LUYOR UCL-3200紫外交联仪用于吉林大学第一医院斑点印迹实验

信息摘要：

2026年，吉林大学第一医院神经内科、神经外科团队在《Cell Biology and Toxicology(ISSN 0742-2091)》(SCI期刊，Springer出版社)发表文献《SIRT5-mediated HSDL2 desuccinylation promotes diabetic-associated cognitive dysfunction via disrupting mitochondrial TRAP1》，文献中使用LUYOR UCL-3200紫外交联仪对斑点印迹(Dot blot)实验的硝酸纤维素膜进行紫外交联固定，用于验证K42位点琥珀酰化(Succ-K42)位点特异性抗体的识别特异性，为糖尿病相关认知功能障碍(DACD)中SIRT5/HSDL2/TRAP1信号轴的机制研究提供关键实验证据。

吉林大学第一医院将LUYOR UCL-3200用于斑点印迹实验

2026年，吉林大学第一医院神经内科、神经外科团队在《Cell Biology and Toxicology(ISSN 0742-2091)》(SCI期刊，Springer出版社)发表文献《SIRT5-mediated HSDL2 desuccinylation promotes diabetic-associated cognitive dysfunction via disrupting mitochondrial TRAP1》，文献中使用LUYOR UCL-3200紫外交联仪用于斑点印迹实验，对点样后的硝酸纤维素膜进行紫外交联固定，验证K42位点琥珀酰化位点特异性抗体的识别特异性。UCL-3200紫外交联仪在斑点印迹流程中承担关键的交联固定环节，通过紫外辐照将点样肽段稳定固定于硝酸纤维素膜上，确保后续封闭、一抗孵育、二抗孵育及化学发光检测等步骤中样品不脱落，UCL-3200紫外交联仪为抗体特异性验证结果的可重复性与可靠性提供保障。

吉林大学第一医院位于长春，是集医疗、教学、科研于一体的大型综合性医院。该研究团队围绕糖尿病相关认知功能障碍(DACD)的发病机制开展研究，利用生物信息学分析锁定线粒体相关蛋白HSDL2，并通过体内外实验系统揭示了SIRT5介导的HSDL2 K42位点去琥珀酰化修饰、经下调线粒体伴侣蛋白TRAP1引起线粒体功能障碍与神经元凋亡、最终导致认知功能损害的SIRT5/HSDL2/TRAP1信号轴机制。UCL-3200紫外交联仪用于的斑点印迹实验作为验证K42位点特异性抗体的关键手段，为上述分子机制的确认提供了重要实验证据。

本实验采用LUYOR UCL-3200作为斑点印迹实验的核心交联设备，用于对点样后的硝酸纤维素膜进行紫外交联固定。实验将未修饰(Unmodified)与琥珀酰化(Succinylated)的合成肽段变性后直接点样至硝酸纤维素膜，经UCL-3200紫外交联仪紫外辐照交联，使点样肽段稳定固定于膜表面；随后以5%脱脂牛奶封闭，与抗Succ-K42一抗4℃孵育过夜，再与HRP标记羊抗兔二抗室温孵育2 h，采用增强化学发光(ECL)底物显色检测斑点信号；平行膜以0.1%亚甲基蓝染色确认肽段上样量一致，保证结果判读的严谨性与可重复性。UCL-3200紫外交联仪用于斑点印迹结果表明，抗Succ-K42抗体特异性识别K42琥珀酰化肽段，而不识别未修饰对照肽段(Fig. 6G)，证实该位点特异性抗体可精确定量检测HSDL2的K42琥珀酰化修饰，UCL-3200紫外交联仪为揭示SIRT5/HSDL2/TRAP1信号轴在糖尿病相关认知功能障碍中的致病机制提供了直接实验证据。

该研究证实，LUYOR UCL-3200紫外交联仪可用于斑点印迹实验中硝酸纤维素膜的紫外交联固定，适用于位点特异性抗体识别特异性验证、蛋白/多肽膜固定等分子生物学应用场景。LUYOR UCL-3200紫外交联仪在国内外高校和科研院所得到广泛好评，欢迎私信或留言联系上海路阳了解详情！

原文段落

斑点印迹实验方法原文

The specificity of the custom anti-Succ-K42 antibody was validated by dot blot assay. Synthetic peptides (unmodified and succinylated) were denatured and spotted directly onto a nitrocellulose membrane. The membrane was cross-linked using a UV crosslinker (#UCL-3200, Luyang Instruments, Shanghai, China), followed by blocking with 5% skim milk. The membrane was then incubated with the primary anti-Succ-K42 antibody (#4408-M-R1, Youke Biotechnology) overnight at 4 °C, followed by incubation with an HRP-conjugated goat anti-rabbit secondary antibody (#AB0101, Abways) for 2 h at room temperature. Protein spots were visualized using an enhanced chemiluminescence substrate (#WBKLS0100, Millipore). For normalization, a parallel membrane was stained with 0.1% methylene blue (#G1300, Solarbio, Beijing, China) to confirm equal peptide loading.

斑点印迹实验结果原文

Dot blot assay revealed that the anti-Succ-K42 antibody preferentially recognized the K42-succinylated peptide but not the unsuccinylated control peptide (Fig. 6G).

研究结论原文

In summary, this study established HSDL2 as a critical pathogenic driver in DACD. We delineated a novel molecular pathway wherein SIRT5-mediated desuccinylation stabilized HSDL2 protein. The upregulated HSDL2 subsequently interacted with and downregulated TRAP1, leading to mitochondrial dysfunction and neuronal apoptosis. These findings unveiled the SIRT5/HSDL2/TRAP1 axis as a central mechanism contributing to cognitive decline in diabetes. Therefore, targeting this pathway represents a promising therapeutic strategy for mitigating DACD.

DOI:10.1007/s10565-026-10210-2