广东医学
廣東醫學
엄동의학
GUNAGDONG MEDICAL JOURNAL
2014年
7期
982-984
,共3页
赵蕾%张晓红%吴柏成%吴晓光%杜娈英%陈晓宁
趙蕾%張曉紅%吳柏成%吳曉光%杜孌英%陳曉寧
조뢰%장효홍%오백성%오효광%두련영%진효저
山楂叶总黄酮%PI3K/Akt信号通路%脑缺血
山楂葉總黃酮%PI3K/Akt信號通路%腦缺血
산사협총황동%PI3K/Akt신호통로%뇌결혈
Hawthorn leaves flavonoids%PI3K/Akt signaling pathway%cerebral ischemia
目的:探讨山楂叶总黄酮对脑缺血大鼠脑组织PI3K/Akt信号通路的影响。方法雄性SD大鼠随机分为假手术组、模型组、银杏叶片组和山楂叶总黄酮组,每组20只。后3组采用双侧颈总动脉结扎法制备慢性脑缺血大鼠模型,银杏叶片组给予银杏叶片5.2 mg/kg,山楂叶总黄酮组给予山楂叶总黄酮140 mg/kg灌胃,模型组和假手术组给予等量的生理盐水。免疫组化法检测PI3K、Akt蛋白的表达,干湿重法检测脑组织水含量,甲酰胺法测定血脑屏障通透性。结果与模型组比较,银杏叶片组和山楂叶总黄酮组PI3K、Akt蛋白均明显升高( P<0.05,P<0.01),脑组织含水量及伊文思蓝含量显著降低(P<0.05,P<0.01)。结论山楂叶总黄酮对缺血性脑损伤具有保护作用,其作用机制可能与调控PI3 K/Akt信号通路有关。
目的:探討山楂葉總黃酮對腦缺血大鼠腦組織PI3K/Akt信號通路的影響。方法雄性SD大鼠隨機分為假手術組、模型組、銀杏葉片組和山楂葉總黃酮組,每組20隻。後3組採用雙側頸總動脈結扎法製備慢性腦缺血大鼠模型,銀杏葉片組給予銀杏葉片5.2 mg/kg,山楂葉總黃酮組給予山楂葉總黃酮140 mg/kg灌胃,模型組和假手術組給予等量的生理鹽水。免疫組化法檢測PI3K、Akt蛋白的錶達,榦濕重法檢測腦組織水含量,甲酰胺法測定血腦屏障通透性。結果與模型組比較,銀杏葉片組和山楂葉總黃酮組PI3K、Akt蛋白均明顯升高( P<0.05,P<0.01),腦組織含水量及伊文思藍含量顯著降低(P<0.05,P<0.01)。結論山楂葉總黃酮對缺血性腦損傷具有保護作用,其作用機製可能與調控PI3 K/Akt信號通路有關。
목적:탐토산사협총황동대뇌결혈대서뇌조직PI3K/Akt신호통로적영향。방법웅성SD대서수궤분위가수술조、모형조、은행협편조화산사협총황동조,매조20지。후3조채용쌍측경총동맥결찰법제비만성뇌결혈대서모형,은행협편조급여은행협편5.2 mg/kg,산사협총황동조급여산사협총황동140 mg/kg관위,모형조화가수술조급여등량적생리염수。면역조화법검측PI3K、Akt단백적표체,간습중법검측뇌조직수함량,갑선알법측정혈뇌병장통투성。결과여모형조비교,은행협편조화산사협총황동조PI3K、Akt단백균명현승고( P<0.05,P<0.01),뇌조직함수량급이문사람함량현저강저(P<0.05,P<0.01)。결론산사협총황동대결혈성뇌손상구유보호작용,기작용궤제가능여조공PI3 K/Akt신호통로유관。
Objective To study the effects of Hawthorn leaves flavonoids ( HLF) on the PI3K/Akt signaling pathway in rats with cerebral ischemia .Methods Chronic cerebral ischemia rat model was constructed by bilateral carot-id artery ligation.PI3K and Akt protein expression was assessed by immunohistochemical assay .Water content of brain tissue was detected by dry-wet method , while brain barrier permeability was measured by formamide method blood .Re-sults Compared with the model group , significant up-regulations in PI3K and Akt proteins were observed in Ginkgo bi-loba group and HLF group (P<0.05).Significant reductions in cerebral water content and EB content were also observed (P<0.05).Conclusion HLF can protect the brain from ischemia injury , probably via regulation of PI3K/Akt signaling pathway .