Project/Area Number |
19590700
|
Research Category |
Grant-in-Aid for Scientific Research (C)
|
Allocation Type | Single-year Grants |
Section | 一般 |
Research Field |
General internal medicine (including Psychosomatic medicine)
|
Research Institution | Josai University |
Principal Investigator |
OKAZAKI Mari Josai University, 薬学部, 准教授 (50272901)
|
Co-Investigator(Kenkyū-buntansha) |
HIBINO Yasuhide 城西大学, 薬学部, 教授 (10189805)
KAMIUCHI Shinya 城西大学, 薬学部, 助教 (80433647)
IWATA Naohiro 城西大学, 薬学部, 助手 (50552759)
|
Project Period (FY) |
2007 – 2009
|
Project Status |
Completed (Fiscal Year 2009)
|
Budget Amount *help |
¥4,680,000 (Direct Cost: ¥3,600,000、Indirect Cost: ¥1,080,000)
Fiscal Year 2009: ¥650,000 (Direct Cost: ¥500,000、Indirect Cost: ¥150,000)
Fiscal Year 2008: ¥910,000 (Direct Cost: ¥700,000、Indirect Cost: ¥210,000)
Fiscal Year 2007: ¥3,120,000 (Direct Cost: ¥2,400,000、Indirect Cost: ¥720,000)
|
Keywords | 酸化ストレス / 糖尿病 / 霊芝菌糸体培養培地抽出物(MAK) / 一過性脳虚血 / 炎症性サイトカイン / グルタミン酸トランスポーター / ストレプトゾトシン糖尿病 / 中大脳動脈閉塞術(MCAO) / 虚血再灌流障害 / HMGB1 / 霊芝菌糸体培養培地抽出物 / 抗酸化食品 / 炎症 / 霊芝糸体培養地抽出物 / 抗酸化酸素活性 |
Research Abstract |
Diabetic Mellitus (DM) have been shown to enhance oxidative stress leading to aggravation of cerebral ischemic injury following stroke. In this study, we examined the effects of oral administration of a water-soluble extract from culture medium of Ganoderma lucidum mycelia (MAK) on blood glucose level (BG), total plasma oxidative stress, and activity of antioxidant enzymes in DM animals. Furthermore, neuroprotective effects of MAK against exacerbation of neuronal damage induced by cerebral ischemia/reperfusion in the DM animals were investigated. DM animals had increased BG and decreased activity of antioxidant enzymes in the brain. DM animals treated with MAK had significantly lower BG and normal activity of the antioxidant enzyme. Treatment of MAK remarkably improved aggravated neurological deficits and cerebral injury induced by ischemia/reperfusion in diabetic animals. These results show that daily intake of MAK relieves the exacerbation of cerebral ischemic injury in a diabetic state, which may be attributed to improvement of augmented oxidative stress.
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