| Project/Area Number |
07671543
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| Research Category |
Grant-in-Aid for Scientific Research (C)
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| Allocation Type | Single-year Grants |
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| Section | 一般 |
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| Research Field |
Cerebral neurosurgery
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| Research Institution | Teikyo Univ.School of Med. |
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Principal Investigator |
KUBOTA Masaru Teikyo Univ.School of Med., Neurosurgery, Assistant Prof., 医学部, 講師 (30246061)
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| Co-Investigator(Kenkyū-buntansha) |
NARITA Koji Teikyo Univ School of Med., Neurosurgery, Assistant, 医学部, 助手 (90237602)
KANEMITSU Hideaki Teikyo Univ School of Med., Neurosurgery, Assistant Prof, 医学部, 講師 (10129992)
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| Project Period (FY) |
1995 – 1997
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| Project Status |
Completed (Fiscal Year 1997)
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| Budget Amount *help |
¥2,400,000 (Direct Cost: ¥2,400,000)
Fiscal Year 1997: ¥300,000 (Direct Cost: ¥300,000)
Fiscal Year 1996: ¥1,300,000 (Direct Cost: ¥1,300,000)
Fiscal Year 1995: ¥800,000 (Direct Cost: ¥800,000)
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| Keywords | Focal cerebral ischemia / sphingomyelin / middle cerebral artery / programd cell death / sphingolipid / forebrain ischemia / 一過性前脳虚血 / 神経細胞死 / 薄層クロマトグラフィー / 局所脳虚血 / セレブロシド / セラミド / ガングリオシド / スフィンゴミエリン / 脂肪酸 |
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| Research Abstract |
Focal cerebral ischemia was induced in anesthetized rats by occluding the stem of the proximal middle cerebral artery. To better define the sphingolipid metabolism during focal brain ischemia, levels of ceramide, sphingomyelin, cerebroside and gangliosides were determined in rat cerebral cortex during focal ischemia produced by occlusion of the middle cerebral artery. Sphingomyelin began to decrease at 2 hours of ischemia and continued to decrease for 96 hours. In contrast, ceramide increased at 6 hours and increased to 4.2-fold at 96 hours after ischemia, and the fatty acid composition of ceramide was solely nonhydroxylated fatty acid similar to sphingomyelin. Hydroxylated fatty acid-linked cerebroside decreased at 6 hours of ischemia, whereas any significant decrease of non-hydroxylated fatty acid-linked cerebroside didn't occur for 96 hours of ischemia. There were no measurable changes in the levels of gangliosides. These results suggested that ceramide was produced in the cerebral cortex by the breakdown of sphingomyelin during early ischemia.
Recently ceramide generated by sphingomyelin degradation has been described as a second messenger involved in programd cell death, cell growth and differentiation in HL-60 leukemic cells. We studied on the differences in sphingomylin levels in gerbil hippocampus induced by lethal or sublethal ischemia using the transient forebrain ischemia-reperfusion gerbil model. Sphingomyelin was separated by thin layr chromatography (TLC) from hippocampal total lipids and analyzed by gas liquid chromatography (GLC). The sphingomyelin levels during recirculation after lethal ischemia (a 5-min.of ischemia) were significantly decreased at 30 min.and then returned to the control level at 60 min. The recirculation after a sublethal ischemia (2 min ischemia and 5 min.ischemia after acquired ischemic tolerance) did not induce any changes in sphingomyelin levels.
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