在神經元的發育、突觸形成及突觸可塑性的調節中，小分子核醣核酸如何參與這些過程近幾年得到相當多的重視，並且在許多的神經疾病中，如：腦部缺血、神經興奮性毒性及阿茲海默症中，皆曾被報導過小分子核醣核酸有神經保護性功效。本實驗室過去研究指出，在亨丁頓氏手舞足蹈症的細胞、基因轉殖小鼠或人類誘導性多功能幹細胞模式中，特定的小分子核醣核酸-196a具有保護性功效並且改善了病理上及行為學上的表現型態。以上結果暗示，小分子核醣核酸-196a在神經保護作用中扮演重要的角色。近年文獻指出小分子核醣核酸-196a可以藉由抑制IκBα表現量，促使NF-κB活性提升，因此我們推測小分子核醣核酸-196a能藉由調控NF-κB活性而達到神經保護功效。在本篇論文中，我們著重於小分子核醣核酸-196a對神經保護功效中的增加突觸可塑性及增進細胞抗凋亡能力此兩方向進行探討。本論文實驗結果發現在小鼠神經瘤母細胞中及基因轉殖小鼠中，小分子核醣核酸-196a大量表現之後，確實可增加NF-κB的表現量與活性。我們更進一步的發現與突觸可塑性相關的NF-κB目標基因-鈣結合蛋白D-28K在基因轉殖小鼠模式中其蛋白質的表現量有顯著的增加。除此之外，突觸蛋白基因-囊泡相關膜蛋白-1，及與神經活性相關的基因-c fos，在小分子核醣核酸-196a基因轉殖小鼠中也顯著性的提升。此暗示了小分子核醣核酸-196a在基因轉殖小鼠中模式中能提升突觸可塑性及神經活性。另一部分，我們發現在小鼠神經瘤母細胞處於氧化逆境下時，小分子核醣核酸-196a能藉由降低NF-κB目標基因-促凋亡蛋白Bim的表達，進而減少細胞凋亡，增進神經細胞抵抗氧化壓力的能力。綜合我們的結果，發現小分子核醣核酸-196a能提升NF-κB活性，並且也提升了突觸可塑性及增加細胞抗凋亡功能，此發現也許能提供未來對亨丁頓氏手舞足蹈症潛在的治療策略。

MicroRNAs (miRNAs) have attracted much attention at neuronal development, synapse formation and synaptic plasticity regulation. Besides, emerging evidences suggest that miRNAs are involved in the neuroprotective effects in many neurological disorders, such as brain ischemia, excitotoxicity and Alzheimer's disease. One previous study published from our laboratory indicated that miR-196a ameliorates phenotypes of Huntington’s disease in cells, transgenic mice and patient-derived induced pluripotent stem cell models, indicating that miR-196a may play an important role in neuroprotection. Recently, studies have revealed that miR-196a could directly interact with nuclear factor-keppa B inhibitor alpha (IĸBα) 3'UTR to suppress IκBα expression and subsequently promotes nuclear factor kappa B (NF-κB) activation. Therefore, we hypothesize miR-196a might have neuroprotective effects through NF-ĸB activation. Here, we focuse on the effects of miR-196a on synaptic plasticity and anti-apoptotic functions. Our results suggest that IĸBα is down-regulated and NF-ĸB is activated as miR-196a was overexpressed in cells and transgenic mouse models. Additionally, the brains of miR-196a transgenic mice display higher expression of calbindinD-28k, related to synaptic plasticity. Furthermore, the miR-196a transgenic mice express higher vesicle-associated membrane protein 1 and c-fos, markers for synaptic proteins and neuron activities respectively, compared to those of wild type mice. Besides, miR-196a down-regulates the expression of pro-apoptotic protein Bim and elevates cell viability in the presence of oxidative stress in vitro. Our results identify a possible function of miR-196a on neuroprotection through NF-ĸB activation, and may provide a potential therapeutic strategy for several neurodegenerative diseases.

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