世界科学技术-中医药现代化
世界科學技術-中醫藥現代化
세계과학기술-중의약현대화
WORLD SCIENCE AND TECHNOLOGY-MODERNIZATION OF TRADITIONAL CHINESE MEDICINE
2013年
8期
1682-1687
,共6页
张胜威%董世芬%李俊青%武汀%孙建宁%玄振玉
張勝威%董世芬%李俊青%武汀%孫建寧%玄振玉
장성위%동세분%리준청%무정%손건저%현진옥
脑缺血%脑含水量%白细胞介素-6%白细胞介素-10%核转录因子Bp65%神经行为评分
腦缺血%腦含水量%白細胞介素-6%白細胞介素-10%覈轉錄因子Bp65%神經行為評分
뇌결혈%뇌함수량%백세포개소-6%백세포개소-10%핵전록인자Bp65%신경행위평분
Cerebral ischemia%brain water content%intedeukin-6%intedeukin-10%nuclear factor kappa Bp65%neurobehavioral symptom scores
目的:探讨梓醇对永久性脑缺血模型急性期脑组织梗死体积、含水量及亚急性期炎性反应的影响。方法:采用化学刺激法建立局灶性脑缺血(MCAT)模型,检测急性期(24 h)神经行为学症状、脑梗死面积和脑含水量;线栓法制作永久性大鼠脑缺血(pMCAO)模型,酶联免疫吸附法(ELISA)测定缺血侧脑组织白细胞介素-6(IL-6)、白细胞介素-10(IL-10)和核转录因子Bp65(NF-κBp65)的含量。结果:大鼠MCAT后24 h,梓醇15~60 mg·kg-1剂量组可以显著改善模型动物神经症状损伤(P<0.01或P<0.001),梓醇15 mg·kg-1组可显著降低模型动物梗塞区面积(P<0.05),30 mg·kg-1组和60 mg·kg-1组可显著降低脑水肿(P<0.05);大鼠pMCAO术后7天开始,梓醇30 mg·kg-1组或60 mg·kg-1组开始改善模型动物神经症状损伤;术后14天,与假手术组比较,缺血侧脑组织IL-10和核转录因子NF-κBp65的含量变化与模型组已经不明显,IL-6水平显著降低(P<0.05),梓醇15 mg·kg-1灌胃14天可以降低模型动物缺血侧脑组织NF-κBp65含量(P<0.05)。结论:梓醇能改善局灶性脑缺血模型动物急性期及亚急性期神经症状损伤,缩小梗死灶,减轻脑部水肿,其作用可能与抑制脑缺血引起的炎症损伤无关。
目的:探討梓醇對永久性腦缺血模型急性期腦組織梗死體積、含水量及亞急性期炎性反應的影響。方法:採用化學刺激法建立跼竈性腦缺血(MCAT)模型,檢測急性期(24 h)神經行為學癥狀、腦梗死麵積和腦含水量;線栓法製作永久性大鼠腦缺血(pMCAO)模型,酶聯免疫吸附法(ELISA)測定缺血側腦組織白細胞介素-6(IL-6)、白細胞介素-10(IL-10)和覈轉錄因子Bp65(NF-κBp65)的含量。結果:大鼠MCAT後24 h,梓醇15~60 mg·kg-1劑量組可以顯著改善模型動物神經癥狀損傷(P<0.01或P<0.001),梓醇15 mg·kg-1組可顯著降低模型動物梗塞區麵積(P<0.05),30 mg·kg-1組和60 mg·kg-1組可顯著降低腦水腫(P<0.05);大鼠pMCAO術後7天開始,梓醇30 mg·kg-1組或60 mg·kg-1組開始改善模型動物神經癥狀損傷;術後14天,與假手術組比較,缺血側腦組織IL-10和覈轉錄因子NF-κBp65的含量變化與模型組已經不明顯,IL-6水平顯著降低(P<0.05),梓醇15 mg·kg-1灌胃14天可以降低模型動物缺血側腦組織NF-κBp65含量(P<0.05)。結論:梓醇能改善跼竈性腦缺血模型動物急性期及亞急性期神經癥狀損傷,縮小梗死竈,減輕腦部水腫,其作用可能與抑製腦缺血引起的炎癥損傷無關。
목적:탐토재순대영구성뇌결혈모형급성기뇌조직경사체적、함수량급아급성기염성반응적영향。방법:채용화학자격법건립국조성뇌결혈(MCAT)모형,검측급성기(24 h)신경행위학증상、뇌경사면적화뇌함수량;선전법제작영구성대서뇌결혈(pMCAO)모형,매련면역흡부법(ELISA)측정결혈측뇌조직백세포개소-6(IL-6)、백세포개소-10(IL-10)화핵전록인자Bp65(NF-κBp65)적함량。결과:대서MCAT후24 h,재순15~60 mg·kg-1제량조가이현저개선모형동물신경증상손상(P<0.01혹P<0.001),재순15 mg·kg-1조가현저강저모형동물경새구면적(P<0.05),30 mg·kg-1조화60 mg·kg-1조가현저강저뇌수종(P<0.05);대서pMCAO술후7천개시,재순30 mg·kg-1조혹60 mg·kg-1조개시개선모형동물신경증상손상;술후14천,여가수술조비교,결혈측뇌조직IL-10화핵전록인자NF-κBp65적함량변화여모형조이경불명현,IL-6수평현저강저(P<0.05),재순15 mg·kg-1관위14천가이강저모형동물결혈측뇌조직NF-κBp65함량(P<0.05)。결론:재순능개선국조성뇌결혈모형동물급성기급아급성기신경증상손상,축소경사조,감경뇌부수종,기작용가능여억제뇌결혈인기적염증손상무관。
This study was aimed to explore the effect of Catalpol on the cerebral infarction size in acute phase, water content and inflammatory reaction of early recovery after permanent middle cerebral artery occlusion (pM-CAO). Adult male Sprague-dawley rats were subjected to chemical method to establish MCAT model. The detec-tion was made on neurobehavioral symptoms, cerebral infarction volume and water content at 24 h after surgery. The content of intedeukin-6 (IL-6), intedeukin-10 (IL-10) and nuclear factor kappa Bp65 (NF-κBp65) were de-tected after pMCAO with enzyme-linked immunosorbent assay (ELISA). The results showed that 24 h after MCAT, Catalpol 15-60 mg·kg-1 can significantly improve the neurobehavioral symptoms (P < 0.01, or P <0.001). The Catalpol 15 mg·kg-1 can significantly reduce cerebral infarction volume (P < 0.05). The Catalpol 30-60 mg·kg-1 can significantly reduce water content (P < 0.05). Catalpol 30-60 mg·kg-1 can significantly improve neurobehav-ioral symptoms from the 7th day after pMCAO. On the 14th after pMCAO, the content of IL-10 and NF-κBp65 of ischemia brain had no difference compared with sham-operated group. The IL-6 level of ischemia brain was obvi-ously reduced than the sham-operated group(P < 0.05). The intragastric administration of Catalpol 15 mg·kg-1 for 14 days can reduce the content of NF-κBp65 in the ischemia brain of model rats (P < 0.05). It was concluded that Catalpol can improve neurobehavioral symptoms of acute and subacute phase after cerebral ischemia, reduce infarcts and water content. These effects may not be related with its inhibition of inflammatory derived from cere-bral ischemia.