呼吸氫氣可治療高血糖增強腦出血誘發的腦出血損傷－台灣氫水實驗室

呼吸氫氣可治療高血糖增強腦出血誘發的腦出血損傷

已有2229次閱讀 2010-5-8 11:38 | 個人分類: 呼吸氫氣 | 系統分類: 科研筆記 | 關鍵詞:氫氣

高血糖（糖尿病）是腦缺血後出血的重要誘導因素。本研究利用大鼠模型檢測了氫氣對這類損傷的作用。72只SD大鼠分成4組，假手術組、腦缺血組、腦缺血治療組。所有動物腦缺血模型製備後15分鐘注射50%葡萄糖(6 ml/kg ip)。90分鐘缺血後開始再灌注並同時呼吸氫氣2小時。注射50%葡萄糖後0 h, 0.5 h, 4 h,和6 h後分別檢測血糖水平，缺血後24小時後分別測定缺血和出血體積、神經行為學評分、氧化應激（8OH-dG、HNE和nitrotyrosine分別代表核酸、脂肪和蛋白氧化損傷指標）、MMP9和2活性。結果發現，呼吸氫氣能有效降低缺血和出血體積，提高神經行為學評分，效應與氧化應激MMP9和2活性的降低有關係。特別是發現在註射50%葡萄糖後4 h（就是在呼吸氫氣2小時結束後45分鐘），血糖從500降低到366 mg/dl，但治療對ZO-1, occluding, collagen IV or aquaporin4的表達沒有影響（這說明什麼？應該好好分析一下）。該研究說明呼吸氫氣確實能對高血糖增強腦出血誘發的腦出血損傷有保護作用，但在氧化應激和血糖水平方面的具體機制需要深入研究。

HYDROGEN GAS REDUCED ACUTE HYPERGLYCEMIA-ENHANCED

HEMORRHAGIC TRANSFORMATION IN A FOCAL ISCHEMIA RAT MODEL

CH CHEN,a,b M. ANATOL,a Y. ZHAN,a,c WW LIU,a RP OSTROWKI,a J. TANGa AND JH ZHANGa,d,e*

aDepartment of Physiology and Pharmacology, Loma Linda University, Loma Linda, CA, USA

bDepartment of Anatomy and Embryology, Peking University Health Science Center, Beijing, PR China

cDepartment of Neurosurgery, the First Affiliated Hospital of Chongqing Medical University, Chongqing, PR China

dDepartment of Neurosurgery, Loma Linda University, Loma Linda, CA, USA

eDepartment of Anesthesiology, Loma Linda University, Loma Linda, CA, USA

Neuroscience xx (2010) xxx

Abstract—Hyperglycemia is one of the major factors for hemorrhagic transformation after ischemic stroke. In this study, we tested hydrogen gas on hemorrhagic transformation in a rat focal cerebral ischemia model. Sprague–Dawley rats ( n _ 72) were divided into the following groups : sham; sham treated with hydrogen gas (H2); Middle Cerebral Artery Occlusion (MCAO); and MCAO treated with H2 (MCAO _ H2). All the rats received an injection of 50% dextrose (6 ml/kg ip) and underwent MCAO 15 min later. Following a 90 min ischemic period, hydrogen was inhaled for 2 h during reperfusion. We measured the level of blood glucose at 0 h, 0.5 h, 4 h, and 6 h after dextrose injection. Infarct and hemorrhagic volumes, neurologic score, oxidative stress (evaluating by the level of 8 Hydroxyguanosine (8OHG), 4-Hydroxy-2-Nonenal (HNE) and nitrotyrosine), matrix metalloproteinase (MMP)-2/MMP-9 activity were measured at 24 h after ischemia . We found that hydrogen inhalation for 2 h reduced infarct and hemorrhagic volumes and improved neurological functions. This effect of hydrogen is accompanied by a reduction of the expressions of 8OHG, HNE, nitrotyrosine and the activity of MMP-9. Furthermore, a reduction of the blood glucose level from 500 _ 32.51 to 366 _ 68.22 mg/dl at 4 h after dextrose injection was observed in hydrogen treated animals. However, the treatment had no significant effect on the expression of ZO-1, occluding, collagen IV or aquaporin4 (AQP4). In conclusion, hydrogen gas reduced the infarction, hemorrhagic transformation, and improved neurological functions in rat. The potential mechanisms of decreased oxidative stress and glucose levels after hydrogen treatment warrant further investigation. © 2010 Published by Elsevier Ltd on behalf of IBRO .

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