中国药理学通报
中國藥理學通報
중국약이학통보
CHINESE PHARMACOLOGICAL BULLETIN
2014年
12期
1763-1768
,共6页
彭晓明%高莉%霍仕霞%闫明
彭曉明%高莉%霍仕霞%閆明
팽효명%고리%곽사하%염명
类叶升麻苷%阿尔采末病%D-半乳糖%三氯化铝%小鼠%皮层%Caspase-3%表达
類葉升痳苷%阿爾採末病%D-半乳糖%三氯化鋁%小鼠%皮層%Caspase-3%錶達
류협승마감%아이채말병%D-반유당%삼록화려%소서%피층%Caspase-3%표체
acteoside%Alzheimer′s disease%D-galac-tose%AlCl3%mice%cerebral cortex%caspase-3%expres-sion
目的:探讨类叶升麻苷(acteoside,AS)对阿尔采末病(Alzheimer’s disease,AD)小鼠皮层组织中 Caspase-3基因表达的影响。方法将昆明(kunming,KM)小鼠随机分为正常组,模型组,vitamin E(VitE)组,类叶升麻苷低、中、高剂量组。除正常组外,其余各组小鼠均腹腔注射60 mg·kg -1· d -1的 D-半乳糖和灌胃5 mg·kg -1·d -1的三氯化铝,连续造模60 d 以制备 AD 模型。然后给以30、60、120 mg·kg -1·d -1的 AS 治疗30 d,期间造模继续。给药完成后,利用跳台法测定小鼠的学习和记忆能力,化学比色法测定小鼠血清及脑组织中的 AChE 活性;HE 染色观察各组小鼠皮层组织结构变化;免疫组化分析小鼠皮层组织中 caspase-3基因表达的变化。结果与模型组相比,AS 给药组小鼠的学习记忆能力有所改善,其下台潜伏期和错误次数均明显延长和减少(P <0.05或 P <0.01),血清和脑组织中 AChE 活性明显降低(P <0.05或 P <0.01),皮层组织中神经细胞的形态和数量明显改善(P <0.01),且皮层组织中 caspase-3基因表达明显下调(P <0.05或 P <0.01)。结论AS 对 D-半乳糖联合三氯化铝诱导的小鼠脑损伤具有明显保护作用,其保护机制可能是通过抑制小鼠皮层组织 caspase-3基因表达,进而维持皮层组织神经细胞的正常形态及数量。
目的:探討類葉升痳苷(acteoside,AS)對阿爾採末病(Alzheimer’s disease,AD)小鼠皮層組織中 Caspase-3基因錶達的影響。方法將昆明(kunming,KM)小鼠隨機分為正常組,模型組,vitamin E(VitE)組,類葉升痳苷低、中、高劑量組。除正常組外,其餘各組小鼠均腹腔註射60 mg·kg -1· d -1的 D-半乳糖和灌胃5 mg·kg -1·d -1的三氯化鋁,連續造模60 d 以製備 AD 模型。然後給以30、60、120 mg·kg -1·d -1的 AS 治療30 d,期間造模繼續。給藥完成後,利用跳檯法測定小鼠的學習和記憶能力,化學比色法測定小鼠血清及腦組織中的 AChE 活性;HE 染色觀察各組小鼠皮層組織結構變化;免疫組化分析小鼠皮層組織中 caspase-3基因錶達的變化。結果與模型組相比,AS 給藥組小鼠的學習記憶能力有所改善,其下檯潛伏期和錯誤次數均明顯延長和減少(P <0.05或 P <0.01),血清和腦組織中 AChE 活性明顯降低(P <0.05或 P <0.01),皮層組織中神經細胞的形態和數量明顯改善(P <0.01),且皮層組織中 caspase-3基因錶達明顯下調(P <0.05或 P <0.01)。結論AS 對 D-半乳糖聯閤三氯化鋁誘導的小鼠腦損傷具有明顯保護作用,其保護機製可能是通過抑製小鼠皮層組織 caspase-3基因錶達,進而維持皮層組織神經細胞的正常形態及數量。
목적:탐토류협승마감(acteoside,AS)대아이채말병(Alzheimer’s disease,AD)소서피층조직중 Caspase-3기인표체적영향。방법장곤명(kunming,KM)소서수궤분위정상조,모형조,vitamin E(VitE)조,류협승마감저、중、고제량조。제정상조외,기여각조소서균복강주사60 mg·kg -1· d -1적 D-반유당화관위5 mg·kg -1·d -1적삼록화려,련속조모60 d 이제비 AD 모형。연후급이30、60、120 mg·kg -1·d -1적 AS 치료30 d,기간조모계속。급약완성후,이용도태법측정소서적학습화기억능력,화학비색법측정소서혈청급뇌조직중적 AChE 활성;HE 염색관찰각조소서피층조직결구변화;면역조화분석소서피층조직중 caspase-3기인표체적변화。결과여모형조상비,AS 급약조소서적학습기억능력유소개선,기하태잠복기화착오차수균명현연장화감소(P <0.05혹 P <0.01),혈청화뇌조직중 AChE 활성명현강저(P <0.05혹 P <0.01),피층조직중신경세포적형태화수량명현개선(P <0.01),차피층조직중 caspase-3기인표체명현하조(P <0.05혹 P <0.01)。결론AS 대 D-반유당연합삼록화려유도적소서뇌손상구유명현보호작용,기보호궤제가능시통과억제소서피층조직 caspase-3기인표체,진이유지피층조직신경세포적정상형태급수량。
Aim To investigate the effect of acteoside (AS)on the expression of caspase-3 in cerebral cortex of mouse models of Alzheimer’s disease(AD).Meth-ods Kunming (KM)strain mice were assigned into control group,model group,positive control group (VitE)and acteoside group.Every group was induced by a combination of D-galactose(i.p.60mg·kg -1 · d -1 )and AlCl3 (i.g.5mg·kg -1 ·d -1 )for 60ds ex-cept for control group,then mice were treated by dif-ferent concentrations(30,60,1 20 mg·kg -1 ·d -1 )of acteoside for 30ds.During the time,mice were in-duced continuously by a combination of D-galactose and AlCl3 .The learning and memory of mice were de-tected by step-down test,the activity of AChE in serum and brain of mice was measured by chemical colorime-try,the structure changes in cerebral cortex were ob-served by HE staining,and the expression of caspase-3 in cerebral cortex was analyzed through the immunohis-tochemical staining.Results Compared with model group,acteoside could improve the learning and mem-ory abilities(P <0.05 or P <0.01 ),decrease the ac-tivity of AChE in serum and brain(P <0.05 or P <0.01 ),and improve the morphology and number of neuron in cerebral cortex(P <0.01 ).Moreover,acte-oside could significantly inhibit the expression of caspase-3 in cerebral cortex (P <0.05,P <0.01 ). Conclusion Acteoside has significantly protective effects on brain damage of mice induced by a combina-tion of D-galactose and AlCl3 , and it′s protective mechanism probably relate to inhibiting the expression of caspase-3 and maintainings the normal morphology and number of neuron in cerebral cortex.