抗氧化碳点用于对乙酰氨基苯酚诱导的急性肝损伤的改善

李燕, 蔡皓, 毕红

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高等学校化学学报 ›› 2025, Vol. 46 ›› Issue (6) : 107-114. DOI: 10.7503/cjcu20240130
研究论文

抗氧化碳点用于对乙酰氨基苯酚诱导的急性肝损伤的改善

作者信息 +

Antioxidative Carbon Dots Improving Acute Liver Injury Induced by Acetaminophen

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摘要

对乙酰氨基苯酚(APAP)是一种用于治疗头疼和发烧症状的药物, 其代谢产物会消耗肝脏内的谷胱甘肽(GSH), 引起氧化应激. 短时间内服用大量APAP会导致肝功能衰竭. 本文以邻苯二酚(CAT)和2,5-二羟基对苯二甲酸(DHTA)为前驱体, 采用一步水热法合成了具有强抗氧化能力和良好生物相容性的黄光碳点(D-CDs). 在斑马鱼APAP肝损伤模型中, 体内成像显示D-CDs可有效富集在斑马鱼肝脏部位. D-CDs增加了斑马鱼体内的超氧化物歧化酶(SOD)和GSH含量, 减少了丙二醛(MDA)含量, 有效改善了由APAP引起的氧化应激损伤.

Abstract

Acetaminophen(APAP) is a drug used to treat headaches and fever symptoms, and its metabolites deplete glutathione(GSH) in the liver and cause oxidative stress. Taking large amounts of APAP in a short period of time can lead to liver failure. Yellow-emissive carbon dots(D-CDs) with strong antioxidant ability and good biocompatibility were synthesized by one-step hydrothermal method using catechol(CAT) and 2,5-dihydroxyterephthalic acid(DHTA) as precursors. In the APAP-induced zebrafish liver injury model, in vivo imaging showed that D-CDs could be effectively enriched in the zebrafish liver. The superoxide dismutase(SOD) activity and GSH content was increased and the content of malondialdehyde(MDA) was reduced, which finally effectively improved APAP- induced oxidative stress injury in zebrafish.

关键词

碳点 / 抗氧化 / 对乙酰氨基苯酚 / 肝损伤 / 斑马鱼

Key words

Carbon dots / Antioxidant / Acetaminophen / Liver injury / Zebrafish

中图分类号

O614 / R318

引用本文

导出引用
李燕 , 蔡皓 , 毕红. 抗氧化碳点用于对乙酰氨基苯酚诱导的急性肝损伤的改善. 高等学校化学学报. 2025, 46(6): 107-114 https://doi.org/10.7503/cjcu20240130
LI Yan, CAI Hao, BI Hong. Antioxidative Carbon Dots Improving Acute Liver Injury Induced by Acetaminophen[J]. Chemical Journal of Chinese Universities. 2025, 46(6): 107-114 https://doi.org/10.7503/cjcu20240130

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致谢

感谢安徽大学杂化材料结构与功能调控教育部重点实验室和绿色高分子材料安徽省重点实验室的支持.

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