CAJ | 학술논문

目的：探讨木犀草素和芦丁组合物( MLR)对帕金森病( PD)模型小鼠的治疗作用及其机制。方法C57BL/6小鼠72只,随机分为6组(n=12),分别为正常对照组,模型对照组,美多巴组(50 mg·kg-1)和MLR小、中、大剂量组(140,280,560 mg·kg-1)。小鼠腹腔注射1-甲基-4-苯基-1,2,3,6-四氢吡啶(MPTP)30 mg·kg-1,建立亚急性 PD模型。采用爬杆实验和悬挂实验评价小鼠肢体运动协调能力和体力；免疫组织化学法检测小鼠 MPTP 损伤通路中酪氨酸羟化酶( TH)阳性神经元数、多巴胺转运体( DAT)、胶质源性纤维蛋白( GFAP)；高效液相色谱法检测中脑神经递质及其代谢产物含量。结果 MLR 可显著改善 PD 模型小鼠运动协调能力( P<0.01或 P<0.05)。 MLR (280和560 mg·kg-1)可增加 TH 阳性神经元数目(可分别达到正常对照组的69.00%和77.95%,P<0.01)和 DAT 阳性神经元数目(可分别达到正常对照组的68.53%和70.40%,P<0.05),显著抑制星形胶质细胞反应性(P<0.01)。 MLR 各剂量组脑内单胺递质紊乱均显著改善。结论 MLR 可显著改善 MPTP 致小鼠运动协调能力损伤,并可能通过调节脑内递质水平、抑制炎性反应、减轻神经元损伤发挥治疗 PD 的作用。
목적：탐토목서초소화호정조합물( MLR)대파금삼병( PD)모형소서적치료작용급기궤제。방법C57BL/6소서72지,수궤분위6조(n=12),분별위정상대조조,모형대조조,미다파조(50 mg·kg-1)화MLR소、중、대제량조(140,280,560 mg·kg-1)。소서복강주사1-갑기-4-분기-1,2,3,6-사경필정(MPTP)30 mg·kg-1,건립아급성 PD모형。채용파간실험화현괘실험평개소서지체운동협조능력화체력；면역조직화학법검측소서 MPTP 손상통로중락안산간화매( TH)양성신경원수、다파알전운체( DAT)、효질원성섬유단백( GFAP)；고효액상색보법검측중뇌신경체질급기대사산물함량。결과 MLR 가현저개선 PD 모형소서운동협조능력( P<0.01혹 P<0.05)。 MLR (280화560 mg·kg-1)가증가 TH 양성신경원수목(가분별체도정상대조조적69.00%화77.95%,P<0.01)화 DAT 양성신경원수목(가분별체도정상대조조적68.53%화70.40%,P<0.05),현저억제성형효질세포반응성(P<0.01)。 MLR 각제량조뇌내단알체질문란균현저개선。결론 MLR 가현저개선 MPTP 치소서운동협조능력손상,병가능통과조절뇌내체질수평、억제염성반응、감경신경원손상발휘치료 PD 적작용。
Objective To study the therapeutic effect of the complex mixture of luteolin and rutin ( MLR) on 1-methyl-4-phenyl-1,2,3,6-tetrahydropyridin ( MPTP) induced Parkinson’ s disease ( PD) mouse model. Methods Seventy-two C57BL/6 mice were divided into six groups randomly ( n=12 in each group): the normal control , model control , madopar (50 mg·kg-1) group, MLR at low (140 mg·kg-1), middle (280 mg·kg-1) and high (560 mg·kg-1) dose groups. PD mouse models were established by intraperitoneal injection of MPTP ( 30 mg · kg-1 ) . Pole test and traction performance were recorded to access the body coordinate capability and strength. The tyrosine hydroxylase (TH), dopamine transport protein ( DAT) , and glial fibrillary acidic protein ( GFAP ) positive cells were detected by immunohistochemical method. Dopamine ( DA ) , dihydroxyphenylacetic acid ( DOPAC ) , homovanilic acid ( HVA ) , 5-hydroxytryptamine ( 5-HT ) and 5-hydroxyindoleacetic acid (5-HIAA) in striatum were quantified by HPLC-ECD. Results MLR significantly ameliorated mouse motor coordination ability (P<0. 01 or P<0. 05). MLR at 280 and 560 mg·kg-1 could increase TH-positive neurons by 69. 00%and 77. 95% compared with the normal control group (P<0. 01) and DAT-positive neurons by 68. 53% and 70. 40% compared with the normal control group(P<0. 05), and decrease GFAP-postive astrocyte reactivity. The treatment with MLR at three doses attenuated the monoamine neurotransmitter disorder. Conclusion MLR markedly improves MPTP caused movement coordinate ability injury in mice and exerts therapeutic action on PD by regulating neurotransmitters in brain, inhibiting the inflammatory reaction and alleviating the neuron injury.