首页 | 本学科首页   官方微博 | 高级检索  
相似文献
 共查询到20条相似文献，搜索用时 31 毫秒
1.
AIM:To investigate effects of factors derived from activated macrophages on survival of retinal ganglion cells (RGCs) after optic nerve crush. METHODS:Adult Wistar rats were randomly divided into normal control, crush control, medium treatment and zymosan treatment groups. All the rats were retrogradly by injecting fluorogold into superior colliculi of both sides. Partial optic nerve injury model was induced in the left eyes by a special designed optic nerve clip with 40 gram power for 9 seconds at optic nerve 2 mm behind the eyeball except for normal control group. The numbers of the labeled RGCs in each group were counted. RESULTS:The numbers of RGCs in crush group was 92.6%, 82.9%, 72.6% and 57.6% of normal controls on the third, 7th, 15th and 21th day, respectively. In the group with zymosan injection, the number of RGCs were much higher than that in controls on the third, 7th, 15th and 21th day (P<0.01). CONCLUSION:Intravitreal injection of zymosan activates macrophages. Macrophages-derived factors might protect RGCs after optic nerve crush and improve their survival.  相似文献   

2.
AIM: In order to understand the pathological changes, characteristic of degeneration in optic nerve and retina after strike of optic nerve. METHODS: According to methods of Allen's spinal injury, a 600gcm-strike power was put on the intraocular portion of the optic nerve and created a striking injury on optic nerve. After a survival interval of 48 h, 1 week, 2 weeks, 4 weeks, 3 months, the animal's optic nerves and retinas were collected and fixed for morphological examination. RESULTS: Forty-eight hours after nerve injuries, the optic nerves were slight enlargement and vacuolation. In 1 week, the optic nerve began to degenerate in injured part and the glia cell had proliferated, but the forms of retinal ganglion cells(RGCs) were normal. In 2 weeks, the vacuolation and focal necrosis were appeared between nerve fiber. The number of RGCs began to decrease. Condensed nuclei presented in the retina. In three month, the diameter of the optic nerve decreased in injury part and collo-scar was formed. The phenomenon mentioned above was more obviously. The internal nuclear neurons and outer nuclear neurons appeared rare. The thickness of retina decreased. The number of RGCs began to decrease in 48 hours and progressed thereafter. It decreased about 3.35%, 13.23%, 19.74%, 23.20%, 29.28% in 48 h, 1 week, 2 weeks, 1 month, 3 months compared with the number of normal RGCs. RGCs began to apoptosis in 48 h. CONCLUSION: The model in this experiment could make definite uncompleted optic nerve and retina injuries. The degree of neuron injuries decreased from RGC, internal nuclear neurons to outer nuclear neurons. The number of RGCs began to decrease in 48 hours, and most quickly periods from 48 hours to one week.  相似文献   

3.
AIM: To evaluate the effect of senegenin (Sen) on H2O2-treated retinal ganglion cells (RGCs) and to explore its underlying mechanisms. METHODS: RGCs were retrograde labeled by injection of fluorogold into the superior colliculi of SD rats on the postnatal day 3. On the postnatal days 6 to 8, the retinas were dissociated with papain and cultured. Primary RGCs cultured in vitro were treated with H2O2 and/or various doses of Sen. The viability of RGCs was evaluated by counting the fluorescence-labeled neurons under microscope. The morphological changes of the nuclei in the retinal neurons were observed by Hoechst 33258 staining. Western blotting was applied to determine the expression of cleaved caspase-3, cytochrome C and Bcl-2 in cultured retinal neurons. RESULTS: Compared with the control cells, Sen at doses of 10, 20 or 40 μmol/L had no toxicity to RGCs (P>0.05). However, Sen at doses of 80 and 160 μmol/L had significant toxicity to RGCs (P<0.01). Compared with H2O2-injured group, Sen at doses of 10, 20 and 40 μmol/L effectively protected against H2O2-induced injury in RGCs (P<0.05) with the best efficiency at 40 μmol/L. Hoechst 33258 staining showed that the neuronal apoptosis caused by H2O2 was reduced by Sen. The results of Western blotting showed an up-regulation of Bcl-2, and decreased cytochrome C and cleaved caspase-3 levels by Sen in H2O2-treated retinal neurons. CONCLUSION: Sen is able to protect RGCs from H2O2-induced injury by enhancing Bcl-2 expression and inhibiting cell apoptosis.  相似文献   

4.
会讯     
AIM:To investigate the pulmonary expresson of macrophage migration inhibitory factor(MIF) in acute lung injury (ALI) rats induced by intravenous injection of oleic acid and its correlation with blood gas change, pulmonary weight index (PWI) and pulmonary pathological injuries.METHODS: ALI rats model were made by injecting oleic acid as the oleic acid group while rats injection with saline solution as control. After injecting oleic acid or saline for six hours, the PaO2 and PaCO2 of the left heart and pulmonary weight index were measured. At the same time, by using a microwave-base double immunohistochemistry labeling, the number of MIF＋, ED1+ (anti-CD68 antibody), ED1+/MIF＋cell in pulmonary tissue of different groups and their correlation with blood gas and pulmonary weight index were examined. RESULTS: The blood gas parameters of the oleic acid group were far worse than that of the control group (P＜0.01). The PWI of the oleic acid group was significantly higher than that of the control group (P＜0.01). There was marked upregulation of MIF expression on injured lung tissue. The number of cell expressed MIF＋ , ED1+ and MIF with ED1 showed a strong positive correlation with PaO2, PWI and histological changes. CONCLUSION: MIF may play a pivotal role in mediation of progressive lung injuries induced by intravenous oleic acid injection. In addition, the number of cells expressed MIF, especially macrophage, may reflect the severity of lung injury.  相似文献   

5.
AIM: To investigate the role of mitochondrial calcium uniporter (MCU) in bupivacaine (B)-induced spinal cord injury in diabetic (D) rats.METHODS: Healthy male Sprague-Dawley rats, weighing 180~220 g, were divided into normal rats and diabetic rats. After intraperitoneal injection of streptozotocin for building diabetic rat mo-del, 48 male rats were randomly divided into 6 groups with 8 rats in each group as following:control (C) group (normal rats by intrathecal injection of normal saline), D group (diabetic rats by intrathecal injection of normal saline), C+B group (normal rats by intrathecal injection of bupivacaine), D+B group (diabetic rats by intrathecal injection of bupivacaine), D+R1+B group (diabetic rats by intrathecal injection of 10 μmol/L Ru360 and bupivacaine) and D+R2+B group (diabetic rats by intrathecal injection of 50 μmol/L Ru360 and bupivacaine). The changes of paw withdrawal mechanical threshold (PWMT) and paw withdrawal thermal latency (PWTL) were measured before modeling, after modeling, and 12 h, 24 h and 48 h after intrathecal injection. Lumbar enlargement was removed from spinal cord after rats were killed. MCU expression was tested by RT-qPCR and Western bolt. The levels of malondialdehyde (MDA) and 8-hydroxydeoxyguanosine (8-OHdG) were determined by ELISA. Spinal neuronal apoptosis was measured using TUNEL assay.RESULTS: Compared with D group, the expression of MCU, the values of PWMT and PWTL, the levels of MDA and 8-OHdG, and the apoptotic rate of spinal cord neurons were significantly increased in D+B group (P<0.05). Compared with D+B group, the expression of MCU, the values of PWMT and PWTL, the levels of MDA and 8-OHdG, and the apoptotic rate of spinal cord neurons were significantly decreased in D+R2+B group (P<0.05).CONCLUSION: Bupivacaine enhances oxidative stress and aggravates spinal cord injury via up-regulating MCU activity in diabetic rats.  相似文献   

6.
AIM: To investigate the differentiation of neural stem cells (NSCs) after transplanted into vitreous and the effects on the regeneration of retina ganglion cells (RGCs) after optic nerve microcrushed.METHODS: After optic nerve microcrushed in adult rat,2×104/2 μL NSCs or 2 μL 0.1 mol/L PBS was injected into vitreous.Animals were divided into control group (MC group,MC+PBS group) and experiment group (MC+NSCs).Animals in each group were allowed to survive for 3,4,5 weeks,respectively.The regenerating RGCs were labeled retrogradely with granular blue,and the numbers of regenerating RGCs in each retina were observed under fluorescent microscope.In addition after 5 animals in MC+NSCs group survived for 4 weeks,rat eyeballs were removed and prepared as freezing microtome sections for observing the migration of NSCs and NF,GFAP,CNP immumodetection.RESULTS: Compared the mean numbers of regenerating RGCs between experiment group and control group at 3,4,5 weeks,the difference was significant (P<0.01).NSCs expressed NF,GFAP and CNP at 4 weeks and were not found to incorporate into retina.CONCLUSION: It suggests that NSCs enhance the RGCs regeneration after ON microcrushed and differentiate into neurons,astrocytes and oligodendrocytes.  相似文献   

7.
  相似文献   

8.
AIM: To study the change of electrophysiological property of dorsal root ganglion (DRG) C-type primary sensory neurons with sialic acid on the membrane surface after rat sciatic nerve injury. METHODS: The operation to induce chronic constriction nerve injury (CCI) for establishing CCI pain model was performed in the rats, and normal rats served as controls. The thermal hyperalgesia behavior was observed to select CCI pain rats, and electrophysiological property of injured and normal C-type neurons was studied by intracellular recording. Ca2+ and neuraminidase (NA) were topically added on the extracellular membrane of C-type neurons to counteract or selectively remove the negatively charged sialic acid residues, and at the same time the change of electrophysiological property was observed. RESULTS: The rest potential (RP) of injured C-type neurons shifted to depolarizing direction. The incidence of evoked action potential (AP) was higher, and the rheobase to evoke AP was lower than the control. After topical application of Ca2+ and NA on injured C-type neurons, hyperpolarized RP and increased rheobase to evoke AP were observed, indicating the excitability of injured C-type neurons diminished. However, these treatments to normal neurons had no effect on electrophysiological property. CONCLUSION: Increased negative charge on the injured C-type neuron surface, carried by the sialic acid residues, contributes to the change of electrophysiological property.  相似文献   

9.
AIM:To study the apoptotic effect of TNFα on rat pulmonary microvascular endothelial cells(PMVEC)and the role of Fas, NF-κB in its mechanism. METHODS: Apoptosis of PMVEC was analyzed and quantitated with TUNEL, flow cytometer. Northern blot was applied to assess the influence of TNFα on PMVEC Fas expression. Fas antibody was used to investigate the apoptotic effect of Fas on PMVEC. Activation of caspase-8 was examined by Western blot. Expression of caspase-3 was analyzed with histo-immunochemical staining. RESULTS:Growth curve showed that TNFα suppressed endothelial cell proliferation in a dose-dependent manner. After treatment with 5×106U/LTNFα, apoptotic rate was 14.0%±3.1% detected with TUNEL, and 13.1% with flow cytometer. When the cells were co-cultured with TNFα and APDC, an NF-κB inhibitor, less cells were viable and more cells were positively stained with TUNEL. Fas expression in PMVEC was elevated after TNFα treatment. Co-culturing with Anti-Fas antibody aggravated PMVEC apoptosis. Caspase-8 activity and caspase-3 expression was elevated. Caspase-3 inhibitor significantly ameliorated PMVEC apoptosis. CONCLUSION: Large dose of TNFα(5×106U/L) can induce apoptosis in rat PMVEC. NF-κB has an anti-apoptotic effect in PMVEC. TNFα up-regulates Fas expression in PMVEC, and the latter takes a part in apoptosis. Caspase-8 and caspase-3 are involved in PMVEC apoptosis induced by TNFα.  相似文献   

10.
AIM: To investigate the role of endoplasmic reticulum (ES) stress in cardiomyocyte apoptosis induced by β1-adrenoceptor autoantibody (β1-AA). METHODS: The rat model of active immunization with the second extracellular loop of β1-adrenoceptor was established, and SA-ELISA was applied to detect the level of β1-AA in serum of actively immunized rats. The apoptosis of cardiomyocytes was detected by TUNEL staining, and the protein expression levels of glucose-regulated protein 78 (GRP78), C/EBP homologous protein (CHOP) and caspase-12 in rat heart tissues were determined by Western blot and immunohistochemistry. After purified β1-AA obtained by affinity chromatography was used to treat H9c2 myocardial cells, the cell viability was measured by CCK-8 assay and the apoptosis was analyzed by flow cytometry with Annexin V-FITC/PI double staining. The H9c2 cells were treated with ER stress inhibitor 4-phenoxybutyric acid (4-PBA) before interfered with β1-AA, and the changes of cell viability and apoptosis were determined by CCK-8 assay and flow cytometry. RESULTS: Compared with vehicle group, the level of β1-AA in the serum of rats was significantly increased after active immunization for 2 weeks and further rised in 8 weeks, and increased apoptosis was observed in cardiomyocytes after active immunization for 2 weeks, lasting till 8 weeks. Compared with vehicle group, the protein expression of GRP78, CHOP and caspase-12 increased after active immunization for 4 weeks and 8 weeks. Continuous reduction of cell viability and increased apoptosis of H9c2 cells were induced by β1-AA. ER stress inhibitor 4-PBA pretreatment in H9c2 cells reversed the increased apoptosis and decreased cell viability induced by β1-AA, indicating that suppression of ER stress effectively reduced cardiomyocyte apoptosis. CONCLUSION: β1-AA induces increased apoptosis in cardiomyocytes by activating ER stress.  相似文献   

11.
AIM: To clarify whether sulforaphane (SF) has protective effects on retina neuronal cells in diabetic rats and to identify the related mechanisms involved in this process. METHODS: The diabetic rat model was induced by single intraperitoneal injection of streptozotocin (STZ). The protective effects of SF were evaluated by measuring the generation of reactive oxygen species (ROS), detecting apoptosis of retina neuronal cells with TUNEL staining and counting the survival retinal ganglion cells (RGCs). The nuclear translocation of nuclear factor E2-related factor 2 (Nrf2) and the protein expression of heme oxygenase-1 (HO-1) were examined by immunofluorescence analysis and Western blot. RESULTS: SF treatment significantly attenuated ROS generation, decreased the apoptosis of retina neuronal cells and increased the numbers of survival RGCs in the diabetic rats. Meanwhile, SF significantly increased the nuclear accumulation of Nrf2 and the protein level of HO-1 in the retinas of diabetic rats. However, HO-1 inhibitor, protoporphyrin IX zinc (Ⅱ) diminished the inhibitory effects of SF on RGCs apoptosis. CONCLUSION: SF partially exerts the beneficial neuroprotective effects via the activation of the Nrf2/HO-1 antioxidant pathway, therefore alleviating retinal oxidative stress and decreasing the apoptosis of retina neuronal cells.  相似文献   

12.
LI Jiang  HU Shen-jiang 《园艺学报》2010,26(10):1928-1931
  相似文献   

13.
AIM: To investigate the effects of integrin-linked kinase (ILK) overexpression on survival and proliferation of cardiac c-Kit+ cells, and the role of ILK-overexpressing c-Kit+ cell transplantation in cardiac function in a rat myocardial infarction (MI) model.METHODS: Cardiac c-Kit+ cells were isolated from the hearts of neonatal Sprague-Dawley (SD) rats and cultured to prepare the ILK-c-Kit+ cells by infected with recombinant adenoviral vector harboring human wild-type ILK cDNA. The survival and proliferation of cardiac c-Kit+ cells were detected by cell counting and CCK-8 assay at 48 h after infection, respectively. The protein levels of cyclin D1 and proliferating cell nuclear antigen (PCNA) in the cardiac c-Kit+ cells were examined by Western blot. MI was induced by coronary artery ligation in 40 adult rats. After 15 min, ILK-c-Kit+ cells were transplanted into the hearts by myocardial injection at 3 different sites in the infracted zone and border zone. All rats were randomly divided into 4 groups:sham group, MI plus saline injection group (MI group), MI plus null vector-infected cardiac c-Kit+ cell injection group (Ad-null-c-Kit+ cell group), and MI plus ILK-overexpressing cardiac c-Kit+ cells injection group (ILK-c-Kit+ cell group), with 10 rats in each group. At 2 weeks after MI, the protein levels of c-Kit in MI hearts were investigated by immunohistochemical assay. At 4 weeks, left ventricular function was examined by hemodynamic measurement.RESULTS: The survival and proliferation of cardiac c-Kit+ cells and the protein levels of cyclin D1 and PCNA were enhanced by ILK overexpression compared with Ad-null group. In MI rat model, the number of c-Kit+ cells was increased by ILK-c-Kit+ cell injection compared with Ad-null-c-Kit+ cell group at 2 weeks after MI. Cardiac function was significantly improved in ILK-c-Kit+ cell-transplanted rats.CONCLUSION: ILK overexpression improves survival and proliferation of cardiac c-Kit+ cells by increasing the protein levels of cyclin D1 and PCNA. ILK-c-Kit+ cell transplantation enhances the therapeutic efficiency of cardiac c-Kit+ cells in the post-MI hearts of rats.  相似文献   

14.
AIM: To determine whether triptolide induce apoptosis of synovial cells in collagen-induced arthritis (CIA) in rats. METHODS: The male Wistar rats were used to make CIA models by immunized with Bovine collagen Ⅱ (BCⅡ) in Freund's complete adjuvant (FCA). A total of 20 CIA rats were randomly divided into 2 groups, triptolide group (10 rats) and CIA control group (10 rats). Triptolide group were administered with triptolide at 40 μg/kg body weight intramuscularly every three days. CIA control group and another 10 age-matched normal rats were given normal saline instead. The rats were sacrificed on the 31st day after the triptolide administration. The pieces of synovium of the rat knee joints were harvested. The synovium was examined by HE staining and electron microscope. The apoptosis was tested by TUNEL and flow cytometer. RESULTS: The earlier phase of apoptotic synoviocytes were observed under the electron microscope. The flow cytometry showed that the percentage of the apoptotic cells was (3.98±1.16)% in the triptolide group, (1.83±0.82)% in the CIA control group, and (0.87±0.24)% in the normal group (P<0.01: triptolide vs control group). While the percentage of the cells in DNA synthesis phase was (3.3±1.2)% in the triptolide group, (8.0±1.4)% in the CIA control group, and (3.4±0.7)% in the normal group. There is significantly different in the apoptosis changes between the triptolide group and the CIA control group (P<0.01: triptolide vs CIA control group). The TUNEL labeling demonstrated that the percentage of the apoptotic cells was (4.5±1.0)% in the triptolide group, (2.2±1.0)% in the CIA control group, and (1.0±0.4)% in the normal group. The difference of apoptotic rate between the triptolide group and the CIA control group is significant (P<0.01). CONCLUSION: This study demonstrates that triptolide can induce apoptosis in CIA rats, which may be one of the mechanisms that triptolide treats the rheumatoid arthritis.  相似文献   

15.
AIM: To investigate the role of autophagy inhibitor 3-methyladenine(3-MA) in the injury of U251 glioma cells induced by H2O2. METHODS: The following groups in this study were set up: control group, 10 mmol/L 3-MA group, 1 mmol/L H2O2 group and 1 mmol/L H2O2 +10 mmol/L 3-MA group. The viability of U251 cells in each group was detected by MTT assay. Autophagic vacuoles in the cells were observed by staining with MDC. The cells were stained with Hoechst 33342 to determine the chromatin condensation. Cell apoptotic ratio was measured by flow cytometry analysis. RESULTS: Compared with control group, no effect of 3-MA on the viability of U251 cells was observed. In H2O2 group, the cell viability decreased and cell apoptotic ratio increased.The autophagic vacuoles and nuclear chromatin condensation in the cells were also detected. Compared with H2O2 group, addition of 3-MA inhibited the increase in autophagic vacuoles but exacerbated the apoptosis. CONCLUSION: Autophagy inhibitor 3-MA inhibits autophagy partially, but exacerbates apoptosis in U251 cells, indicating that autophagy exerts protective effect in the process of injury in U251 cells induced by H2O2.  相似文献   

16.
AIM: To explore the effects of rhynchophylline (RHL) on rat renal injury induced by adriamycin. METHODS: Fifty-two female SD rats were randomly divided into normal saline group (NSG, n=10), model group (MG, n=14), low-dose RHL treatment group (RHL-LG, n=14) and high-dose RHL treatment group (RHL-HG, n=14). The animals in the latter 3 groups were injected with adriamycin at a dose of 5 mg/kg through the tail vein. The animals in RHL-LG and RHL-HG were treated with RHL at doses of 5 mg/kg and 15 mg/kg, respectively, by intraperitoneal injection for 8 weeks. The animals in NSG and MG were treated with normal saline only. Urine and blood samples were collected to detect the urine protein, blood urea nitrogen (BUN) and serum creatinine (SCr). The renal tissues of the animals were collected for detection of malondialdehyde (MDA) content, superoxide dismutase (SOD) activity, pathological changes and mRNA expression of angiotension Ⅱreceptors 1,2 (AT1,2-R), angiotensin-converting enzyme (ACE) and angiotensinogen (AGT). RESULTS: The urine protein, BUN and SCr in RHL-LG were significantly lower than those in MG, but higher than those in RHL-HG (P<0.05). The SOD activity in MG was significantly lower than that in RHL-LG in the renal tissues. The SOD activity in RHL-LG was significantly lower than that in RHL-HG (P<0.05), but the content of MDA was on the contrary. The renal pathological damages in RHL-LG were weaker than that in MG, and that in RHL-HG were weaker than that in RHL-LG. The mRNA expression of AT1-R, ACE and AGT in MG was significantly higher than that in RHL-LG in the renal tissues, and that in RHL-LG was higher than that in RHL-HG (P<0.05). The mRNA expression of AT2-R in MG was significantly lower than that in RHL-LG, and that in RHL-LG was significantly lower than that in RHL-HG (P<0.05). CONCLUSION: RHL reduces adriamycin-induced renal injury in rats by attenuating the injury of lipid peroxidation in renal tissue, regulating the mRNA expression of AT1, 2-R, ACE and AGT, and increasing renal blood flow.  相似文献   

17.
AIM: To investigate the effects of nitric oxide (NO) and NO synthase (NOS) inhibitor NG-nitro-L arginine (L-NA) on LPS induced-lung injury in rats. METHODS: Forty healthy male SD rats, weighing 300±20 g, were used. The animals were anesthetized with 20% urethane 1 g·kg-1. Common carotid artery (CAA) and jugular vein were exposed through a median incision in the neck. Mean arterial pressure (MAP) was measured through a pressure transducer connected with intubation of CAA. The animals were randomly divided into five groups: group 1: control; group 2: LPS (5 mg·kg-1, iv); group 3: high dose L-NA (20 mg·kg-1 intraperitoneal injection, ip); gropu 4: middle dose L-NA (10 mg·kg-1, ip); group 5: low dose L-NA (5 mg·kg-1, ip). Group1 : 0.9% saline solution was given and the animals were killed 6 h after the saline solution. Gruop 2: saline solution was given 3 h after LPS and the animals were killed 3 h after administration. Group 3, 4 and 5: L-NA was given 3 h after LPS iv and the animals were killed 3 h after administration, respectively. The pulmonary was removed immediately. The pulmonary coefficient and water content in pulmonary tissue were calculated (%). The NO2-/NO3- content in plasma, MDA content and NOS, SOD activity in the pulmonary tissue were measured. RESULTS: L-NA significantly decreased pulmonary coefficient and water content in pulmonary tissue and ameliorated LPS induced lung injury. The effect in high dose group was better than that in low dose group. L-NA significantly decreased NO2-/NO3- content in plasm, decreased MDA content and inhibited NOS activity and enhanced SOD activity in the pulmonary tissue. CONCLUSION: It may be concluded that L-NA has a beneficial effect on lung injury induced by LPS.  相似文献   

18.
AIM: To investigate the role of infiltration of macrophages and expression of intracellular adhesion molecule-1 in the pathogenesis of oleic-acid-induced acute lung injury rats. METHODS:The rats were subjected to injection of oleic acid (oleic acid group) or saline solution (control). After injecting oleic acid or saline for 4 hours, the PaO2 of the left heart, lung permeability index(LPI), the number of macrophage and the levels of soluble intercellular molecule-1 (sICAM-1) in the bronchial alveolar lavage fluid (BALF) were measured. The levels of expression of ICAM-1 mRNA were evaluated by in situ hybridization and the degree of macrophage infiltration and the expression of ICAM-1 were evaluated by double staining immunocytochemistry. RESULTS:The PaO2 of the oleic acid group was significantly lower than that of the control group (P＜0.01) and the LPI of the oleic acid group was significantly higher than that of the control group (P＜0.01). The cell number of macrophage and sICAM-1 level were significantly higher in the oleic acid group than those of the control group (P＜0.01). There were marked upregulation of ICAM-1 mRNA expression in injuried lung tissue compared with the normal lung tissue. Furthermore, the infiltrated number of macrophage and the level of ICAM-1 expression showed strong positive correlation with the lung injury parameters, PaO2 and LPI.CONCLUSION:The infiltration of macrophage may play a pivotal role in the pathogenesis of progressive lung injuries induced by intravenous oleic acid injection,ICAM-1 may mediate the infiltrat ion and adhesion of macrophage in the injuried lung t issue and contribute to the development of acute lung injury.  相似文献   

19.
AIM:To observe the dynamic expression of cannabinoid receptor type 1 (CB1 receptor) in peri-pheral injured area during pain and to explore whether activation of CB1 receptor is regulated by potassium channel. METHODS:A mouse model of chronic constriction injury (CCI) was established to observe the changes of pain behavior by von Frey and Hargreaves tests. Western blot was used to detect the dynamic changes of CB1 receptor. The discharge frequency of sciatic nerve single fiber was recorded to investigate whether CB1 receptor activation was regulated by potassium channel. RESULTS:With the decrease in the pain threshold, the expression of CB1 receptor in the area of sciatic nerve injury was increased, and injection of CB1 receptor agonist HU210 in the area of peripheral injury had a significant analgesic effect. However, after injection of CB1 receptor antagonist AM281 or potassium channel non-specific blocker tetraethylammonium (TEA) for 20 min, the analgesic effect of the HU210 injection disappeared. The perfusion of HU210 in the injured area significantly reduced the spontaneous ectopic discharge frequency of the injured nerve fibers, but the early perfusion of AM281 or TEA suppressed this effect. CONCLUSION:The analgesic effect of CB1 receptor is mediated by potassium channel.  相似文献   

20.
AIM: To dynamically observe the protective effect of magnesium on the brain with ischemia and reperfusion injury in the middle cerebral artery occlusion (MCAO) rat model using the device of laser Doppler flowmetry (LDF) .METHODS: Twenty-four Sprague-Dawley male rats (280-300 g) were used to establish MCAO model with the conventional line-embolism method.The rats were divided into 4 groups according to the initial time of peritoneal injection of magnesium sulfate (MgSO4).The rats in MgSO4 groups were treated with 25% MgSO4 at 160 mg/kg at time points of 20 min, 30 min and 40 min after ischemia.The rats in control group were treated with the same volume of normal saline.The real-time fluctuation of the local cerebral blood flow (CBF) was dynamically monitored by LDF.The degree of nervous functional defect was evaluated by calculating the neurological impairment score of the rats after suffered from 2 h ischemia and followed with 24 h reperfusion.All the rats were killed with an end breaking method, and the volumes of brain infarction were evaluated by TTC staining at the brain slices obtained by autopsy.RESULTS: The fluctuating features in 3 MgSO4 treatment groups were as follows: when reperfusion began, the local CBF appeared and increased smoothly, then approached to its baseline step by step, and kept at the stable level in the whole reperfusion period.The CBF in control group fluctuated sharply in the whole reperfusion period associated with the heart beating, which was significantly different from those in MgSO4 treatment groups.The average volume of brain infarction in MgSO4 treatment groups was 26.5%, 36.5% and 24.5%, respectively, and was 54.0% in control group.The local nervous defect scores in MgSO4 treatment groups were 5.670±1.003, 8.670±1.211 and 7.170±1.472, respectively, and was 11.170±0.983 in control group.CONCLUSION: Vasomotor functional improvement might be one of the protective mechanisms of magnesium on the brain with cerebral ischemia and reperfusion injury in acute ischemic stroke.  相似文献   

设为首页 | 免责声明 | 关于勤云 | 加入收藏

Copyright©北京勤云科技发展有限公司  京ICP备09084417号