BACKGROUND： Cerebral ischemia/reperfusion injury has been shown to induce inflammatory reactions, including white blood cell activation and adhesion molecule expression. These reactions often lead to aggravated neuro...BACKGROUND： Cerebral ischemia/reperfusion injury has been shown to induce inflammatory reactions, including white blood cell activation and adhesion molecule expression. These reactions often lead to aggravated neuronal injury. OBJECTIVE： To observe corticocerebral pathology, as well as ultrastructural changes, in a rat model of focal cerebral ischemia/reperfusion injury through optical and electron microscopy, and to investigate interventional effects of ＂Xingnao Kaiqiao＂ acupuncture （a brain-activating and orifice-opening acupuncture method）. DESIGN, TIME AND SETTING： A randomized, controlled, neuropathology, animal experiment was performed at the Laboratory of Molecular Biology, First Affiliated Hospital of Tianjin University of Traditional Chinese Medicine between April and June 2004. MATERIALS： A total of 50 healthy, male, Wistar rats were randomized into 5 groups, with 10 rats per group： control, sham-operated, model, non-acupoint, and ＂Xingnao Kaiqiao ＂. Transmission electron microscope （TEM 400ST） was provided by Philips, Netherlands. Electro-acupuncture treatment apparatus （KWD-8082） was provided by Changzhou Wujin Great Wall Medical Instrument, China. METHODS： Focal cerebral ischemia/reperfusion injury was induced by occlusion of the middle cerebral artery in the model, non-acupoint, and ＂Xingnao Kaiqiao＂ groups. Rats from the control group did not undergo any treatment. The sham-operated group received identical experimental procedures as the model group, except that the nylon suture was not inserted into the right internal carotid artery. At 1, 3, 6, and 12 hours following focal cerebral ischemia/reperfusion injury induction, rats from the Xingnao Kaiqiao group underwent 1-minute acupuncture at the bilateral ＂Neiguan＂ （PC 6） acupoint, using a reducing method of lifting-thrusting and twirling-rotating. Subsequently, the rats were subjected to acupuncture at the ＂Renzhong＂ （DU26） acupoint 10 times by a heavy bird-pecking method. The non-acupoint group received acupuncture administration at the bilateral costal region. MAIN OUTCOME MEASURES： After ischemia for 1 hour and reperfusion for 24 hours, corticocerebral morphology and ultrastructural changes were observed on the injured side through the use of optical and electron microscopy. RESULTS： Cerebral ischemia/reperfusion resulted in damage to neurons, glial cells, and capillary vessels in the rat brain. ＂Xingnao Kaiqiao＂ acupuncture produced superior curative effects when it was performed 3 hours after cerebral ischemia/reperfusion induction, resulting in slightly recovered neuronal structures, alleviated cellular interstitial edema, and more capillary vessels. At each corresponding time point, the ＂Xingnao Kaiqiao＂ group exhibited improved neuronal structure and cellular interstitial edema, compared with the non-acupoint group. CONCLUSION： ＂Xingnao Kaiqiao＂ acupuncture results in protective effects on corticocerebral neuronal morphology and ultrastructure in rats following focal cerebral ischemia/reperfusion.展开更多
文摘BACKGROUND： Cerebral ischemia/reperfusion injury has been shown to induce inflammatory reactions, including white blood cell activation and adhesion molecule expression. These reactions often lead to aggravated neuronal injury. OBJECTIVE： To observe corticocerebral pathology, as well as ultrastructural changes, in a rat model of focal cerebral ischemia/reperfusion injury through optical and electron microscopy, and to investigate interventional effects of ＂Xingnao Kaiqiao＂ acupuncture （a brain-activating and orifice-opening acupuncture method）. DESIGN, TIME AND SETTING： A randomized, controlled, neuropathology, animal experiment was performed at the Laboratory of Molecular Biology, First Affiliated Hospital of Tianjin University of Traditional Chinese Medicine between April and June 2004. MATERIALS： A total of 50 healthy, male, Wistar rats were randomized into 5 groups, with 10 rats per group： control, sham-operated, model, non-acupoint, and ＂Xingnao Kaiqiao ＂. Transmission electron microscope （TEM 400ST） was provided by Philips, Netherlands. Electro-acupuncture treatment apparatus （KWD-8082） was provided by Changzhou Wujin Great Wall Medical Instrument, China. METHODS： Focal cerebral ischemia/reperfusion injury was induced by occlusion of the middle cerebral artery in the model, non-acupoint, and ＂Xingnao Kaiqiao＂ groups. Rats from the control group did not undergo any treatment. The sham-operated group received identical experimental procedures as the model group, except that the nylon suture was not inserted into the right internal carotid artery. At 1, 3, 6, and 12 hours following focal cerebral ischemia/reperfusion injury induction, rats from the Xingnao Kaiqiao group underwent 1-minute acupuncture at the bilateral ＂Neiguan＂ （PC 6） acupoint, using a reducing method of lifting-thrusting and twirling-rotating. Subsequently, the rats were subjected to acupuncture at the ＂Renzhong＂ （DU26） acupoint 10 times by a heavy bird-pecking method. The non-acupoint group received acupuncture administration at the bilateral costal region. MAIN OUTCOME MEASURES： After ischemia for 1 hour and reperfusion for 24 hours, corticocerebral morphology and ultrastructural changes were observed on the injured side through the use of optical and electron microscopy. RESULTS： Cerebral ischemia/reperfusion resulted in damage to neurons, glial cells, and capillary vessels in the rat brain. ＂Xingnao Kaiqiao＂ acupuncture produced superior curative effects when it was performed 3 hours after cerebral ischemia/reperfusion induction, resulting in slightly recovered neuronal structures, alleviated cellular interstitial edema, and more capillary vessels. At each corresponding time point, the ＂Xingnao Kaiqiao＂ group exhibited improved neuronal structure and cellular interstitial edema, compared with the non-acupoint group. CONCLUSION： ＂Xingnao Kaiqiao＂ acupuncture results in protective effects on corticocerebral neuronal morphology and ultrastructure in rats following focal cerebral ischemia/reperfusion.
