Objective:To investigate the change of the hs-CRP,sVC AM-1,NT-proBNP levels of the patients with pregnancy-induced hypertension(PIH) syndrome.Methods:A total of 200 patients with PIH were divided into mild,moderate an...Objective:To investigate the change of the hs-CRP,sVC AM-1,NT-proBNP levels of the patients with pregnancy-induced hypertension(PIH) syndrome.Methods:A total of 200 patients with PIH were divided into mild,moderate and severe group,and 50 healthy pregnancy patients served as the control group.The serum sVCAM-1 levels were detected by enzyme-linked immunosorbent assay,hs-CRP were detected by immunity transmission turbidity,and NT-proBNP levels were determined by the colloidal gold method.Patients were treated with magnesium sulfate and nifudipine and the contrastive analysis was performed before and after treatment.And the pathological changes in placental of PIH patients were delected by hematoxylin-eosin staining at the same time.Results:The hs-CRP,sVCAM-l,NT-proBNP levels of patients in the mild, moderate and severe PHI group were significantly higher than that in the control group(P<0.05). The hs-CKP,sVCAM-l,NT-proBNP levels in the severe group were significantly higher than the mild group and the moderate group,the difference was statistically significant(P<0.05).The hsCRP,sVCAM-l,NT-proBNP of the moderate group were significantly higher than the mild group(P<0.05).There was a positive correlation between hs-CRP,sVCAM-1,NT-proBNP expression levels and the degree of the PIH.The expression of hs-CRP,sVCAM-1,NT-proBNP levels of the moderate and the severe group were significantly decreased(P<0.05).The number of placental villi and interstitial blood vessel in the moderate and severe PIH group were significantly less than the control group(P<0.05).Conclusions:The increased levels of serum hs-CRP,sVCAM-1, NT-proBNP may be involved in the process of vascular endothelial cell injury of the PIH,and the hs-CRP,sVCAM-1,NT-proBNP can be used as the auxiliary index for diagnosis of PIH and determination of PIH severity.展开更多
Background： Percutaneous coronary intervention （PCI） causes endothelial damage, resulting in an inflammatory response with elevation of markers such as high-sensitive C-reactive protein （hs-CRP） and vascular cell...Background： Percutaneous coronary intervention （PCI） causes endothelial damage, resulting in an inflammatory response with elevation of markers such as high-sensitive C-reactive protein （hs-CRP） and vascular cell adhesion molecule-1（VCAM-1）, which are associated with restenosis after PCI. Evidence suggests that microRNA-126 （miR-126） plays an important role in vascular inflammation, but its correlation with PCl-mediated inflammation has not been investigated. In this study, we investigated the effect of PCI on circulating miR-126 and inflammation markers such as hs-CRP and VCAM-1. Methods： We enrolled 130 patients with coronary artery disease （CAD） in the Second Hospital of Jilin University from October 2015 to December 2015. Among them, 82 patients with CAD, defined as at least one major epicardial vessel with 〉70% stenosis who planned to undergo PCI, were divided into acute coronary syndrome （ACS） group （46 patients） and stable angina （SA） group （36 patients）. Forty-eight patients confirmed by coronary angiography without PCI were used as controls. The plasmas of all patients were collected prior to PCI and at 30 min, 24 h, and 72 h after PCI. The plasma VCAM-1 and hs-CRP were detected by enzyme-linked immunosorbent assay, and the miR-126 was evaluated by quantitative reverse transcription-polymerase chain reaction. Results： Plasma concentrations of hs-CRP and VCAM-I in patients with either ACS （n = 46） or SA （n = 36） were significantly higher than in controls （n = 48） （P 〈 0.01） prior to PCI, and increased further at 24 h and 72 h after PCI, compared with prior PCI. Moreover, VCAM-1 was positively correlated with balloon time and pressure. In contrast, the plasma concentration of miR-126 was significantly lower in patients with CAD than in controls, and further decreased with time post-PCl. A negative correlation was observed between miR-126 and hs-CRP and VCAM-1 at 72 h after PCI. Conclusion： There was a negative correlation of miR-126 with the PCI-induced markers of inflammation such as hs-CRP and VCAM-1.展开更多
INTRODUCTIONMultiple organ dysfunction syndrome (MODS) isthought to be a frequent consequence of sepsis[1-3].Despite substantial advances in our knowledge and understanding of the basic pathophysiologic mechanisms[4-7...INTRODUCTIONMultiple organ dysfunction syndrome (MODS) isthought to be a frequent consequence of sepsis[1-3].Despite substantial advances in our knowledge and understanding of the basic pathophysiologic mechanisms[4-7], in critically ill patients infections and sepsis are still associated with a high mortality[8,9].展开更多
Pingyangmycin (bleomycin A5 hydrochloride,PYM) is one of the anti-neoplastic agents which have been commonly used to treat venous malformations.However,the underlying mechanism by which PYM treats venous malformations...Pingyangmycin (bleomycin A5 hydrochloride,PYM) is one of the anti-neoplastic agents which have been commonly used to treat venous malformations.However,the underlying mechanism by which PYM treats venous malformations remains poorly understood.It was reported that venous endothelial cells could recruit neutrophils via adhesion molecules (E-selectin,ICAM-1,ICAM-3,VCAM-1) during the acute/chronic inflammation and subsequent histological fibrosis after sclerotherapy with PYM.This study explored if the expression of E-selectin,ICAM-1,ICAM-3 and VCAM-1 in human venous malformation endothelial cells could be affected by PYM.HVMECs were cultured from human venous malformation tissue.Expressions of E-selectin,ICAM-1,ICAM-3 and VCAM-1 on HVMECs in response to PYM were analyzed by cell ELISA.The relative levels of mRNA expression in the cells were semi-quantified.The results showed that PYM up-regulated the expressions of E-selectin,ICAM-3,VCAM-1 and ICAM-1 in both time-and concentration-dependent manner.Our findings suggested that PYM could induce the expression of adhesion molecules in HVMECs,which might be a possible mechanism by which sclerotherapy by intralesional injection of PYM treats venous malformations.展开更多
CD151 is a member of the tetraspanin family that is implicated as a promoter of pathological or physiological angiogenesis. C-Met is expressed on a variety of cells including vascular endothelial cells（VECs） and up-...CD151 is a member of the tetraspanin family that is implicated as a promoter of pathological or physiological angiogenesis. C-Met is expressed on a variety of cells including vascular endothelial cells（VECs） and up-regulated during angiogenesis. In this study, we investigated whether CD151 regulated migration, proliferation, tube formation and angiogenesis of human umbilical VECs（HUVECs） with activation of C-Met. Moreover, we studied whether CD151 could affect the angiogenic molecules such as nitric oxide（NO）, vascular cell adhesion molecule-1（VCAM-1） and vascular endothelial growth factor（VEGF）. The expression of CD151 was determined by Western blotting. The cell proliferation assay was performed using the cell counting kit-8（CCK-8） method and cell migration was assessed in microchemotaxis chambers by using fetal bovine serum（FBS） as the chemotactic stimulus. The angiogenic molecules were evaluated using ELISA. The NO level was detected using NO detection kit. The potential involvement of various signaling pathways was explored using relevant antibodies. We found that proliferation, migration and tube formation of HUVECs were promoted by CD151 with activation of C-Met, FAK and CDC42, while they were suppressed with CD151 knockdown by RNAi. Similarly, the levels of NO, VCAM-1 and VEGF in HUVECs were increased by CD151, but they were inhibited with CD151 knockdown by RNAi. These data suggested that CD151 could promote migration, proliferation, tube formation and angiogenesis of HUVECs, which was possibly related to the C-Met signaling pathways.展开更多
Objective: To explore the hemostatic mechanism of Jianpi Yiqi Shexue decoction(JYSD) by regulating vascular factors in an immune thrombocytopenia(ITP) mouse model.Methods: An ITP mouse model was established by the pas...Objective: To explore the hemostatic mechanism of Jianpi Yiqi Shexue decoction(JYSD) by regulating vascular factors in an immune thrombocytopenia(ITP) mouse model.Methods: An ITP mouse model was established by the passive-immune modeling method, and interventional drugs used were prednisone tablets and JYSD. The platelet count;vascular activity-related factors v WF, VCAM-1, and TM;and VEGF and b FGF were used as observational indicators.Results: On the 8th day of administration, compared with the model group, platelet counts in the prednisone and JYSD groups increased(both P <.001). Compared with the control group, the levels of v WF, VCAM-1, and TM in the other groups were lower(all P <.05). The VCAM-1 level in the JYSD group was higher than that in the prednisone group(P =.012), but without significant difference compared with the model group(P =.051). The TM level in the JYSD group was the lowest(vs. the model group,P =.047;vs. the prednisone group, P =.006). Compared with the control group, the IOD values of VEGF and b FGF in the other three groups were lower(all P <.01). The IOD values of VEGF in the prednisone and JYSD groups were both higher than those in the model group(P =.002 and P <.001, respectively). The IOD values of b FGF among the model, prednisone, and JYSD groups were not statistically significant(P >.05).Conclusion: A vascular factor disorder is involved in the pathogenesis of ITP. JYSD can increase the platelet count, upregulate VEGF expression, and reduce the TM level. JYSD has the same effect as prednisone tablets in regulating platelet, v WF, VEGF, and b FGF, with a stronger effect in normalizing VCAM-1 and TM levels. The hemostatic mechanism of JYSD is closely related to the effective balance of vascular factors.展开更多
Background Intercellular adhesion molecule-1 (ICAM-1) and vascular cell adhesion molecule-1 (VCAM-1) are two important cytokines in inflammatory response, which may induce rolling and adhesion of both leukocytes and l...Background Intercellular adhesion molecule-1 (ICAM-1) and vascular cell adhesion molecule-1 (VCAM-1) are two important cytokines in inflammatory response, which may induce rolling and adhesion of both leukocytes and lymphocytes, while modulating vascular permeability at the same time. These adhesion molecules usually serve as surrogate markers of activation and injury of vascular endothelial cells. Tumor necrosis factor-α (TNF-α) is a key factor to induce the expression and production of the above cell adhesion molecules. However, it remains to be elucidated whether exogenous ubiquitin exerts any effect on the cytokines in sepsis-induced ALI. Methods Sixty mice were devided randomly into five groups with twelve mice in each group, i.e. CLP group, SHAM group, UB1 group (10 mg/kg), UB2 group (5 mg/kg) and UB3 group(1 mg/kg). Mice of SHAM group underwent sham operation, and other four groups underwent CLP. Six hours after surgery, mice of three UB groups received ubiquitin by caudal vein injection while CLP and SHAM group received vehicle. Seven hours after surgery, blood and lungs of all mice were collected. ICAM-1, VCAM-1 and TNF-α level of 9% lung homogenate and serum TNF-α level were measured by ELISA. Results Pulmonary ICAM-1, VCAM-1 and TNF-α level of three UB groups were lower than CLP and SHAM group, and there were several comparisons with a statistically significant difference. Serum TNF-α level of three UB groups were slightly lower than CLP group, but far higher than SHAM group. Pulmonary ICAM-1 level, VCAM-1 level and serum TNF-α level of UB3 group were lower than UB1 and UB2 group, and there was a significant difference in VCAM-1 between UB3 and UB1 group. Pulmonary TNF-α level of UB3 group was slightly higher than UB1 and UB2 group.展开更多
BACKGROUND： Nuclear factor-κB （NF-κB）, intercellular adhesion molecule-1 （ICAM-1）, and vascular cell adhesion molecule-1 （VCAM-1） in brain tissue can participate in inflammatory reactions after cerebral ische...BACKGROUND： Nuclear factor-κB （NF-κB）, intercellular adhesion molecule-1 （ICAM-1）, and vascular cell adhesion molecule-1 （VCAM-1） in brain tissue can participate in inflammatory reactions after cerebral ischemia. Acupuncture treatment for acute cerebral ischemia produces abnormal protein expression. OBJECTIVE： To investigate the effects of acupuncture on NF-KB, ICAM-1, and VCAM-1 mRNA and protein expression in the brain tissue of rats with cerebral ischemiaJreperfUsion injury. DESIGN, TIME AND SETTING： Randomized, controlled, animal experiments were performed at the Laboratory of Department of Neurosurgery, Xiangya Hospital, Central South University, China between December 2008 and October 2009. MATERIALS： Rabbit anti-NF-KB polyclonal antibody, rabbit anti-ICAM-1 polyclonal antibody, and rabbit anti-VCAM-1 polyclonal antibody were purchased from Santa Cruz Biotechnology, USA. METHODS： A total of 46 healthy, Sprague Dawley rats were randomly assigned to sham surgery （n= 10）, model （n = 12）, acupuncture pretreatment （n = 12）, and acupuncture intervention （n = 12） groups. Models of middle cerebral artery occlusion were established by right common carotid artery ligation. In the acupuncture pretreatment group, rats received acupuncture for 3 consecutive days, and then models were established. In the acupuncture intervention group, rats received acupuncture for 3 consecutive days at Waiguan （SJ 5）, Sanyinjiao （SP 6）, and Dazhui （DU 14） acupoints following model establishment. MAIN OUTCOME MEASURES： Somatosensory asymmetry and forelimb use asymmetry were tested, as well as NF-KB, ICAM-1, and VCAM-1 mRNA and protein expression in the frontal and parietal cortex at 4, 12, 24, 48 and 72 hours following cerebral ischemia/reperfusion injury. RESULTS： Acupuncture improved neurological function and significantly decreased NF-KB, ICAM-1, and VCAM-1 mRNA and protein expression in the frontal and parietal cortex of rats with cerebral ischemia/reperfusion injury （P 〈 0.05）. CONCLUSION： Acupuncture can improve neurological function, potentially via inhibition of NF-κB, ICAM,I, and VCAM-1 mRNA and protein expression in the frontal and parietal cortex of rats with cerebral ischemia/reperfusion injury.展开更多
文摘Objective:To investigate the change of the hs-CRP,sVC AM-1,NT-proBNP levels of the patients with pregnancy-induced hypertension(PIH) syndrome.Methods:A total of 200 patients with PIH were divided into mild,moderate and severe group,and 50 healthy pregnancy patients served as the control group.The serum sVCAM-1 levels were detected by enzyme-linked immunosorbent assay,hs-CRP were detected by immunity transmission turbidity,and NT-proBNP levels were determined by the colloidal gold method.Patients were treated with magnesium sulfate and nifudipine and the contrastive analysis was performed before and after treatment.And the pathological changes in placental of PIH patients were delected by hematoxylin-eosin staining at the same time.Results:The hs-CRP,sVCAM-l,NT-proBNP levels of patients in the mild, moderate and severe PHI group were significantly higher than that in the control group(P<0.05). The hs-CKP,sVCAM-l,NT-proBNP levels in the severe group were significantly higher than the mild group and the moderate group,the difference was statistically significant(P<0.05).The hsCRP,sVCAM-l,NT-proBNP of the moderate group were significantly higher than the mild group(P<0.05).There was a positive correlation between hs-CRP,sVCAM-1,NT-proBNP expression levels and the degree of the PIH.The expression of hs-CRP,sVCAM-1,NT-proBNP levels of the moderate and the severe group were significantly decreased(P<0.05).The number of placental villi and interstitial blood vessel in the moderate and severe PIH group were significantly less than the control group(P<0.05).Conclusions:The increased levels of serum hs-CRP,sVCAM-1, NT-proBNP may be involved in the process of vascular endothelial cell injury of the PIH,and the hs-CRP,sVCAM-1,NT-proBNP can be used as the auxiliary index for diagnosis of PIH and determination of PIH severity.
基金This study was supported by grants from the National Natural Science Foundation of China （No. 81470024）, the Development and Reform Commission of Jilin Province （No. 2013C023）, and the Doctoral Fund of Ministry of Education of China （No. 2013061120051）.
文摘Background： Percutaneous coronary intervention （PCI） causes endothelial damage, resulting in an inflammatory response with elevation of markers such as high-sensitive C-reactive protein （hs-CRP） and vascular cell adhesion molecule-1（VCAM-1）, which are associated with restenosis after PCI. Evidence suggests that microRNA-126 （miR-126） plays an important role in vascular inflammation, but its correlation with PCl-mediated inflammation has not been investigated. In this study, we investigated the effect of PCI on circulating miR-126 and inflammation markers such as hs-CRP and VCAM-1. Methods： We enrolled 130 patients with coronary artery disease （CAD） in the Second Hospital of Jilin University from October 2015 to December 2015. Among them, 82 patients with CAD, defined as at least one major epicardial vessel with 〉70% stenosis who planned to undergo PCI, were divided into acute coronary syndrome （ACS） group （46 patients） and stable angina （SA） group （36 patients）. Forty-eight patients confirmed by coronary angiography without PCI were used as controls. The plasmas of all patients were collected prior to PCI and at 30 min, 24 h, and 72 h after PCI. The plasma VCAM-1 and hs-CRP were detected by enzyme-linked immunosorbent assay, and the miR-126 was evaluated by quantitative reverse transcription-polymerase chain reaction. Results： Plasma concentrations of hs-CRP and VCAM-I in patients with either ACS （n = 46） or SA （n = 36） were significantly higher than in controls （n = 48） （P 〈 0.01） prior to PCI, and increased further at 24 h and 72 h after PCI, compared with prior PCI. Moreover, VCAM-1 was positively correlated with balloon time and pressure. In contrast, the plasma concentration of miR-126 was significantly lower in patients with CAD than in controls, and further decreased with time post-PCl. A negative correlation was observed between miR-126 and hs-CRP and VCAM-1 at 72 h after PCI. Conclusion： There was a negative correlation of miR-126 with the PCI-induced markers of inflammation such as hs-CRP and VCAM-1.
基金Supported by the National Natural Science Foundation of China, No. 39870796
文摘INTRODUCTIONMultiple organ dysfunction syndrome (MODS) isthought to be a frequent consequence of sepsis[1-3].Despite substantial advances in our knowledge and understanding of the basic pathophysiologic mechanisms[4-7], in critically ill patients infections and sepsis are still associated with a high mortality[8,9].
基金supported by the Natural Science Foundation of Hubei province,China (No.2010CDB07907)
文摘Pingyangmycin (bleomycin A5 hydrochloride,PYM) is one of the anti-neoplastic agents which have been commonly used to treat venous malformations.However,the underlying mechanism by which PYM treats venous malformations remains poorly understood.It was reported that venous endothelial cells could recruit neutrophils via adhesion molecules (E-selectin,ICAM-1,ICAM-3,VCAM-1) during the acute/chronic inflammation and subsequent histological fibrosis after sclerotherapy with PYM.This study explored if the expression of E-selectin,ICAM-1,ICAM-3 and VCAM-1 in human venous malformation endothelial cells could be affected by PYM.HVMECs were cultured from human venous malformation tissue.Expressions of E-selectin,ICAM-1,ICAM-3 and VCAM-1 on HVMECs in response to PYM were analyzed by cell ELISA.The relative levels of mRNA expression in the cells were semi-quantified.The results showed that PYM up-regulated the expressions of E-selectin,ICAM-3,VCAM-1 and ICAM-1 in both time-and concentration-dependent manner.Our findings suggested that PYM could induce the expression of adhesion molecules in HVMECs,which might be a possible mechanism by which sclerotherapy by intralesional injection of PYM treats venous malformations.
基金supported by the National Natural Science Foundation of China(No.81000047)Hubei Natural Science Foundation(No.2014CFB437)
文摘CD151 is a member of the tetraspanin family that is implicated as a promoter of pathological or physiological angiogenesis. C-Met is expressed on a variety of cells including vascular endothelial cells（VECs） and up-regulated during angiogenesis. In this study, we investigated whether CD151 regulated migration, proliferation, tube formation and angiogenesis of human umbilical VECs（HUVECs） with activation of C-Met. Moreover, we studied whether CD151 could affect the angiogenic molecules such as nitric oxide（NO）, vascular cell adhesion molecule-1（VCAM-1） and vascular endothelial growth factor（VEGF）. The expression of CD151 was determined by Western blotting. The cell proliferation assay was performed using the cell counting kit-8（CCK-8） method and cell migration was assessed in microchemotaxis chambers by using fetal bovine serum（FBS） as the chemotactic stimulus. The angiogenic molecules were evaluated using ELISA. The NO level was detected using NO detection kit. The potential involvement of various signaling pathways was explored using relevant antibodies. We found that proliferation, migration and tube formation of HUVECs were promoted by CD151 with activation of C-Met, FAK and CDC42, while they were suppressed with CD151 knockdown by RNAi. Similarly, the levels of NO, VCAM-1 and VEGF in HUVECs were increased by CD151, but they were inhibited with CD151 knockdown by RNAi. These data suggested that CD151 could promote migration, proliferation, tube formation and angiogenesis of HUVECs, which was possibly related to the C-Met signaling pathways.
基金supported by the National Basic Research Program of China (973 Program, 2013CB531705)the National Natural Science Foundation Youth Project of China(81703903 and 81803904)
文摘Objective: To explore the hemostatic mechanism of Jianpi Yiqi Shexue decoction(JYSD) by regulating vascular factors in an immune thrombocytopenia(ITP) mouse model.Methods: An ITP mouse model was established by the passive-immune modeling method, and interventional drugs used were prednisone tablets and JYSD. The platelet count;vascular activity-related factors v WF, VCAM-1, and TM;and VEGF and b FGF were used as observational indicators.Results: On the 8th day of administration, compared with the model group, platelet counts in the prednisone and JYSD groups increased(both P <.001). Compared with the control group, the levels of v WF, VCAM-1, and TM in the other groups were lower(all P <.05). The VCAM-1 level in the JYSD group was higher than that in the prednisone group(P =.012), but without significant difference compared with the model group(P =.051). The TM level in the JYSD group was the lowest(vs. the model group,P =.047;vs. the prednisone group, P =.006). Compared with the control group, the IOD values of VEGF and b FGF in the other three groups were lower(all P <.01). The IOD values of VEGF in the prednisone and JYSD groups were both higher than those in the model group(P =.002 and P <.001, respectively). The IOD values of b FGF among the model, prednisone, and JYSD groups were not statistically significant(P >.05).Conclusion: A vascular factor disorder is involved in the pathogenesis of ITP. JYSD can increase the platelet count, upregulate VEGF expression, and reduce the TM level. JYSD has the same effect as prednisone tablets in regulating platelet, v WF, VEGF, and b FGF, with a stronger effect in normalizing VCAM-1 and TM levels. The hemostatic mechanism of JYSD is closely related to the effective balance of vascular factors.
文摘Background Intercellular adhesion molecule-1 (ICAM-1) and vascular cell adhesion molecule-1 (VCAM-1) are two important cytokines in inflammatory response, which may induce rolling and adhesion of both leukocytes and lymphocytes, while modulating vascular permeability at the same time. These adhesion molecules usually serve as surrogate markers of activation and injury of vascular endothelial cells. Tumor necrosis factor-α (TNF-α) is a key factor to induce the expression and production of the above cell adhesion molecules. However, it remains to be elucidated whether exogenous ubiquitin exerts any effect on the cytokines in sepsis-induced ALI. Methods Sixty mice were devided randomly into five groups with twelve mice in each group, i.e. CLP group, SHAM group, UB1 group (10 mg/kg), UB2 group (5 mg/kg) and UB3 group(1 mg/kg). Mice of SHAM group underwent sham operation, and other four groups underwent CLP. Six hours after surgery, mice of three UB groups received ubiquitin by caudal vein injection while CLP and SHAM group received vehicle. Seven hours after surgery, blood and lungs of all mice were collected. ICAM-1, VCAM-1 and TNF-α level of 9% lung homogenate and serum TNF-α level were measured by ELISA. Results Pulmonary ICAM-1, VCAM-1 and TNF-α level of three UB groups were lower than CLP and SHAM group, and there were several comparisons with a statistically significant difference. Serum TNF-α level of three UB groups were slightly lower than CLP group, but far higher than SHAM group. Pulmonary ICAM-1 level, VCAM-1 level and serum TNF-α level of UB3 group were lower than UB1 and UB2 group, and there was a significant difference in VCAM-1 between UB3 and UB1 group. Pulmonary TNF-α level of UB3 group was slightly higher than UB1 and UB2 group.
基金the National Natural Science Foundation of China,No.30472115,30500644the Natural Science Foundation of Hunan Province,No.07JJ5019
文摘BACKGROUND： Nuclear factor-κB （NF-κB）, intercellular adhesion molecule-1 （ICAM-1）, and vascular cell adhesion molecule-1 （VCAM-1） in brain tissue can participate in inflammatory reactions after cerebral ischemia. Acupuncture treatment for acute cerebral ischemia produces abnormal protein expression. OBJECTIVE： To investigate the effects of acupuncture on NF-KB, ICAM-1, and VCAM-1 mRNA and protein expression in the brain tissue of rats with cerebral ischemiaJreperfUsion injury. DESIGN, TIME AND SETTING： Randomized, controlled, animal experiments were performed at the Laboratory of Department of Neurosurgery, Xiangya Hospital, Central South University, China between December 2008 and October 2009. MATERIALS： Rabbit anti-NF-KB polyclonal antibody, rabbit anti-ICAM-1 polyclonal antibody, and rabbit anti-VCAM-1 polyclonal antibody were purchased from Santa Cruz Biotechnology, USA. METHODS： A total of 46 healthy, Sprague Dawley rats were randomly assigned to sham surgery （n= 10）, model （n = 12）, acupuncture pretreatment （n = 12）, and acupuncture intervention （n = 12） groups. Models of middle cerebral artery occlusion were established by right common carotid artery ligation. In the acupuncture pretreatment group, rats received acupuncture for 3 consecutive days, and then models were established. In the acupuncture intervention group, rats received acupuncture for 3 consecutive days at Waiguan （SJ 5）, Sanyinjiao （SP 6）, and Dazhui （DU 14） acupoints following model establishment. MAIN OUTCOME MEASURES： Somatosensory asymmetry and forelimb use asymmetry were tested, as well as NF-KB, ICAM-1, and VCAM-1 mRNA and protein expression in the frontal and parietal cortex at 4, 12, 24, 48 and 72 hours following cerebral ischemia/reperfusion injury. RESULTS： Acupuncture improved neurological function and significantly decreased NF-KB, ICAM-1, and VCAM-1 mRNA and protein expression in the frontal and parietal cortex of rats with cerebral ischemia/reperfusion injury （P 〈 0.05）. CONCLUSION： Acupuncture can improve neurological function, potentially via inhibition of NF-κB, ICAM,I, and VCAM-1 mRNA and protein expression in the frontal and parietal cortex of rats with cerebral ischemia/reperfusion injury.
