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
2014年
10期
2131-2136
,共6页
孙玉芝%雒晓东%赵贝贝%吴寿海%崔晓峰
孫玉芝%雒曉東%趙貝貝%吳壽海%崔曉峰
손옥지%락효동%조패패%오수해%최효봉
帕病2号方%帕金森病%Nrf2%HO-11
帕病2號方%帕金森病%Nrf2%HO-11
파병2호방%파금삼병%Nrf2%HO-11
Pa-Bing Formula No. 2%Parkinson's disease%Nrf2%HO-1
目的：探讨帕病2号方对帕金森病（PD）模型大鼠中脑黑质神经元的保护作用。方法：采用6-羟基多巴胺（6-OHDA）左侧纹状体两点注射法建立PD大鼠模型，经阿扑吗啡（APO）诱导表现恒定右侧旋转且30 min内旋转速度大于7 r·min-1者，视为成功PD大鼠模型。14只PD大鼠随机分为模型组、治疗组，同时设立正常组、假手术组。正常组、假手术组、模型组给予等容积蒸馏水，治疗组给予帕病2号方（32.0 g·kg-1），连续灌胃给药4周。通过Nissl染色及免疫组化方法检测中脑黑质神经元Nissl小体的变化及酪氨酸羟化酶（TH）、核因子E2相关性因子2（Nrf2）、血红加氧酶1（HO-1）的变化。结果：与正常组比较，模型组PD大鼠黑质神经元Nissl小体严重损伤，TH阳性细胞数目显著减少（P<0.01），Nrf2核蛋白、HO-1蛋白表达显著增强（P<0.01）。与模型组比较，帕病2号方治疗组能明显增加PD大鼠黑质神经元内Nissl小体数量，增加TH阳性细胞数目（P<0.05），同时明显上调Nrf2核内表达及HO-1蛋白的表达（P<0.05）。结论：帕病2号方干预对PD大鼠模型黑质神经元具有明显保护作用，可能与上调Nrf2核内表达和HO-1表达有关。
目的：探討帕病2號方對帕金森病（PD）模型大鼠中腦黑質神經元的保護作用。方法：採用6-羥基多巴胺（6-OHDA）左側紋狀體兩點註射法建立PD大鼠模型，經阿撲嗎啡（APO）誘導錶現恆定右側鏇轉且30 min內鏇轉速度大于7 r·min-1者，視為成功PD大鼠模型。14隻PD大鼠隨機分為模型組、治療組，同時設立正常組、假手術組。正常組、假手術組、模型組給予等容積蒸餾水，治療組給予帕病2號方（32.0 g·kg-1），連續灌胃給藥4週。通過Nissl染色及免疫組化方法檢測中腦黑質神經元Nissl小體的變化及酪氨痠羥化酶（TH）、覈因子E2相關性因子2（Nrf2）、血紅加氧酶1（HO-1）的變化。結果：與正常組比較，模型組PD大鼠黑質神經元Nissl小體嚴重損傷，TH暘性細胞數目顯著減少（P<0.01），Nrf2覈蛋白、HO-1蛋白錶達顯著增彊（P<0.01）。與模型組比較，帕病2號方治療組能明顯增加PD大鼠黑質神經元內Nissl小體數量，增加TH暘性細胞數目（P<0.05），同時明顯上調Nrf2覈內錶達及HO-1蛋白的錶達（P<0.05）。結論：帕病2號方榦預對PD大鼠模型黑質神經元具有明顯保護作用，可能與上調Nrf2覈內錶達和HO-1錶達有關。
목적：탐토파병2호방대파금삼병（PD）모형대서중뇌흑질신경원적보호작용。방법：채용6-간기다파알（6-OHDA）좌측문상체량점주사법건립PD대서모형，경아복마배（APO）유도표현항정우측선전차30 min내선전속도대우7 r·min-1자，시위성공PD대서모형。14지PD대서수궤분위모형조、치료조，동시설립정상조、가수술조。정상조、가수술조、모형조급여등용적증류수，치료조급여파병2호방（32.0 g·kg-1），련속관위급약4주。통과Nissl염색급면역조화방법검측중뇌흑질신경원Nissl소체적변화급락안산간화매（TH）、핵인자E2상관성인자2（Nrf2）、혈홍가양매1（HO-1）적변화。결과：여정상조비교，모형조PD대서흑질신경원Nissl소체엄중손상，TH양성세포수목현저감소（P<0.01），Nrf2핵단백、HO-1단백표체현저증강（P<0.01）。여모형조비교，파병2호방치료조능명현증가PD대서흑질신경원내Nissl소체수량，증가TH양성세포수목（P<0.05），동시명현상조Nrf2핵내표체급HO-1단백적표체（P<0.05）。결론：파병2호방간예대PD대서모형흑질신경원구유명현보호작용，가능여상조Nrf2핵내표체화HO-1표체유관。
This article was aimed to study the protection effects of Pa-Bing Formula No. 2 (PBFN-2) on neurons of substantia nigra in Parkinson's disease (PD) rats models in order to explore the possible mechanism of PBFN-2 in PD treatment. Rats were stereotaxically injected with 6-hydroxydopamine (6-OHDA) solution into the left stria-tum in two-site. Rat showed consistent right whirling and the number of rotation was more than 7 r·min-1 induced by APO in 30 min, then the rat was judged as PD model. A total of 14 rats modeled successfully were randomly di-vided into the model group and the treatment group. At the same time, the normal group and sham operation group were also established. Same volume of distilled water was given to the normal group, sham operation group and the model group. PBFN-2 (32.0 g·kg-1) was given to the treatment group for 4 weeks. Microscope was used to observe pathological changes of substantia nigra by nissl stain and changes of TH, Nrf2 and HO-1 immunohistochemical stain. The results showed that compared with the normal group, the nissl bodies were badly injured. Expressions of TH-positive cells were obviously reduced (P<0.01). The expression of Nrf2 nucleus protein and HO-1 protein were obviously increased in substantia nigra of PD rats in model group (P<0.01). Compared to the model group, PBFN-2 effectively increased nissl bodies in neuronal cells of substantia nigra of PD rats, and elevated the number of TH-immunoreactive cells in substantia nigra (P<0.05). The expressions of Nrf2 nucleus protein, HO-1 protein were significantly up-regulated (P<0.05). It was concluded that PBFN-2 had an obvious neuroprotection on the neuronal cells in substantia nigra of PD rats induced by 6-OHDA. The underlying mechanisms may be associated with regu-lation of Nrf2 nucleus protein and HO-1 protein expressions.
