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長期餵食六味地黃丸對大鼠被動迴避學習反應之影響

Effects of Liu-Wei-Di-Huang-Wan after Long-term Consecutive Treatment on Inhibitory Avoidance Response in Rats

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摘要


Vanillyl alcohol (香芙醇蘭)是天麻的成份之一,先前我們的研究發現vanillyl alcohol 可以減少FeCl3 所誘發的癲癎發作,它的抗癲癎作用部份來自於它對自由基的清除或抑制自由基的產生,因此本研究的目標是更進一步探討它的抗癲癎機轉。方法是於Sprague - Dawley ( SD )大鼠的腹腔注射kainic acid (KA,12mg/kg )誘發痛痛發作模型。實驗A是分別接受Vanillyl alcohol100mg/kg, 200mg/kg 腹腔注射, 以wet dog shakes (WDS)的發作次數為指標觀察vanillyl alcohol 的抗癱摘效用,以及觀察KA誘發WDS發作頻率的時間超過。實驗B 是於KA腹腔注射後的60分鐘同時測量末梢血液中的luminol chemilumines-ence(CL) counts 和lucigenin chemiluminesence counts,以及腦組織中的su-peroxidedismutase (SOD)活性來觀察vanillyl alcohol 的抗癲癎機轉結果顯示於KA注射後60分鐘左右WDS的發作頻率達到高峰。Vanillyl alcohol00mg/kg 和200mg/kg兩者都能減少KA所誘發的WDS次數。另外,在KA 治療的大鼠, vanillyl alcohol 1O0mg/kg和200mg./均可以降低血液中luminol - CL counts 與lucigenin - CL counts'同時左右大腦中的SOD活性較低,但小腦則無變化。結論是Vanillyl alcohol 能減少KA誘發WDS的次數,這些說明vanillyl al-cohol對於KA誘發的癲癎發作具有抗癲癎的作用。另外, Vanillyl alcohol 能減少末梢血液KA所誘發的luminol - CL 和lucigenin - CL counts,以及大腦組織的SOD 活性,說明vanillyl alcohol 的抗癲癎機轉和它的清除或抑制自由基有關, 而這些作用可能先經曲SOD的消耗而來,或vanillyl alchol對自由基及SOD兩者同時都有抑制作用的結果須進一步的探討。

並列摘要


In present study we aimed to investigate the attenuating effects of LWw on various drugs (SCOP and PCA)─induced memory impairment in the passive avoidance task. Moreover, the effect on motivational or motor systems can in turn affect the acquisition of the avoidance response. We also investigated the motor activity and pain threshold of LWw to separate the attenuating effect of LWw on memory impairment from those on motivational or motor systems. After two - week concurrent administration, LWw at any dosage attenuated the SCOP - and PCA─induced acquisition impairment. Furthermore, the counteracting effect of LWw on PCA - induced memory deficit was antagonized by 8 ─ OHDPAT and DOL M - SCOP also partially blocked the counteracting affect of LWw on SCOP - induced memory deficit. From our present data, it suggested LWw at any dosage attenuated the SCOP - and PCA - induced acquisition impairment. LW w at any dosage did not possessed sedative or analgesic activities, and the attenuating effects of it might be re-1ated to memory processes. The mechanism of the atternuating effects of LWw on memory deficit was related to decreasing the serotonergic neuronal activity via 5 ─ HT1A and 5 – HT2 receptors, and activating the peripheral nervous systems.

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