摘要
背景：蛋白酶体抑制剂硼替佐米(BTZ)诱导细胞内氧化应激导致周围神经病变的观点已被普遍接受。米托孔德协会Al功能障碍、细胞凋亡和内质网应激与细胞内氧化应激的关系尚不明确，尚需进一步研究。激活转录FActor 3(ATF 3)是周围神经损伤后在背根神经节(DRG)神经元中表达的一种应激中枢基因。 目的：通过激活ATF 3，探讨BTZ诱导细胞内氧化应激、线粒体功能障碍、细胞凋亡和ER应激的作用机制。 方法：采用原代培养的BTZ诱导神经毒性的DRG神经元和BTZ诱导的痛性周围神经病变大鼠的DRG来探讨这些问题。 结果：BTZ诱导DRG神经元ATF 3的上调与细胞内氧化应激、线粒体功能障碍、细胞凋亡和ER应激平行。在体内。用小干扰RNA(SiRNA)基因沉默技术阻断ATF 3信号转导可降低细胞内氧化应激、线粒体功能障碍、细胞凋亡和ER stres。BTZ处理后DRG神经元的S。 结论：本研究揭示了BTZ通过激活ATF 3导致细胞内氧化应激、线粒体功能紊乱而诱导神经毒性的重要机制。、细胞凋亡、ER应激，并通过阻断ATF 3信号通路提供了新的治疗靶点。
关键词: 氧化应激、线粒体功能障碍、细胞凋亡、内质网应激、激活转录因子3、硼替佐米、神经病、背根神经节。
图形摘要
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