CAJ | 학술논문

目的：探讨红景天苷对大鼠局灶性脑缺血-再灌注损伤的保护作用机制与磷脂酰肌醇-3激酶/丝氨酸-苏氨酸蛋白激酶（ PI3-K/AKT）信号通路的相关性。方法将48只SD雄性大鼠按随机数字表法分为四组：假手术组、模型组及红景天苷低、高剂量组。采用线栓法制备右侧大脑中动脉闭塞模型，缺血2 h再灌注24 h后进行神经功能缺损评分及相关指标检测。氯化三苯基四氮唑（ TTC）染色检测脑梗死面积，苏木素-伊红（ HE）染色观察脑组织病理学改变，原位末端标记技术（ TUNEL）法检测细胞凋亡数，免疫组化法检测PI3-K、p-AKT表达。结果与模型组比较，红景天苷高、低剂量组神经功能缺损程度明显减轻，脑梗死体积及凋亡阳性细胞数均明显减少，PI3-K、p-AKT阳性细胞表达明显增加，差异均有统计学意义（ P ＜0.05）；与红景天苷低剂量组相比较，红景天苷高剂量组神经功能缺损程度减轻，脑梗死体积及凋亡阳性细胞数均减少，PI3-K、p-AKT阳性细胞表达增加，差异均有统计学意义（ P ＜0.05）。结论红景天苷通过激活PI3-K/AKT信号通路，从而抑制神经细胞凋亡可能是其对脑缺血-再灌注损伤的保护作用机制之一。
목적：탐토홍경천감대대서국조성뇌결혈-재관주손상적보호작용궤제여린지선기순-3격매/사안산-소안산단백격매（ PI3-K/AKT）신호통로적상관성。방법장48지SD웅성대서안수궤수자표법분위사조：가수술조、모형조급홍경천감저、고제량조。채용선전법제비우측대뇌중동맥폐새모형，결혈2 h재관주24 h후진행신경공능결손평분급상관지표검측。록화삼분기사담서（ TTC）염색검측뇌경사면적，소목소-이홍（ HE）염색관찰뇌조직병이학개변，원위말단표기기술（ TUNEL）법검측세포조망수，면역조화법검측PI3-K、p-AKT표체。결과여모형조비교，홍경천감고、저제량조신경공능결손정도명현감경，뇌경사체적급조망양성세포수균명현감소，PI3-K、p-AKT양성세포표체명현증가，차이균유통계학의의（ P ＜0.05）；여홍경천감저제량조상비교，홍경천감고제량조신경공능결손정도감경，뇌경사체적급조망양성세포수균감소，PI3-K、p-AKT양성세포표체증가，차이균유통계학의의（ P ＜0.05）。결론홍경천감통과격활PI3-K/AKT신호통로，종이억제신경세포조망가능시기대뇌결혈-재관주손상적보호작용궤제지일。
Objective To explore the mechanism of protective effect of Rhodioloside in cerebral ischemia-reperfusion rats and its relevance to phosphatidylinositol 3-kinases ( PI3-K)/protein serine-threonine kinases ( AKT) signaling pathway .Methods Forty eight Sprague-Dawley rats were randomly divided into four groups: sham-operation group , ischemia-reperfusion group , and Rhodiolo-side treatment groups (5 and 10 mg/kg).The model of right middle cerebral artery occlusion was established with thread ligation meth -od.The score of the neurological deficit was estimated 2 h followed by 24 h reperfusion.Histopathological changes were observed by hematoxylin-eosin(HE) staining.The infarct volume was measured with triphenyltetrazolium chloride (TTC) staining.Apoptotic cells were assessed with terminal deoxynucleotidyl transferase (TdT)-mediated dUTP nick end labeling (TUNEL) method.The expressions of PI3-K and p-AKT were evaluated with immunohistochemistry .Results The score of the neurological deficit was decreased more ob-viously, the number of apoptotic were decreased more significantly , the expressions of PI3-K and p-AKT were increased more signifi-cantly in the Rhodioloside treatment groups (5 and 10 mg/kg) than in the ischemia-reperfusion group ( P <0.05).The score of the neurological deficit was decreased , the number of apoptotic was decreased , and the expressions of PI 3-K and p-AKT were increased in the Rhodioloside treatment group (10 mg/kg) than the Rhodioloside treatment group (5 mg/kg) ( P <0.05).Conclusions The protective mechanism of Rhodioloside therapy against cerebral ischemia r-eperfusion injury might be associated with activating the PI 3-K/AKT signaling pathway and then inhibiting neuronal apoptosis .