目的:探讨右美托咪定复合超声引导下腹横肌平面(TAP)阻滞麻醉对腹腔镜下腹股沟疝修补术病人血清β-42淀粉样蛋白(Aβ-42)和Tau蛋白的影响。方法:选取行腹腔镜下腹股沟疝修补术病人100例,随机分为对照组和观察组,各50例。对照组行喉罩全...目的:探讨右美托咪定复合超声引导下腹横肌平面(TAP)阻滞麻醉对腹腔镜下腹股沟疝修补术病人血清β-42淀粉样蛋白(Aβ-42)和Tau蛋白的影响。方法:选取行腹腔镜下腹股沟疝修补术病人100例,随机分为对照组和观察组,各50例。对照组行喉罩全麻,观察组采用超声引导下TAP阻滞联合右美托咪定麻醉。记录2组病人切皮时(T1)、手术开始1 h(T2)、手术结束即刻(T3)的平均动脉压和心率(HR)、血氧饱和度。比较2组疼痛视觉模拟评分(VAS)、简易智能状态检查量表(MMSE)评分、术后认知功能障碍(POCD)的发生率及Aβ-42和Tau蛋白表达水平。结果:2组病人术后即刻和术后6、24、48 h VAS评分逐渐降低降低(P<0.05);观察组术后6、24、48 h VAS评分均明显低于对照组(P<0.01)。观察组T2、T3 HR均明显低于对照组(P<0.01),且T2、T3时HR低于T1(P<0.05)。术后观察组POCD的发生率为6.00%(3/50),低于对照组的22.00%(11/50)(P<0.05)。术后1、7 d 2组MMSE评分均低于麻醉前(P<0.05),且观察组MMSE评分明显高于对照组(P<0.01)。术后7 d 2组Tau蛋白水平均高于麻醉前(P<0.05),Aβ-42蛋白水平均低于麻醉前(P<0.05),Tau/Aβ-42值高于麻醉前(P<0.05);且观察组Tau蛋白水平及Tau/Aβ-42值均低于对照组(P<0.05和P<0.01),Aβ-42水平明显高于对照组(P<0.01)。结论:超声引导下TAP阻滞麻醉联合右美托咪定在腹腔镜下腹股沟疝修补术中镇痛效果显著,同时有效改善病人的认知功能,调节术后血清Aβ-42和Tau蛋白水平,降低POCD发生率。展开更多
BACKGROUND: The pharmacological actions of Panax notoginseng saponins (PNS) lie in removing free radicals, anti-inflammation and anti-oxygenation. It can also improve memory and behavior in rat models of Alzheimer’s ...BACKGROUND: The pharmacological actions of Panax notoginseng saponins (PNS) lie in removing free radicals, anti-inflammation and anti-oxygenation. It can also improve memory and behavior in rat models of Alzheimer’s disease. OBJECTIVE: Using the Morris water maze, immunohistochemistry, real-time PCR and RT-PCR, this study aimed to measure improvement in spatial learning, memory, expression of amyloid precursor protein (App) and β-amyloid (Aβ), to investigate the mechanism of action of PNS in the treatment of AD in the senescence accelerated mouse-prone 8 (SAMP8) and compare the effects with huperzine A. DESIGN, TIME AND SETTING: A completely randomized grouping design, controlled animal experiment was performed in the Center for Research & Development of New Drugs, Guangxi Traditional Chinese Medical University from July 2005 to April 2007. MATERIALS: Sixty male SAMP8 mice, aged 3 months, purchased from Tianjin Chinese Traditional Medical University of China, were divided into four groups: PNS high-dosage group, PNS low-dosage group, huperzine A group and control group. PNS was provided by Weihe Pharmaceutical Co., Ltd. (batch No.: Z53021485, Yuxi, Yunan Province, China). Huperzine A was provided by Zhenyuan Pharmaceutical Co., Ltd. (batch No.: 20040801, Zhejiang, China). METHODS: The high-dosage group and low-dosage group were treated with 93.50 and 23.38 mg/kg PNS respectively per day and the huperzine A group was treated with 0.038 6 mg/kg huperzine A per day, all by intragastric administration, for 8 consecutive weeks. The same volume of double distilled water was given to the control group. MAIN OUTCOME MEASURES: After drug administration, learning and memory abilities were assessed by place navigation and spatial probe tests. The recording indices consisted of escape latency (time-to-platform), and the percentage of swimming time spent in each quadrant. The number of Aβ1-40, Aβ1-42 and App immunopositive neurons in the brains of SAMP8 mice was analyzed by immunohistochemistry. The mRNA content of App, tau, acetylcholinesterase, and synaptophysin (Syp) was tested by real time PCR and RT-PCR. RESULTS: The PCR results show that PNS can downregulate the expression of the App gene and upregulate the expression of the Syp gene in the parietal cortex and hippocampus of SAMP8 mice. The therapeutic effects of the PNS high-dosage group were greater than those of the PNS low-dosage group and the huperzine A group (P < 0.05). The results of the Morris water maze and immunohistochemistry indicated that PNS can improve the capacity for spatial learning and memory in SAMP8 mice, and reduce the content of Aβ1-40, Aβ1-42 and expression of App in the brains of SAMP8 mice. The therapeutic effects of the PNS high-dosage group were greater than that of the PNS low-dosage group and the huperzine A group (P < 0.05). CONCLUSION: These results support the hypothesis that PNS plays a therapeutic and protective role on the pathological lesions and learning dysfunction of Alzheimer’s disease. The therapeutic effects of PNS for Alzheimer’s disease are possibly achieved through downregulating the expression of the App gene and upregulating the expression of the Syp gene. The therapeutic effects of PNS are dose-dependent and are greater than the effect of huperzine A.展开更多
文摘目的:探讨右美托咪定复合超声引导下腹横肌平面(TAP)阻滞麻醉对腹腔镜下腹股沟疝修补术病人血清β-42淀粉样蛋白(Aβ-42)和Tau蛋白的影响。方法:选取行腹腔镜下腹股沟疝修补术病人100例,随机分为对照组和观察组,各50例。对照组行喉罩全麻,观察组采用超声引导下TAP阻滞联合右美托咪定麻醉。记录2组病人切皮时(T1)、手术开始1 h(T2)、手术结束即刻(T3)的平均动脉压和心率(HR)、血氧饱和度。比较2组疼痛视觉模拟评分(VAS)、简易智能状态检查量表(MMSE)评分、术后认知功能障碍(POCD)的发生率及Aβ-42和Tau蛋白表达水平。结果:2组病人术后即刻和术后6、24、48 h VAS评分逐渐降低降低(P<0.05);观察组术后6、24、48 h VAS评分均明显低于对照组(P<0.01)。观察组T2、T3 HR均明显低于对照组(P<0.01),且T2、T3时HR低于T1(P<0.05)。术后观察组POCD的发生率为6.00%(3/50),低于对照组的22.00%(11/50)(P<0.05)。术后1、7 d 2组MMSE评分均低于麻醉前(P<0.05),且观察组MMSE评分明显高于对照组(P<0.01)。术后7 d 2组Tau蛋白水平均高于麻醉前(P<0.05),Aβ-42蛋白水平均低于麻醉前(P<0.05),Tau/Aβ-42值高于麻醉前(P<0.05);且观察组Tau蛋白水平及Tau/Aβ-42值均低于对照组(P<0.05和P<0.01),Aβ-42水平明显高于对照组(P<0.01)。结论:超声引导下TAP阻滞麻醉联合右美托咪定在腹腔镜下腹股沟疝修补术中镇痛效果显著,同时有效改善病人的认知功能,调节术后血清Aβ-42和Tau蛋白水平,降低POCD发生率。
基金the National Natural Science Foundation of China, No: 30560189
文摘BACKGROUND: The pharmacological actions of Panax notoginseng saponins (PNS) lie in removing free radicals, anti-inflammation and anti-oxygenation. It can also improve memory and behavior in rat models of Alzheimer’s disease. OBJECTIVE: Using the Morris water maze, immunohistochemistry, real-time PCR and RT-PCR, this study aimed to measure improvement in spatial learning, memory, expression of amyloid precursor protein (App) and β-amyloid (Aβ), to investigate the mechanism of action of PNS in the treatment of AD in the senescence accelerated mouse-prone 8 (SAMP8) and compare the effects with huperzine A. DESIGN, TIME AND SETTING: A completely randomized grouping design, controlled animal experiment was performed in the Center for Research & Development of New Drugs, Guangxi Traditional Chinese Medical University from July 2005 to April 2007. MATERIALS: Sixty male SAMP8 mice, aged 3 months, purchased from Tianjin Chinese Traditional Medical University of China, were divided into four groups: PNS high-dosage group, PNS low-dosage group, huperzine A group and control group. PNS was provided by Weihe Pharmaceutical Co., Ltd. (batch No.: Z53021485, Yuxi, Yunan Province, China). Huperzine A was provided by Zhenyuan Pharmaceutical Co., Ltd. (batch No.: 20040801, Zhejiang, China). METHODS: The high-dosage group and low-dosage group were treated with 93.50 and 23.38 mg/kg PNS respectively per day and the huperzine A group was treated with 0.038 6 mg/kg huperzine A per day, all by intragastric administration, for 8 consecutive weeks. The same volume of double distilled water was given to the control group. MAIN OUTCOME MEASURES: After drug administration, learning and memory abilities were assessed by place navigation and spatial probe tests. The recording indices consisted of escape latency (time-to-platform), and the percentage of swimming time spent in each quadrant. The number of Aβ1-40, Aβ1-42 and App immunopositive neurons in the brains of SAMP8 mice was analyzed by immunohistochemistry. The mRNA content of App, tau, acetylcholinesterase, and synaptophysin (Syp) was tested by real time PCR and RT-PCR. RESULTS: The PCR results show that PNS can downregulate the expression of the App gene and upregulate the expression of the Syp gene in the parietal cortex and hippocampus of SAMP8 mice. The therapeutic effects of the PNS high-dosage group were greater than those of the PNS low-dosage group and the huperzine A group (P < 0.05). The results of the Morris water maze and immunohistochemistry indicated that PNS can improve the capacity for spatial learning and memory in SAMP8 mice, and reduce the content of Aβ1-40, Aβ1-42 and expression of App in the brains of SAMP8 mice. The therapeutic effects of the PNS high-dosage group were greater than that of the PNS low-dosage group and the huperzine A group (P < 0.05). CONCLUSION: These results support the hypothesis that PNS plays a therapeutic and protective role on the pathological lesions and learning dysfunction of Alzheimer’s disease. The therapeutic effects of PNS for Alzheimer’s disease are possibly achieved through downregulating the expression of the App gene and upregulating the expression of the Syp gene. The therapeutic effects of PNS are dose-dependent and are greater than the effect of huperzine A.
