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樟芝萃取物馬偕一號增加神經細胞的活性

Evaluation of Antrodia cinnamomea Extract MMH01 Effect on IMR-32 Neural Cells Activity

Abstracts


Senile Dementia (老年失智症) 是老化常見疾病之一,其中神經退化性病因所造成的疾病包括阿茲海默症及帕金森症等。由於人口老化且全世界目前都有阿茲海默氏症病患增加的趨勢,讓人不得不重視此議題。由於可能造成老年失智症的原因仍然不清楚,若能有效提升神經的保護作用,抑制發炎與神經細胞凋亡,或許可進而減緩神經認知功能的衰退與阿茲海默症發生率,達到保健預防或減緩失智的產生。最近的研究曾指出,樟芝的培養菌絲體萃取物能藉由抑制人類白血球的reactive oxygen species (ROS)生成,達到抗發炎的效果。而研究也顯示樟芝具有良好的抗氧化性,其子實體萃取物能抑制嗜中性細胞的ROS製造,並降低其附著能力,因此亦具有抗發炎及抗氧化的功效。最近,由牛樟芝子實體中萃取出特有的活性化合物「去氫硫色多孔菌酸化合物」(MMH01)。發現其能啟動癌細胞不正常分裂,導致癌細胞壞死,抑制癌細胞效果高達97%,讓癌細胞快速凋亡。因此本研究以神經細胞IMR-32 為對象,測試MMH01 是否可以增加其神經細胞活性。神經細胞大多為生長停滯或生長速度較為緩慢之細胞,但卻在此研究中意外發現MMH01可以提升具活性健康之神經細胞的比率,細胞抗氧化酵素之活性也有所上升,可知在適當劑量作用下MMH01能夠維持神經細胞株的健康活性。另外,在觀察MMH01 馬偕一號誘導發炎相關基因的表現後,結果顯示如IL-1β 、IL-6 及iNOS 等發炎基因都呈現了劑量依賴性的正相關;而CCL2 因子與MMH01 在神經細胞活性調節作用中扮演相當重要的角色。

Parallel abstracts


Senile dementia is an important aging problem, including Alzheimer’s disease and Parkinson’s disease which occur as neurodegenerative processes. People have to pay attention to this topic due to aging population and current trend of increased Alzheimer's disease patients worldwide. So far the causal agent of senile dementia is still unknown, but we may reduce the incidence of Alzheimer’s disease and the neurodegeneration rate through increasing neuroprotection and suppressing neuronal inflammation and apoptosis. Recent study reveals that several ingredients of the extracts isolated from Antrodia cinnamomea (AC) mycelia possess complicated pharmacological and biological activities, which can decrease the production of reactive oxygen species (ROS). In addition, the extracts from AC fruiting body with anti-inflammatory effect can inhibit ROS production and decrease attached ability of neutrophils. Previously, researchers isolate a new compound, 24-Methylen elanosta-7, 9(11)-diene-3 , 15 -diol-21-oicacid, designated as MMH01, from the fruiting body of AC, and found that possesses toxicity against human leukemia and pancreatic cancer cells, even up to 97% in anti-cancer effect. Therefore, this study used human neuroblastoma cell line, IMR-32 to detect whether AC could enhance the neural cell activity. Most of neural cells are growth arrest or growth slowness; however we found that MMH01 with an appropriate-dose manner was able to increase the healthy cells ratio and raise the activity of antioxidant enzyme. We also found that the expressions of inflammatory genes like IL-1β, IL-6, iNOS et al are dose-dependently correlated with the concentration of MMH01, while CCL2 may play a vital role in regulation of neural cells activity. Further study of the mechanisms of AC action is needed to define how MMH01 contribute to increase IMR-32 cell activity.

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