Electroacupuncture attenuates cerebral hypoxia and neuronal apoptosis induced by cerebral ischemia/reperfusion injury.To further identify the involved mechanisms,we assumed that electroacupuncture used to treat cerebr...Electroacupuncture attenuates cerebral hypoxia and neuronal apoptosis induced by cerebral ischemia/reperfusion injury.To further identify the involved mechanisms,we assumed that electroacupuncture used to treat cerebral ischemia/reperfusion injury was associated with the p38 mitogen-activated protein kinase（MAPK） signaling pathway.We established rat models of cerebral ischemia/reperfusion injury using the modified Zea-Longa＇s method.At 30 minutes before model establishment,p38 MAPK blocker SB20358 was injected into the left lateral ventricles.At 1.5 hours after model establishment,electroacupuncture was administered at acupoints of Chize（LU5）,Hegu（LI4）,Zusanli（ST36）,and Sanyinjiao（SP6） for 20 minutes in the affected side.Results showed that the combination of EA and SB20358 injection significantly decreased neurologic impairment scores,but no significant differences were determined among different interventional groups.Hematoxylin-eosin staining also showed reduced brain tissue injuries.Compared with the SB20358 group,the cells were regularly arranged,the structures were complete,and the number of viable neurons was higher in the SB20358 ＋ electroacupuncture group.Terminal deoxynucleotidyl transferase（Td T）-mediated d UTP nick-end labeling assay showed a decreased apoptotic index in each group,with a significant decrease in the SB20358 ＋ electroacupuncture group.Immunohistochemistry revealed reduced phosphorylated p38 expression at 3 days in the electroacupuncture group and SB20358 ＋ electroacupuncture group compared with the ischemia/reperfusion group.There was no significant difference in phosphorylated p38 expression between the ischemia/reperfusion group and SB20358 group.These findings confirmed that the electroacupuncture effects on mitigating cerebral ischemia/reperfusion injury are possibly associated with the p38 MAPK signaling pathway.A time period of 3 days could promote the repair of ischemic cerebral nerves.展开更多
BACKGROUND： Several studies have shown that midkine directly participates in tumor cell growth and invasion, as well as the regulation of angiogenesis. OBJECTIVE： To investigate midkine expression in meningioma tiss...BACKGROUND： Several studies have shown that midkine directly participates in tumor cell growth and invasion, as well as the regulation of angiogenesis. OBJECTIVE： To investigate midkine expression in meningioma tissue in relation to angiogenesis, invasion, peritumoral edema, and clinicopathology. DESIGN, TIME AND SETTING： The present clinical, case-controlled, neuropathological study was performed at the Laboratory of Molecular Organism, People＇s Hospital of Deyang City between May 2007 and April 2008. MATERIALS： Fifty-two meningioma tissues were classified by WHO tumor classification of the central nervous system, comprising 40 grade Ⅰ meningioma, five grade Ⅱ meningioma, and seven grade Ⅲ meningioma. Ten normal, human cerebral maters were selected from cerebral trauma patients. METHODS： Midkine protein expression and mean microvessel density were detected using immunohistochemical techniques. Simultaneously, all data were statistically analyzed. MAIN OUTCOME MEASURES： Midkine expression and microvessel density in meningiomas and normal cerebral maters. RESULTS： The positive midkine expression rate was 64% in the meningioma tissues. However, midkine expression was not detected in normal cerebral mater tissue. The mean microvessel density was 82.0 ± 22.7 in the meningiomas, and 25.8± 6.2 in the normal cerebral mater tissues. There was significant difference in midkine expression and mean microvessel density between meningioma tissues and human cerebral maters （P 〈 0.05）. Midkine expression positively correlated with microvessel density （r = 0.756, P 〈 0.05）. Midkine expression did not correlate to patient age, gender, or tumor size, location, and shape （P 〉 0.05）. However, it closely correlated with patient clinical condition, pathological grade, invasion, and peritumoral edema （r = 0.3785,0.741 2,0.6518, 0.614 2, P 〈 0.05）. CONCLUSION： Midkine protein was overexpressed in meningiomas and correlated to tumor angiogenesis, invasion, pefitumoral edema, and clinicopathology.展开更多
基金supported by the National Natural Science Foundation of China,No.81173355
文摘Electroacupuncture attenuates cerebral hypoxia and neuronal apoptosis induced by cerebral ischemia/reperfusion injury.To further identify the involved mechanisms,we assumed that electroacupuncture used to treat cerebral ischemia/reperfusion injury was associated with the p38 mitogen-activated protein kinase（MAPK） signaling pathway.We established rat models of cerebral ischemia/reperfusion injury using the modified Zea-Longa＇s method.At 30 minutes before model establishment,p38 MAPK blocker SB20358 was injected into the left lateral ventricles.At 1.5 hours after model establishment,electroacupuncture was administered at acupoints of Chize（LU5）,Hegu（LI4）,Zusanli（ST36）,and Sanyinjiao（SP6） for 20 minutes in the affected side.Results showed that the combination of EA and SB20358 injection significantly decreased neurologic impairment scores,but no significant differences were determined among different interventional groups.Hematoxylin-eosin staining also showed reduced brain tissue injuries.Compared with the SB20358 group,the cells were regularly arranged,the structures were complete,and the number of viable neurons was higher in the SB20358 ＋ electroacupuncture group.Terminal deoxynucleotidyl transferase（Td T）-mediated d UTP nick-end labeling assay showed a decreased apoptotic index in each group,with a significant decrease in the SB20358 ＋ electroacupuncture group.Immunohistochemistry revealed reduced phosphorylated p38 expression at 3 days in the electroacupuncture group and SB20358 ＋ electroacupuncture group compared with the ischemia/reperfusion group.There was no significant difference in phosphorylated p38 expression between the ischemia/reperfusion group and SB20358 group.These findings confirmed that the electroacupuncture effects on mitigating cerebral ischemia/reperfusion injury are possibly associated with the p38 MAPK signaling pathway.A time period of 3 days could promote the repair of ischemic cerebral nerves.
文摘BACKGROUND： Several studies have shown that midkine directly participates in tumor cell growth and invasion, as well as the regulation of angiogenesis. OBJECTIVE： To investigate midkine expression in meningioma tissue in relation to angiogenesis, invasion, peritumoral edema, and clinicopathology. DESIGN, TIME AND SETTING： The present clinical, case-controlled, neuropathological study was performed at the Laboratory of Molecular Organism, People＇s Hospital of Deyang City between May 2007 and April 2008. MATERIALS： Fifty-two meningioma tissues were classified by WHO tumor classification of the central nervous system, comprising 40 grade Ⅰ meningioma, five grade Ⅱ meningioma, and seven grade Ⅲ meningioma. Ten normal, human cerebral maters were selected from cerebral trauma patients. METHODS： Midkine protein expression and mean microvessel density were detected using immunohistochemical techniques. Simultaneously, all data were statistically analyzed. MAIN OUTCOME MEASURES： Midkine expression and microvessel density in meningiomas and normal cerebral maters. RESULTS： The positive midkine expression rate was 64% in the meningioma tissues. However, midkine expression was not detected in normal cerebral mater tissue. The mean microvessel density was 82.0 ± 22.7 in the meningiomas, and 25.8± 6.2 in the normal cerebral mater tissues. There was significant difference in midkine expression and mean microvessel density between meningioma tissues and human cerebral maters （P 〈 0.05）. Midkine expression positively correlated with microvessel density （r = 0.756, P 〈 0.05）. Midkine expression did not correlate to patient age, gender, or tumor size, location, and shape （P 〉 0.05）. However, it closely correlated with patient clinical condition, pathological grade, invasion, and peritumoral edema （r = 0.3785,0.741 2,0.6518, 0.614 2, P 〈 0.05）. CONCLUSION： Midkine protein was overexpressed in meningiomas and correlated to tumor angiogenesis, invasion, pefitumoral edema, and clinicopathology.
