2010年2月
Cholinergic agonist physostigmine suppresses excessive superoxide anion radical generation in blood, oxidative stress, early inflammation, and endothelial injury in rats with forebrain ischemia/reperfusion
BRAIN RESEARCH
- 巻
- 1313
- 号
- 開始ページ
- 242
- 終了ページ
- 249
- 記述言語
- 英語
- 掲載種別
- 研究論文(学術雑誌)
- DOI
- 10.1016/j.brainres.2009.11.077
- 出版者・発行元
- ELSEVIER SCIENCE BV
The cholinergic anti-inflammatory pathway is reportedly important in modulating the inflammatory response in local and systemic diseases, including ischemia/reperfusion pathophysiology. in this study, we investigated the effects of the cholinergic agonist, physostigmine, on jugular venous superoxide radical (O-2(-)center dot) generation, oxidative stress, early inflammation, and endothelial activation during forebrain ischemia/reperfusion (FBI/R) in rats. Fourteen male Wistar rat were allocated to the control group (n=7) or physostigmine group (n=7). The physostigmine group received 80 ng/g physostigmine intraperitoneally 24h and 1 h before forebrain ischemia was established. The jugular venous O-2(-)center dot current was measured for 10 min during forebrain ischemia and for 120 min after reperfusion. The O-2(-)center dot current increased gradually during forebrain ischemia in both groups. The current increased markedly immediately after reperfusion in the control group but was significantly attenuated in the physostigmine group after reperfusion. Brain and plasma malondialdehyde, high-mobility group box 1 (HMGB1) protein, and intercellular adhesion molecule 1 (ICAM1) were significantly attenuated in the physostigmine group compared with the control group, except for brain HMGB1. The amount of O-2(-)center dot generated during FBI/R correlated with malondialdehyde, HMGB1, and ICAM1 in both the brain and plasma. in conclusion, the cholinergic agonist physostigmine suppressed jugular venous O-2(-)center dot
- リンク情報
- ID情報
-
- DOI : 10.1016/j.brainres.2009.11.077
- ISSN : 0006-8993
- eISSN : 1872-6240
- Web of Science ID : WOS:000274869100024