Elevation of jugular venous superoxide anion radical is associated with early inflammation, oxidative stress, and endothelial injury in forebrain ischemia–reperfusion rats

详细信息    查看全文

• 作者：Hiromi Shinagawa Aki ; Motoki Fujita ; Susumu Yamashita ; Kenji Fujimoto ; Kazumi Kumagai ; Ryosuke Tsuruta ; Shunji Kasaoka ; Tetsuya Aoki ; Masahiro Nanba ; Hidenori Murata ; Makoto Yuasa ; Ikuro Maruyama ; Tsu
• 关键词：Forebrain ischemia ; Reperfusion ; Electrochemical sensor ; Superoxide anion radical ; Malondialdehyde ; High-mobility group box 1 (HMGB1) ; Intercellular adhesion molecule 1 (ICAM-1)
• 刊名：Brain Research
• 出版年：2009
• 出版时间：25 September 2009
• 年：2009
• 卷：1292
• 期：Complete
• 页码：180-190
• 全文大小：766 K

文摘

A novel electrochemical sensor was used in this study to determine the correlations between jugular venous O₂⁻ and HMGB1, malondialdehyde (MDA), and intercellular adhesion molecule-1 (ICAM-1) in rats with forebrain ischemia/reperfusion (FBI/R). Twenty-one male rats were divided into a Sham group, a hemorrhagic shock/reperfusion (HS/R) group, and a forebrain ischemia/reperfusion (FBI/R) group. The O₂⁻ sensor in the jugular vein detected the current derived from O₂⁻ generation (abbreviated as “O₂⁻ current”), which was integrated as the partial value of quantified electricity during ischemia (Q_I) and after reperfusion (Q_R). The plasma O₂⁻ current showed a gradual increase during forebrain ischemia in the HS/R and the FBI/R groups. The current showed a marked increase immediately after reperfusion and continued for more than 60 min in the FBI/R group. In the HS/R group, the current was gradually attenuated to the baseline level. Brain and plasma HMGB1 increased significantly in the FBI/R group compared with those in the Sham and the HS/R groups, and both brain and plasma HMGB1 correlated significantly with the sum of Q_I and Q_R (total Q). Brain and plasma MDA and plasma soluble ICAM-1 also correlated significantly with total Q. Here, we report the correlation between O₂⁻ and HMGB1, MDA, and sICAM-1 in rats with cerebral ischemia–reperfusion, using a novel electrochemical sensor. These data indicated that excessive production of O₂⁻ after ischemia–reperfusion was associated with early inflammation, oxidative stress, and endothelial activation in the brain and plasma, which might enhance the ischemia–reperfusion injury.