2005•Zhongguo redai yixueRequires access

Effect of pentoxifylline on inflammatory reaction of rats with global cerebral ischemia-reperfusion

Liu De-hon

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Abstract

Objective To explore the protective effects of pentoxifylline (PTX) on rats with global cerebral ischemia-reperfusion. Methods The model of global cerebral ischemia-reperfusion was established by four-vessel occlusion method using immunohistochemical technique, in situ hybridization and in situ end labeling technique (TUNEL), the expressions of NF-κB and TNF-α mRNA and the number of the apoptotic cell were examined in the sham-operated group (group A), the control group (the group after global cerebral ischemia-reperfusion treated with Saline, group B) and the group treated with PTX (the group after global cerebral ischemia-reperfusion treated with PTX, group C) separately. Results Compared with group A, the expressions of NF-κB and TNF-α mRNA in group B increased significantly (P0.01), with a peak at 6h and 12h respectively. As the time of reperfusion was prolonged, the number of apoptotic cell gradually increased (P0.01). Compared with group B, the expressions of NF-κB and TNF-α mRNA and the number of apoptotic cell in group C decreased (P0.01). Conclusion PTX may down-regulate the expressions of NF-κB and TNF-α mRNA after global cerebral ischemia-reperfusion. It inhibited the inflammatory reaction and attenuated cellular apoptosis.

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What this paper is about

Objective To explore the protective effects of pentoxifylline (PTX) on rats with global cerebral ischemia-reperfusion. Methods The model of global cerebral ischemia-reperfusion was established by four-vessel occlusion method using immunohistochemical technique, in situ hybridization and in situ end labeling technique (TUNEL), the expressions of NF-κB and TNF-α mRNA and the number of the apoptotic cell were examined in the sham-operated group (group A), the control group (the group after global cerebral ischemia-reperfusion treated with Saline, group B) and the group treated with PTX (the group after global cerebral ischemia-reperfusion treated with PTX, group C) separately. Results Compared with group A, the expressions of NF-κB and TNF-α mRNA in group B increased significantly (P0.01), with a peak at 6h and 12h respectively. As the time of reperfusion was prolonged, the number of apoptotic cell gradually increased (P0.01). Compared with group B, the expressions of NF-κB and TNF-α mRNA and the number of apoptotic cell in group C decreased (P0.01). Conclusion PTX may down-regulate the expressions of NF-κB and TNF-α mRNA after global cerebral ischemia-reperfusion. It inhibited the inflammatory reaction and attenuated cellular apoptosis.

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Available abstract

Objective To explore the protective effects of pentoxifylline (PTX) on rats with global cerebral ischemia-reperfusion. Methods The model of global cerebral ischemia-reperfusion was established by four-vessel occlusion method using immunohistochemical technique, in situ hybridization and in situ end labeling technique (TUNEL), the expressions of NF-κB and TNF-α mRNA and the number of the apoptotic cell were examined in the sham-operated group (group A), the control group (the group after global cerebral ischemia-reperfusion treated with Saline, group B) and the group treated with PTX (the group after global cerebral ischemia-reperfusion treated with PTX, group C) separately. Results Compared with group A, the expressions of NF-κB and TNF-α mRNA in group B increased significantly (P0.01), with a peak at 6h and 12h respectively. As the time of reperfusion was prolonged, the number of apoptotic cell gradually increased (P0.01). Compared with group B, the expressions of NF-κB and TNF-α mRNA and the number of apoptotic cell in group C decreased (P0.01). Conclusion PTX may down-regulate the expressions of NF-κB and TNF-α mRNA after global cerebral ischemia-reperfusion. It inhibited the inflammatory reaction and attenuated cellular apoptosis.

Key concepts: Pentoxifylline, Ischemia, Apoptosis, In situ hybridization, Medicine, Reperfusion injury, TUNEL assay, Messenger RNA

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