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Endoplasmic Reticulum-Targeted Carbon Monoxide Photoreleaser for Drug-Induced Hepatotoxicity Remediation
Analytical Chemistry ( IF 6.7 ) Pub Date : 2023-05-04 , DOI: 10.1021/acs.analchem.2c03540 Yong Li 1 , Jiangong Zhang 1 , Simiao Cheng 1 , Xu Wang 1 , Jian Zhang 1 , Xilei Xie 1 , Xiaoyun Jiao 1 , Bo Tang 1
Analytical Chemistry ( IF 6.7 ) Pub Date : 2023-05-04 , DOI: 10.1021/acs.analchem.2c03540 Yong Li 1 , Jiangong Zhang 1 , Simiao Cheng 1 , Xu Wang 1 , Jian Zhang 1 , Xilei Xie 1 , Xiaoyun Jiao 1 , Bo Tang 1
Affiliation
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The alleviation of drug-induced liver injury has been a long-term public health concern. Growing evidence suggests that endoplasmic reticulum (ER) stress plays a critical role in the pathogenesis of drug-induced hepatotoxicity. Therefore, the inhibition of ER stress has gradually become one of the important pathways to alleviate drug-induced liver injury. In this work, we developed an ER-targeted photoreleaser, ERC, for controllable carbon monoxide (CO) release with a near-infrared light trigger. By employing peroxynitrite (ONOO–) as an imaging biomarker of hepatotoxicity, the remediating effect of CO was mapped upon drug acetaminophen (APAP) challenge. The direct and visual evidence of suppressing oxidative and nitrosative stress by CO was obtained both in living cells and in mice. Additionally, the ER stress inhibiting the effect of CO was verified during drug-induced hepatotoxicity. This work demonstrated that CO may be employed as a potent potential antidote for APAP-related oxidative and nitrative stress remediation.
中文翻译：
内质网靶向一氧化碳光释放剂用于药物性肝毒性修复
减轻药物性肝损伤一直是一个长期的公共卫生问题。越来越多的证据表明，内质网 (ER) 应激在药物诱导的肝毒性的发病机制中起着关键作用。因此，抑制内质网应激逐渐成为减轻药物性肝损伤的重要途径之一。在这项工作中，我们开发了一种以 ER 为目标的光致释放剂ERC，用于通过近红外光触发来控制一氧化碳 (CO) 的释放。通过使用过氧亚硝酸盐 (ONOO –) 作为肝毒性的成像生物标志物，CO 的补救作用被映射到药物对乙酰氨基酚 (APAP) 挑战上。在活细胞和小鼠中都获得了 CO 抑制氧化应激和亚硝化应激的直接和视觉证据。此外，抑制 CO 作用的内质网应激在药物诱导的肝毒性过程中得到验证。这项工作表明，CO 可用作 APAP 相关氧化和硝化应激修复的有效潜在解毒剂。
更新日期：2023-05-04
中文翻译：
内质网靶向一氧化碳光释放剂用于药物性肝毒性修复
减轻药物性肝损伤一直是一个长期的公共卫生问题。越来越多的证据表明，内质网 (ER) 应激在药物诱导的肝毒性的发病机制中起着关键作用。因此，抑制内质网应激逐渐成为减轻药物性肝损伤的重要途径之一。在这项工作中，我们开发了一种以 ER 为目标的光致释放剂ERC，用于通过近红外光触发来控制一氧化碳 (CO) 的释放。通过使用过氧亚硝酸盐 (ONOO –) 作为肝毒性的成像生物标志物，CO 的补救作用被映射到药物对乙酰氨基酚 (APAP) 挑战上。在活细胞和小鼠中都获得了 CO 抑制氧化应激和亚硝化应激的直接和视觉证据。此外，抑制 CO 作用的内质网应激在药物诱导的肝毒性过程中得到验证。这项工作表明，CO 可用作 APAP 相关氧化和硝化应激修复的有效潜在解毒剂。
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