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川芎嗪对染氟致肝损伤 ICR 小鼠的病理生理学改变及临床作用

The Pathophysiological Changes and Clinical Effects of Tetramethylpyrazine in ICR Mice with Fluoride-Induced Hepatopathy.

机构信息

Department of Basic Veterinary Medicine, Sichuan Agricultural University, Chengdu 611100, China.

Center for Veterinary Sciences, Zhejiang University, Hangzhou 310030, China.

出版信息

Molecules. 2023 Jun 19;28(12):4849. doi: 10.3390/molecules28124849.

Abstract

The excessive intake of fluoride, one of the trace elements required to maintain health, leads to liver injury. Tetramethylpyrazine (TMP) is a kind of traditional Chinese medicine monomer with a good antioxidant and hepatoprotective function. The aim of this study was to investigate the effect of TMP on liver injury induced by acute fluorosis. A total of 60 1-month-old male ICR mice were selected. All mice were randomly divided into five groups: a control (K) group, a model (F) group, a low-dose (LT) group, a medium-dose (MT) group, and a high-dose (HT) group. The control and model groups were given distilled water, while 40 mg/kg (LT), 80 mg/kg (MT), or 160 mg/kg (HT) of TMP was fed by gavage for two weeks, with a maximum gavage volume for the mice of 0.2 mL/10 g/d. Except for the control group, all groups were given fluoride (35 mg/kg) by an intraperitoneal injection on the last day of the experiment. The results of this study showed that, compared with the model group, TMP alleviated the pathological changes in the liver induced by the fluoride and improved the ultrastructure of liver cells; TMP significantly decreased the levels of ALT, AST, and MDA ( < 0.05) and increased the levels of T-AOC, T-SOD, and GSH ( < 0.05). The results of mRNA detection showed that TMP significantly increased the mRNA expression levels of Nrf2, HO-1, CAT, GSH-Px, and SOD in the liver compared with the model group ( < 0.05). In conclusion, TMP can inhibit oxidative stress by activating the Nrf2 pathway and alleviate the liver injury induced by fluoride.

摘要

过量摄入氟(一种维持健康所需的微量元素)会导致肝损伤。川芎嗪(TMP)是一种具有良好抗氧化和保肝作用的中药单体。本研究旨在探讨 TMP 对急性氟中毒性肝损伤的影响。选择 60 只 1 月龄雄性 ICR 小鼠,将其随机分为 5 组:对照组(K)、模型组(F)、低剂量组(LT)、中剂量组(MT)和高剂量组(HT)。对照组和模型组给予蒸馏水,低、中、高剂量组分别灌胃 40mg/kg、80mg/kg、160mg/kg TMP,最大灌胃体积为 0.2mL/10g/d,除对照组外,其余各组于实验最后一天腹腔注射氟(35mg/kg)。结果显示,与模型组相比,TMP 减轻了氟诱导的肝组织病理变化,改善了肝细胞超微结构;TMP 显著降低了 ALT、AST 和 MDA 水平(<0.05),提高了 T-AOC、T-SOD 和 GSH 水平(<0.05)。mRNA 检测结果表明,TMP 可显著增加 Nrf2、HO-1、CAT、GSH-Px 和 SOD 在肝组织中的 mRNA 表达水平(<0.05)。综上所述,TMP 可通过激活 Nrf2 通路抑制氧化应激,缓解氟诱导的肝损伤。

https://cdn.ncbi.nlm.nih.gov/pmc/blobs/4ce4/10302661/f960e7c5ec9f/molecules-28-04849-g001.jpg

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