doi:10.3969/j.issn.1004-583X.2024.06.016

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模型	体内/体外实验	病种	机制	结果	参考文献
无	体外	帕金森病	通过氢键和疏水相互作用强烈结合MAO以可逆竞争方式抑制MAO-和MAO-B	岩藻黄素能可逆性竞争MAO,可用于治疗帕金森病	Zielińska-Nowak等^[25]
大脑中动脉损伤模型	体内体外均有	无	诱导Nrf2核转位并增强HO-1	岩藻黄素可以作为保护神经元免受脑缺血再灌注损伤的治疗药物	Hu等^[51]
创伤性脑损伤模型	体内体外均有	无	激动Nrf2-ARE	岩藻黄素可提高神经元存活率并降低ROS)水平	Zhang等^[52]
帕金森病模型	体内	帕金森病	抑制α-突触核蛋白表达和氧化应激	岩藻黄素可以对抗MPTP介导的帕金森病模型小氧的病理变化	Mumu等^[53]
AD模型	体外	AD	有效减少Aβ纤维和低聚物的形成且显著降低Aβ寡聚物的体外神经毒性	岩藻黄素可能通过抑制Aβ聚集和减弱Aβ神经毒性来改善AD	Xiang等^[54]
AD模型	体内体外均有	AD	抗氧化、抗炎以及抑制乙酰胆碱酯酶酶活性、Aβ (1-42)积累	岩藻黄素对AD的治疗效果较好	Lin等^[55]
无	体外	无	与多巴胺受体结合发挥激动剂作用的潜在机制涉及到特定的氨基酸残基。这些机制包括与D3受体的Ser196和Thr115位点结合,以及与D4受体的Ser196和Asp115位点结合。这种结合促使受体激活,进而发挥其生物学功能	岩藻黄素是一种潜在的D3/D4激动剂,可用于治疗帕金森病等神经退行性疾病	Paudel等^[56]

模型	体内/体外实验	病种	机制	结果	参考文献
无	体外	帕金森病	通过氢键和疏水相互作用强烈结合MAO以可逆竞争方式抑制MAO-和MAO-B	岩藻黄素能可逆性竞争MAO,可用于治疗帕金森病	Zielińska-Nowak等^[25]
大脑中动脉损伤模型	体内体外均有	无	诱导Nrf2核转位并增强HO-1	岩藻黄素可以作为保护神经元免受脑缺血再灌注损伤的治疗药物	Hu等^[51]
创伤性脑损伤模型	体内体外均有	无	激动Nrf2-ARE	岩藻黄素可提高神经元存活率并降低ROS)水平	Zhang等^[52]
帕金森病模型	体内	帕金森病	抑制α-突触核蛋白表达和氧化应激	岩藻黄素可以对抗MPTP介导的帕金森病模型小氧的病理变化	Mumu等^[53]
AD模型	体外	AD	有效减少Aβ纤维和低聚物的形成且显著降低Aβ寡聚物的体外神经毒性	岩藻黄素可能通过抑制Aβ聚集和减弱Aβ神经毒性来改善AD	Xiang等^[54]
AD模型	体内体外均有	AD	抗氧化、抗炎以及抑制乙酰胆碱酯酶酶活性、Aβ (1-42)积累	岩藻黄素对AD的治疗效果较好	Lin等^[55]
无	体外	无	与多巴胺受体结合发挥激动剂作用的潜在机制涉及到特定的氨基酸残基。这些机制包括与D3受体的Ser196和Thr115位点结合,以及与D4受体的Ser196和Asp115位点结合。这种结合促使受体激活,进而发挥其生物学功能	岩藻黄素是一种潜在的D3/D4激动剂,可用于治疗帕金森病等神经退行性疾病	Paudel等^[56]

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