中国药物警戒
中國藥物警戒
중국약물경계
CHINESE JOURNAL OF PHARMACOVIGILANCE
2014年
12期
717-720
,共4页
李冬梅%车薇%李霞%曹军平
李鼕梅%車薇%李霞%曹軍平
리동매%차미%리하%조군평
芍药苷%脑缺血再灌注损伤%ATP 酶%兴奋性氨基酸
芍藥苷%腦缺血再灌註損傷%ATP 酶%興奮性氨基痠
작약감%뇌결혈재관주손상%ATP 매%흥강성안기산
paeoniflorin%cerebral ischemia/reperfusion injury%ATPase%excitatory amino acid(EAA)
目的：探讨芍药苷对沙土鼠脑缺血再灌注（CI/R）损伤的保护作用及其作用机制。方法采用结扎双侧颈总动脉缺血10 min 再灌注6 h，建立沙土鼠 CI/R 模型，随机分为假手术组、模型组、芍药苷3个剂量组（20、10、5 mg·kg-1），每组10只，术前3天开始腹腔注射给药。观察再灌注6 h 内神经症状，计算卒中指数；取脑组织匀浆，定磷法测定ATP酶活性，高效液相色谱法测定谷氨酸（Glu）和天冬氨酸（Asp）含量。结果与模型组比较，芍药苷各剂量均能降低CI/R沙土鼠的卒中指数（P <0.05或 P <0.01），各剂量均可显著升高脑组织 Ca2+-ATP 酶活性（P <0.05），高、中剂量组能显著升高 Na＋-K＋-ATP 酶活性（P <0.05或 P <0.01），各剂量均能降低脑组织 Glu 含量（P <0.05或 P <0.01）。芍药苷对脑组织 Mg2+-ATP 酶活性和 Asp 含量则无明显影响。结论芍药苷预处理对 CI/R 损伤的保护作用与其保护脑细胞膜 ATP 酶的活性、抑制 Glu 的释放、降低兴奋性氨基酸毒性等有关。
目的：探討芍藥苷對沙土鼠腦缺血再灌註（CI/R）損傷的保護作用及其作用機製。方法採用結扎雙側頸總動脈缺血10 min 再灌註6 h，建立沙土鼠 CI/R 模型，隨機分為假手術組、模型組、芍藥苷3箇劑量組（20、10、5 mg·kg-1），每組10隻，術前3天開始腹腔註射給藥。觀察再灌註6 h 內神經癥狀，計算卒中指數；取腦組織勻漿，定燐法測定ATP酶活性，高效液相色譜法測定穀氨痠（Glu）和天鼕氨痠（Asp）含量。結果與模型組比較，芍藥苷各劑量均能降低CI/R沙土鼠的卒中指數（P <0.05或 P <0.01），各劑量均可顯著升高腦組織 Ca2+-ATP 酶活性（P <0.05），高、中劑量組能顯著升高 Na＋-K＋-ATP 酶活性（P <0.05或 P <0.01），各劑量均能降低腦組織 Glu 含量（P <0.05或 P <0.01）。芍藥苷對腦組織 Mg2+-ATP 酶活性和 Asp 含量則無明顯影響。結論芍藥苷預處理對 CI/R 損傷的保護作用與其保護腦細胞膜 ATP 酶的活性、抑製 Glu 的釋放、降低興奮性氨基痠毒性等有關。
목적：탐토작약감대사토서뇌결혈재관주（CI/R）손상적보호작용급기작용궤제。방법채용결찰쌍측경총동맥결혈10 min 재관주6 h，건립사토서 CI/R 모형，수궤분위가수술조、모형조、작약감3개제량조（20、10、5 mg·kg-1），매조10지，술전3천개시복강주사급약。관찰재관주6 h 내신경증상，계산졸중지수；취뇌조직균장，정린법측정ATP매활성，고효액상색보법측정곡안산（Glu）화천동안산（Asp）함량。결과여모형조비교，작약감각제량균능강저CI/R사토서적졸중지수（P <0.05혹 P <0.01），각제량균가현저승고뇌조직 Ca2+-ATP 매활성（P <0.05），고、중제량조능현저승고 Na＋-K＋-ATP 매활성（P <0.05혹 P <0.01），각제량균능강저뇌조직 Glu 함량（P <0.05혹 P <0.01）。작약감대뇌조직 Mg2+-ATP 매활성화 Asp 함량칙무명현영향。결론작약감예처리대 CI/R 손상적보호작용여기보호뇌세포막 ATP 매적활성、억제 Glu 적석방、강저흥강성안기산독성등유관。
Objective To investigate the effects of paeoniflorin (PAE) on gerbils with cerebral ischemia/reperfusion (CI/R) injury and the mechanisms involved. Methods Gerbil model of CI/R was prepared by bilateral common carotid occlusion for 10 min followed by 6-hour reperfusion. Then gerbils were divided into 5 groups at random (n=10), namely sham, model, PAE high, medium and low dose groups (20, 10 and 5 mg·kg-1, respectively). PAE was injected intraperitoneally (i.p.) for 3 days before the carotid occlusion. Stroke index was calculated during the reperfusion. The ATPase activities in brain tissue homogenate were examined by a phosphate assay and glutamate (Glu) and aspirate (Asp) contents were determined by HPLC. Results The results showed that PAE significantly improved stroke index, compared to the model group (P <0.05 or P <0.01). PAE evidently elevated Ca2+-ATPase activities in brain tissue of CI/R gerbils (P <0.05). The Na+-K+-ATPase activities in PAE high and medium dose groups were significantly higher than the model group (P <0.05 or P <0.01). PAE markedly inhibited the Glu contents in brain tissue of CI/R gerbils (P <0.05 or P <0.01). However, PAE showed no influence on Mg2+-ATPase activities or Asp contents in brain tissue. Conclusion The effectiveness of PAE pretreatment in CI/R injury appears to be associated with the enhancement of ATPase activities and inhibition of excitatory amino acid (EAA) toxicity in brain tissue.
