中国康复理论与实践
中國康複理論與實踐
중국강복이론여실천
CHINESE JOURNAL OF REHABILITATION THEORY & PRACTICE
2013年
5期
440-443
,共4页
赵彩燕%雒晓东%林明欣%苏巧珍%郑春叶
趙綵燕%雒曉東%林明訢%囌巧珍%鄭春葉
조채연%락효동%림명흔%소교진%정춘협
帕金森病%帕病1号方%抗氧化作用%Akt信号转导通路%神经保护机制
帕金森病%帕病1號方%抗氧化作用%Akt信號轉導通路%神經保護機製
파금삼병%파병1호방%항양화작용%Akt신호전도통로%신경보호궤제
Parkinson's Disease%Pabing Formula I Granules%antioxidation%Akt signaling pathway%neuroprotection
目的探讨帕病1号方颗粒对帕金森病(PD)模型大鼠发挥神经保护作用的机制.方法采用6-羟基多巴胺纹状体两点注射法造成左侧纹状体损毁模型大鼠,把造模成功的40只大鼠分为3组:模型组(n=12),高剂量组(n=14),低剂量组(n=14).另加正常组(n=8).高、低剂量组每天分别给予帕病1号方颗粒18 g/kg,9 g/kg,模型组、正常组均予等体积蒸馏水.32 d后,行旋转测试;测定大鼠左侧纹状体匀浆中超氧化物歧化酶(SOD)活性及谷胱甘肽(GSH)、丙二醛( MDA)含量,免疫组化法检测中脑黑质P-Akt(ser 473)、Bcl-2、Bax表达.结果治疗后,与同期模型组相比,高、低剂量组旋转行为学明显改善(P<0.01),且存在量效关系(P<0.01).与同期模型组相比,高剂量组SOD活性(P<0.01)和GSH含量明显提高(P<0.01),MDA含量降低(P<0.01);低剂量组GSH含量提高(P<0.01),MDA含量降低(P<0.01);与低剂量相比,高剂量组GSH含量提高(P<0.01), MDA含量降低了(P<0.01).与模型组相比,高、低剂量组P-Akt(ser 473)、Bcl-2、Bax阳性细胞数及Bc1-2/Bax比值有显著性差异(P<0.05),且存在量效关系(P<0.05).结论帕病1号方颗粒能提高大鼠抗氧化能力和清除自由基能力,同时激活Akt信号转导通路,发挥其神经保护作用.其神经保护作用呈一定的量效关系.
目的探討帕病1號方顆粒對帕金森病(PD)模型大鼠髮揮神經保護作用的機製.方法採用6-羥基多巴胺紋狀體兩點註射法造成左側紋狀體損燬模型大鼠,把造模成功的40隻大鼠分為3組:模型組(n=12),高劑量組(n=14),低劑量組(n=14).另加正常組(n=8).高、低劑量組每天分彆給予帕病1號方顆粒18 g/kg,9 g/kg,模型組、正常組均予等體積蒸餾水.32 d後,行鏇轉測試;測定大鼠左側紋狀體勻漿中超氧化物歧化酶(SOD)活性及穀胱甘肽(GSH)、丙二醛( MDA)含量,免疫組化法檢測中腦黑質P-Akt(ser 473)、Bcl-2、Bax錶達.結果治療後,與同期模型組相比,高、低劑量組鏇轉行為學明顯改善(P<0.01),且存在量效關繫(P<0.01).與同期模型組相比,高劑量組SOD活性(P<0.01)和GSH含量明顯提高(P<0.01),MDA含量降低(P<0.01);低劑量組GSH含量提高(P<0.01),MDA含量降低(P<0.01);與低劑量相比,高劑量組GSH含量提高(P<0.01), MDA含量降低瞭(P<0.01).與模型組相比,高、低劑量組P-Akt(ser 473)、Bcl-2、Bax暘性細胞數及Bc1-2/Bax比值有顯著性差異(P<0.05),且存在量效關繫(P<0.05).結論帕病1號方顆粒能提高大鼠抗氧化能力和清除自由基能力,同時激活Akt信號轉導通路,髮揮其神經保護作用.其神經保護作用呈一定的量效關繫.
목적탐토파병1호방과립대파금삼병(PD)모형대서발휘신경보호작용적궤제.방법채용6-간기다파알문상체량점주사법조성좌측문상체손훼모형대서,파조모성공적40지대서분위3조:모형조(n=12),고제량조(n=14),저제량조(n=14).령가정상조(n=8).고、저제량조매천분별급여파병1호방과립18 g/kg,9 g/kg,모형조、정상조균여등체적증류수.32 d후,행선전측시;측정대서좌측문상체균장중초양화물기화매(SOD)활성급곡광감태(GSH)、병이철( MDA)함량,면역조화법검측중뇌흑질P-Akt(ser 473)、Bcl-2、Bax표체.결과치료후,여동기모형조상비,고、저제량조선전행위학명현개선(P<0.01),차존재량효관계(P<0.01).여동기모형조상비,고제량조SOD활성(P<0.01)화GSH함량명현제고(P<0.01),MDA함량강저(P<0.01);저제량조GSH함량제고(P<0.01),MDA함량강저(P<0.01);여저제량상비,고제량조GSH함량제고(P<0.01), MDA함량강저료(P<0.01).여모형조상비,고、저제량조P-Akt(ser 473)、Bcl-2、Bax양성세포수급Bc1-2/Bax비치유현저성차이(P<0.05),차존재량효관계(P<0.05).결론파병1호방과립능제고대서항양화능력화청제자유기능력,동시격활Akt신호전도통로,발휘기신경보호작용.기신경보호작용정일정적량효관계.
Objective To explore the neuroprotection of Pabing Formula I Granules for Parkinson's disease (PD) rats. Methods PD rats were induced with injection of 6-hydroxy dopamine twice stereotaxically into the left striatum. 40 rats modeled successfully were divided in-to model group (n=12), high dose group (n=14) and low dose group (n=14), and the other 8 rats were as normal group. The high dose group and low dose group received Pabing Formula I Granules 18 g/kg and 9 g/kg respectively, while the model group and normal group were giv-en distilled water at the same volume, once a day for 32 d. Then, they were assessed with rotation test. The activities of superoxide dis-mutase (SOD), the levels of glutathione (GSH) and malonaldehyde (MDA) of their left striatum were measured, and the expression of P-Akt (ser 473), Bcl-2, and Bax in substantia nigra were detected with immunohistochemistry. Results The rotation released was significant differ-ent among the model, high dose and the low dose groups after treatment (P<0.01), with the activities of SOD (P<0.01) and the content of GSH (P<0.01) increasing and the content of MDA (P<0.01) descreasing. There was significant difference in the content of GSH (P<0.01) and MDA (P<0.01) between the high and the low dose groups. There was significant difference in expression of P-Akt (ser 473), Bcl-2 and Bax among the model, high dose and the low dose groups, as well as the Bcl-2/Bad ratio (P<0.05). Conclusion Pabing Formula I Granules plays neuroprotective effect through enhancing antioxidation and eliminating free radicals ability and Akt signaling pathway, which appears as dose-effect relationship.