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金银花对乙酰氨基酚诱导的肝损伤的保护作用及其机制。

Protection of Flos Lonicerae against acetaminophen-induced liver injury and its mechanism.

机构信息

The MOE Key Laboratory for Standardization of Chinese Medicines, The SATCM Key Laboratory for New Resources and Quality Evaluation of Chinese Medicines and Shanghai Key Laboratory of Complex Prescription, Institute of Chinese Materia Medica, Shanghai University of Traditional Chinese Medicine, Shanghai 201203, China.

Center for Drug Safety Evaluation and Research, Shanghai University of Traditional Chinese Medicine, Shanghai 201203, China.

出版信息

Environ Toxicol Pharmacol. 2014 Nov;38(3):991-9. doi: 10.1016/j.etap.2014.10.019. Epub 2014 Nov 1.

DOI:10.1016/j.etap.2014.10.019
PMID:25461560
Abstract

This study aims to observe the protective action of Flos Lonicerae (FL) aqueous extract against acetaminophen (AP)-induced liver injury and its mechanism. Results show that FL decreases AP-increased serum alanine/aspartate transaminases (ALT/AST) activity, as well as total bilirubin (TB) amount, in mice. Histological evaluation of the liver further confirms the protection of FL against AP-induced hepatotoxicity. TdT-mediated biotin-dUTP nick-end labeling (TUNEL) assay shows that FL reduces AP-increased apoptotic cells. Furthermore, AP-decreased liver glutamate-cysteine ligase (GCL) enzymatic activity and glutathione (GSH) amount are both reversed by FL because of the increased expression of the catalytic subunit of GCL (GCLC) protein. The amount of chlorogenic acid (CGA), caffeic acid, and luteolin, the main active compounds in FL, is detected by high-performance liquid chromatography (HPLC). In addition, cell viability assay demonstrates that polyphenols in FL, such as CGA, caffeic acid, as well as isochlorogenic acids A, B, and C, can reverse AP-induced cytotoxicity. In conclusion, FL can prevent AP-induced liver injury by inhibiting apoptosis. The cellular antioxidant enzyme GCL is also involved in such protection. Polyphenols may be the main active hepato-protective ingredients in FL.

摘要

本研究旨在观察金银花(FL)水提物对醋氨酚(AP)诱导的肝损伤的保护作用及其机制。结果表明,FL 可降低 AP 升高的血清丙氨酸/天冬氨酸转氨酶(ALT/AST)活性和总胆红素(TB)含量。对肝脏的组织学评价进一步证实了 FL 对 AP 诱导的肝毒性的保护作用。TdT 介导的生物素-dUTP 缺口末端标记(TUNEL)检测显示,FL 可减少 AP 诱导的凋亡细胞。此外,FL 还可逆转 AP 降低的肝谷氨酸半胱氨酸连接酶(GCL)酶活性和谷胱甘肽(GSH)含量,这是由于 GCL 催化亚基(GCLC)蛋白表达增加所致。采用高效液相色谱法(HPLC)检测到 FL 中的主要活性化合物绿原酸(CGA)、咖啡酸和木犀草素的含量。此外,细胞活力测定表明,FL 中的多酚类物质,如 CGA、咖啡酸以及异绿原酸 A、B 和 C,可逆转 AP 诱导的细胞毒性。总之,FL 可通过抑制细胞凋亡来预防 AP 诱导的肝损伤。细胞抗氧化酶 GCL 也参与了这种保护作用。多酚类物质可能是 FL 中主要的具有肝保护作用的活性成分。

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