中华神经医学杂志
中華神經醫學雜誌
중화신경의학잡지
CHINESE JOURNAL OF NEUROMEDICINE
2014年
9期
894-898
,共5页
吴亮%田有勇%周俊山%张颖冬
吳亮%田有勇%週俊山%張穎鼕
오량%전유용%주준산%장영동
帕金森病%鱼藤酮%坎地沙坦酯
帕金森病%魚籐酮%坎地沙坦酯
파금삼병%어등동%감지사탄지
Parkinson's disease%Rotenone%Candesartan cilexetil
目的 研究坎地沙坦酯对鱼藤酮致帕金森病(PD)大鼠的影响. 方法 10周龄雄性Lewis大鼠40只按照随机数字表法分为对照组、鱼藤酮组、鱼藤酮+坎地沙坦酯组和坎地沙坦酯组,每组10只.100 g/L水合氯醛麻醉充分后,微量渗透泵包埋于各组大鼠背部皮下.鱼藤酮[2.5～3.0 mg/(kg· d)]溶于二甲基亚砜和聚乙二醇(1∶1)混合液中,埋于鱼藤酮组大鼠微量渗透泵中;余3组给予等质量的生理盐水装于微量渗透泵中;鱼藤酮+坎地沙坦酯组大鼠同时给予坎地沙坦酯(混于0.5％甲基纤维素中)每天上午8时～12时灌胃[1 mg/(kg· d)],对照组给予等体积生理盐水灌胃.行为学检测评定运动功能等损害症状;免疫组化染色检测大鼠黑质部位酪氨酸羟化酶(TH)和α-共核蛋白表达情况;Western blotting检测黑质部位α-共核蛋白表达水平. 结果 分组4周后鱼藤酮组大鼠体质量明显减轻,降至(297.3±12.2)g;黑质部位TH阳性细胞显著减少,降至(377.0±41.6)个/mm2;α-共核蛋白表达显著增加,达到0.75±0.02;鱼藤酮+坎地沙坦酯组对应的各项值分别为(337.2±26.3)g、(639.7 ±46.0)个/mm2、0.57±0.01;二者差异有统计学意义(P＜0.05).Western blotting结果与之一致. 结论 坎地沙坦酯能够通过减少TH阳性细胞凋亡及α-共核蛋白沉积起到保护PD大鼠作用.
目的 研究坎地沙坦酯對魚籐酮緻帕金森病(PD)大鼠的影響. 方法 10週齡雄性Lewis大鼠40隻按照隨機數字錶法分為對照組、魚籐酮組、魚籐酮+坎地沙坦酯組和坎地沙坦酯組,每組10隻.100 g/L水閤氯醛痳醉充分後,微量滲透泵包埋于各組大鼠揹部皮下.魚籐酮[2.5～3.0 mg/(kg· d)]溶于二甲基亞砜和聚乙二醇(1∶1)混閤液中,埋于魚籐酮組大鼠微量滲透泵中;餘3組給予等質量的生理鹽水裝于微量滲透泵中;魚籐酮+坎地沙坦酯組大鼠同時給予坎地沙坦酯(混于0.5％甲基纖維素中)每天上午8時～12時灌胃[1 mg/(kg· d)],對照組給予等體積生理鹽水灌胃.行為學檢測評定運動功能等損害癥狀;免疫組化染色檢測大鼠黑質部位酪氨痠羥化酶(TH)和α-共覈蛋白錶達情況;Western blotting檢測黑質部位α-共覈蛋白錶達水平. 結果 分組4週後魚籐酮組大鼠體質量明顯減輕,降至(297.3±12.2)g;黑質部位TH暘性細胞顯著減少,降至(377.0±41.6)箇/mm2;α-共覈蛋白錶達顯著增加,達到0.75±0.02;魚籐酮+坎地沙坦酯組對應的各項值分彆為(337.2±26.3)g、(639.7 ±46.0)箇/mm2、0.57±0.01;二者差異有統計學意義(P＜0.05).Western blotting結果與之一緻. 結論 坎地沙坦酯能夠通過減少TH暘性細胞凋亡及α-共覈蛋白沉積起到保護PD大鼠作用.
목적 연구감지사탄지대어등동치파금삼병(PD)대서적영향. 방법 10주령웅성Lewis대서40지안조수궤수자표법분위대조조、어등동조、어등동+감지사탄지조화감지사탄지조,매조10지.100 g/L수합록철마취충분후,미량삼투빙포매우각조대서배부피하.어등동[2.5～3.0 mg/(kg· d)]용우이갑기아풍화취을이순(1∶1)혼합액중,매우어등동조대서미량삼투빙중;여3조급여등질량적생리염수장우미량삼투빙중;어등동+감지사탄지조대서동시급여감지사탄지(혼우0.5％갑기섬유소중)매천상오8시～12시관위[1 mg/(kg· d)],대조조급여등체적생리염수관위.행위학검측평정운동공능등손해증상;면역조화염색검측대서흑질부위락안산간화매(TH)화α-공핵단백표체정황;Western blotting검측흑질부위α-공핵단백표체수평. 결과 분조4주후어등동조대서체질량명현감경,강지(297.3±12.2)g;흑질부위TH양성세포현저감소,강지(377.0±41.6)개/mm2;α-공핵단백표체현저증가,체도0.75±0.02;어등동+감지사탄지조대응적각항치분별위(337.2±26.3)g、(639.7 ±46.0)개/mm2、0.57±0.01;이자차이유통계학의의(P＜0.05).Western blotting결과여지일치. 결론 감지사탄지능구통과감소TH양성세포조망급α-공핵단백침적기도보호PD대서작용.
Objective To investigate the effect of candesartan cilexetil on rotenone-induced Parkinson's disease (PD) in rats.Methods Forty 10-week-old male Lewis rats were chosen in our study and equally randomized into control group,rotenone group,rotenone+candesartan cilexetil group and candesartan cilexetil group (n=10); rotenone (2.5-3.0 mg/[kg· d]) was given for 4 weeks to the rats of rotenone group and rotenone+candesartan cilexetil group by subcutaneous osmotic minipumps implantation under the back; rats in the rotenone+candesartan cilexetil group and candesartan cilexetil group were orally administered candesartan cilexetil.Neurological behavioral measurements were performed to evaluate the motor features; tyrosine hydroxylase (TH) and α-synuclein immunoreactivities in the substantia nigra pars compacta (SNc) were observed.Protein level of α-synuclein was determined by Westem blotting.Results The weight of rats in the rotenone group reduced to (297.3±12.2) g,with significant difference as compared with that of the other three groups (P＜0.05); decreased TH immunoreactivity (377.0±41.6) cells/mm2) and increased α-synuclein immunoreactivity (0.75±0.02) in the SNc of rats in the rotenone group was noted,enjoying significant differences as compared with the other three groups (P＜0.05); these values in the rotenone+candesartan cilexetil group were (337.2±26.3) g,(639.7±46.0) cells/mm2 and 0.57±0.01,respectively (P＜0.05).Western blotting confirmed that rotenone up-regulated the expression ofα-synuclein in the SNc,and candesartan ceilexetil markedly attenuated the increase (P＜0.05).Conclusion Candesartan cilexetil can protect rotenone-induced PD in rats through decreasing TH-positive cell apoptosis and α-synuclein deposition.
