by ELISA. The nitric oxide (NO) level was detected by nitrate reductase method. The protein levels of transient receptor potential channel protein 1 (TRPC1), stromal interaction molecule 1 (STIM1) and endothelial NO synthase (eNOS) were determined by Western blot. RESULTS:QS significantly reduced the arterial damage via inhibiting the formation of atherosclerotic plaque and attenuated intimal thickening and vascular stenosis. Compared with AS group, the serum levels of total cholesterol (TC), triglyceride (TG) and low-density lipoprotein cholesterol (LDL-C) were decreased significantly and the levels of high-density lipoprotein cholesterol (HDL-C) were increased significantly in high-dose QS group (P<0.05). The serum levels of IL-1β, IL-6 and TNF-α in high-dose QS group were lower than those in AS group (P<0.05). Compared with AS group, the serum Ca2+ level was lowered and the arterial tissue NO level was elevated in QS groups (P<0.05). Compared with AS rats, the protein levels of TRPC1 and STIM1 were decreased significantly and the protein level of eNOS was increased significantly in the rats treated with QS (P<0.05). CONCLUSION:QS regulate calcium homeostasis via TRPC1/STIM1 pathway, increase the production of NO and inhibit the inflammatory responses, thus exerting anti-AS effect.  相似文献   

19.
AIM: To study the effect of TNF-α on osteoporosis pain. METHODS: Forty female Sparague-Dawley rats, 5 months old, were either sham-operated (sham) or ovariectomized (Ovx), and assigned to sham group (n=16) and Ovx group (n=24). Pain behavioral tests with up-down method and tail withdrawal test were performed once a week beginning at 5th week after the operation. At 8th week after the operation, 8 rats in each group were sacrificed and the L5 dorsal root ganglions (DRG) were collected. The expression of TNF-α in L5 DRG was measured by immunofluorescence. The remaining rats in Ovx group were assigned to 2 subgroups: Ovx-1 and Ovx-2. The rats in Ovx-2 group were administered with thalidomide (an inhibitor of TNF-α synthesis, 50 mg/kg) once a day, while the animals in Ovx-1 group were given same volume of saline. Pain behavioral tests continued to be performed once a week until 10th week after operation. RESULTS: (1)The results of pain behavioral tests showed that the mechanical paw withdrawal threshold and heat tail withdrawal latency in Ovx group at 5th, 6th, 7th and 8th week after surgery were significantly lower than those in sham group (P<0.01). After administration with thalidomide, the mechanical paw withdrawal threshold and heat tail withdrawal latency in Ovx-2 group were restored to the level of sham group, and significantly higher than those in Ovx-1 group (P<0.05). (2)The expression of TNF-α in L5 DRG was significantly higher in Ovx group than that in sham group (P<0.01). CONCLUSION: TNF-α may play an important role in osteoporosis pain by inducing hyperalgesia through taking action on DRG. Inhibition of TNF-α synthesis may relieve menopause osteoporosis pain.  相似文献   

20.
AIM: To determine the effect of Radix Angelicae Sinensis(RAS) on renal ischemia/reperfusion injury in rabbits and to explore its mechanism. METHODS: Twenty-five rabbits were divided randomly into the sham operated group(Control group), renal ischemia/reperfusion injury group(IR group) and RAS+IR group. At the time point of reperfusion 48 h after renal ischemia 1 h, the renal tissue were observed by electron-microscope and the contents of creatinine(Cr) in serum, tumor necrosis factor-α(TNF-α), interleukin-6(IL-6)and basic fibroblast growth factor(bFGF) in the renal tissue were measured. RESULTS: A remarkably degenerative changes in renal tissue were showed under electronmicroscope in IR group, but the changes in RAS+IR group were slight. The contents of Cr, TNF-α and IL-6 in IR group were higher than those in Control group, these parameters in RAS+IR group were lower than those in IR group, the difference between these groups was significant(P< 0.05 or P< 0.01). At the same time, the content of bFGF in IR group was lower than that in Control group(P< 0.01), while the content of bFGF in RAS+IR group was higher than that in IR group(P< 0.01) and Control group(P< 0.05). CONCLUSION: RAS has an effect of alleviating the renal ischemia/reperfusion injury by modulating the production or release of TNF-α, IL-6 and bFGF.  相似文献   

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