2005Journal of Jilin University ofRequires access

Effect of propofol on expression of TGF-β_1 in cerebral cortexduring transient focal cerebral ischemia-reperfusion in rats

Feng Chun-sheng

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Abstract

Objective To investigate the effect of propofol on the expression of TGF-β1 in cerebral cortex during focal cerebral ischemia-reperfusion in rats. Methods The focal cerebral ischemia-reperfusion model was established by thread embolism of middle cerebral artery. Forty-five male Wistar rats were randomly allocated to sham-operation group (n=5), ischemia-reperfusion group (n=20) and propofol group (n=20), rats were subjected to 2 h of focal ischemia by left middle cerebral artery occlusion and then reperfused. At 3, 6, 24, and 72 h after reperfusion the rats were decapitated, the expressions of TGF-β1 in ischemic cortex were tested by immunohistochemical method. At 24 h after reperfusion, scores of neurological deficit were estimated and the change of histomorphology in ischemic cortex was observed under the light microscope by using HE staining. Results The expression of TGF-β1 increased significantly after focal cerebral ischemia-reperfusion, reached to maximal expression at 24 h after reperfusion (P0.01), and decreased to normal at 72 h after reperfusion. The scores of neurological deficit in rats increased significantly. The followings were observed in histomorphology: congestion and edema in ischemic cortex, degeneration and necrosis of neuron. Expression of TGF-β1 in propofol group increased significantly than that in ischemia-reperfusion group (P0.05). The scores of neurological deficit and the damage of histomorphology in ischemic cortex lowered than that in propofol group. Conclusion The results show that propofol can stimulate the expression of TGF-β_1 to produce neuroprotection.

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Objective To investigate the effect of propofol on the expression of TGF-β1 in cerebral cortex during focal cerebral ischemia-reperfusion in rats. Methods The focal cerebral ischemia-reperfusion model was established by thread embolism of middle cerebral artery. Forty-five male Wistar rats were randomly allocated to sham-operation group (n=5), ischemia-reperfusion group (n=20) and propofol group (n=20), rats were subjected to 2 h of focal ischemia by left middle cerebral artery occlusion and then reperfused. At 3, 6, 24, and 72 h after reperfusion the rats were decapitated, the expressions of TGF-β1 in ischemic cortex were tested by immunohistochemical method. At 24 h after reperfusion, scores of neurological deficit were estimated and the change of histomorphology in ischemic cortex was observed under the light microscope by using HE staining. Results The expression of TGF-β1 increased significantly after focal cerebral ischemia-reperfusion, reached to maximal expression at 24 h after reperfusion (P0.01), and decreased to normal at 72 h after reperfusion. The scores of neurological deficit in rats increased significantly. The followings were observed in histomorphology: congestion and edema in ischemic cortex, degeneration and necrosis of neuron. Expression of TGF-β1 in propofol group increased significantly than that in ischemia-reperfusion group (P0.05). The scores of neurological deficit and the damage of histomorphology in ischemic cortex lowered than that in propofol group. Conclusion The results show that propofol can stimulate the expression of TGF-β_1 to produce neuroprotection.

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Available abstract

Objective To investigate the effect of propofol on the expression of TGF-β1 in cerebral cortex during focal cerebral ischemia-reperfusion in rats. Methods The focal cerebral ischemia-reperfusion model was established by thread embolism of middle cerebral artery. Forty-five male Wistar rats were randomly allocated to sham-operation group (n=5), ischemia-reperfusion group (n=20) and propofol group (n=20), rats were subjected to 2 h of focal ischemia by left middle cerebral artery occlusion and then reperfused. At 3, 6, 24, and 72 h after reperfusion the rats were decapitated, the expressions of TGF-β1 in ischemic cortex were tested by immunohistochemical method. At 24 h after reperfusion, scores of neurological deficit were estimated and the change of histomorphology in ischemic cortex was observed under the light microscope by using HE staining. Results The expression of TGF-β1 increased significantly after focal cerebral ischemia-reperfusion, reached to maximal expression at 24 h after reperfusion (P0.01), and decreased to normal at 72 h after reperfusion. The scores of neurological deficit in rats increased significantly. The followings were observed in histomorphology: congestion and edema in ischemic cortex, degeneration and necrosis of neuron. Expression of TGF-β1 in propofol group increased significantly than that in ischemia-reperfusion group (P0.05). The scores of neurological deficit and the damage of histomorphology in ischemic cortex lowered than that in propofol group. Conclusion The results show that propofol can stimulate the expression of TGF-β_1 to produce neuroprotection.

Key concepts: Ischemia, Medicine, Propofol, Neuroprotection, Anesthesia, Cerebral cortex, Reperfusion injury, Cortex (anatomy)

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