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甘豆汤对铜负荷型肝豆状核变性模型的保护机制：药理学与细胞代谢组学

Protective Mechanism of Gandou Decoction in a Copper-Laden Hepatolenticular Degeneration Model: Pharmacology and Cell Metabolomics.

作者信息

Yin Fengxia, Nian Mengnan, Wang Na, Wu Hongfei, Wu Huan, Zhao Wenchen, Cao Shijian, Wu Peng, Zhou An

机构信息

The Experimental Research Center, Anhui University of Chinese Medicine, Hefei, China.

School of Pharmacy, Anhui University of Chinese Medicine, Hefei, China.

出版信息

Front Pharmacol. 2022 Mar 23;13:848897. doi: 10.3389/fphar.2022.848897. eCollection 2022.

DOI:10.3389/fphar.2022.848897
PMID:35401189
原文链接:https://pmc.ncbi.nlm.nih.gov/articles/PMC8984159/
Abstract

Gandou decoction (GDD) is a classic prescription for the treatment of hepatolenticular degeneration (HLD) in China; however, the liver-protecting mechanism of this prescription needs further evaluation. In the present study, we explored the protective mechanisms of GDD in a copper-laden HLD model using integrated pharmacology and cellular metabolomics . The results revealed that GDD could significantly promote copper excretion in copper-laden HLD model cells and improve the ultrastructural changes in hepatocytes. In addition, GDD could decrease the extent of lipid peroxidation, levels of reactive oxygen species, and the release rate of lactate dehydrogenase while increasing the activity of superoxide dismutase and the ratio of glutathione to oxidized glutathione in the copper-laden HLD model cells. On conducting statistical analysis of significant metabolic changes, 47 biomarkers and 30 related metabolic pathways were screened as pharmacological reactions induced by GDD in HLD model cells. d-glutamate and d-glutamine metabolic pathways showed the highest importance and significance among the 30 metabolic pathways, and the differential expression levels of the glutamine synthetase (GS) and the renal type and liver type GLS (GLS1 and GLS2) proteins were verified by Western blotting. Collectively, our data established the underlying mechanism of GDD therapy, such as the promotion of copper excretion and improvement in oxidative stress by regulating the expressions of GS, GLS1, and GLS2 protein to protect hepatocytes from injury.

摘要

肝豆汤（GDD）是中国治疗肝豆状核变性（HLD）的经典方剂；然而，该方剂的肝脏保护机制需要进一步评估。在本研究中，我们采用整合药理学和细胞代谢组学方法，探讨了GDD在铜负荷HLD模型中的保护机制。结果显示，GDD可显著促进铜负荷HLD模型细胞中铜的排泄，并改善肝细胞的超微结构变化。此外，GDD可降低铜负荷HLD模型细胞中脂质过氧化程度、活性氧水平和乳酸脱氢酶释放率，同时提高超氧化物歧化酶活性以及谷胱甘肽与氧化型谷胱甘肽的比值。对显著的代谢变化进行统计分析后，筛选出47个生物标志物和30条相关代谢途径作为GDD在HLD模型细胞中诱导的药理反应。在30条代谢途径中，d-谷氨酸和d-谷氨酰胺代谢途径的重要性和显著性最高，谷氨酰胺合成酶（GS）以及肾型和肝型谷氨酰胺酶（GLS1和GLS2）蛋白的差异表达水平通过蛋白质免疫印迹法得到验证。总体而言，我们的数据揭示了GDD治疗的潜在机制，如通过调节GS、GLS1和GLS2蛋白的表达促进铜排泄并改善氧化应激，从而保护肝细胞免受损伤。

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