探討暴露聚苯乙烯塑膠微粒對小鼠大腦學習與記憶之分子機制與神經發炎的影響;The effects of polystyrene microplastics exposure on molecular mechanisms of learning and memory and neuroinflammation

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題名:	探討暴露聚苯乙烯塑膠微粒對小鼠大腦學習與記憶之分子機制與神經發炎的影響;The effects of polystyrene microplastics exposure on molecular mechanisms of learning and memory and neuroinflammation
作者:	劉晏均;Liu, Yan-Jun
貢獻者:	生命科學系
關鍵詞:	聚苯乙烯塑膠微粒;海馬迴;學習和記憶;突觸可塑性分子Arc
日期:	2022-07-26
上傳時間:	2022-10-04 11:03:15 (UTC+8)
出版者:	國立中央大學
摘要:	塑膠微粒(MPs)定義為直徑小於5 mm的塑膠顆粒，是一種新興環境污染物。因為塑膠微粒體積較小，它們能夠經由食物鏈進入生物體內，並積聚在周圍組織/器官中，隨後對器官造成損害。本實驗室先前研究發現，聚苯乙烯塑膠微粒(PS-MPs)會影響公鼠學習與記憶能力，然而，PS-MPs如何影響大腦學習及記憶的分子機制仍然未知。本篇研究結果顯示，小鼠口服2μm PS-MPs八周後，利用拉曼光譜分析，可觀察到2 μm PS-MPs在肝臟及大腦海馬迴腦區中累積，而海馬迴是學習與記憶的重要腦區，進一步針對八周PS-MPs公鼠海馬迴進行分子分析後，發現對突觸可塑性和記憶力至關重要的Activity-regulated cytoskeleton-associated protein (Arc)，其mRNA和蛋白質表達在海馬迴中顯著降低，但在PS-MPs母鼠中則沒有明顯差異。由於Arc蛋白會影響α-氨基-3-羥基-5-甲基-4-異噁唑丙酸受體(α-amino-3-hydroxy-5-methyl-4-isoxazolepropionic acid receptor, AMPAR)亞基之一的突觸蛋白GluA1的內吞作用，因此發現GluA1在八周PS-MPs公鼠的海馬迴中異常增加。此外，本篇研究也發現暴露PS-MPs的公鼠八周後會會增加海馬迴促炎因子TNF-α與IL-1β的mRNA表現量及小膠質細胞的活化。綜合上述結果顯示小鼠暴露PS-MPs會改變突觸相關蛋白的表達以及神經發炎，進而削弱海馬迴依賴性學習和記憶。;Microplastics (MPs), defined as plastics particles less than 5 mm in diameter, are an emerging environmental pollutant in worldwide. Sine MPs are smaller in size, they can enter organisms via the food chain and accumulate in tissues/organs, subsequently causing damage to the organs. Previous study has confirmed that polystyrene micropartics (PS-MPs) can affect learning and memory ability in male mice. However, the molecular mechanism on how PS-MPs affecting learning and memory is still unknown. Using Raman spectroscopy analysis, 2 μm PS-MPs were found in the liver and the hippocampus of mice with oral administration of PS-MPs for eight weeks. Since the hippocampus is an important brain areafor learning and memory, Ifurther explored the molecular mechanism in the hippocampus. I found that the mRNA and protein expressions of activity-regulated cytoskeleton-associated protein (Arc), a key regulator for synaptic plasticity and learning and memory, was significantly decreased in the hippocampus, but there was no difference in PS-MPs female mice. The Arc protein can regulate α-amino-3-hydroxy-5-methyl-4-isoxazolepropionic acid receptor (AMPAR) endocytosis. I found that GluA1, a subunit of AMPAR, was aberrantly increased in the hippocampus of PS-MPs male mice.Moreover, I also found that exposure to PS-MPs in male mice for eight weeks increased the mRNA expression of pro-inflammatory cytokines TNF-α and IL-1β in the hippocampus and induced microglia activation. Taken together, these results suggest that exposure to PS-MPs in mice alters synapse-associated protein expression and neuroinflammation, thereby impairing hippocampal-dependent learning and memory.
顯示於類別:	[生命科學研究所 ] 博碩士論文

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