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白藜芦醇对铁过载诱导的小鼠肝损伤的保护机制。

The protective mechanism of resveratrol against hepatic injury induced by iron overload in mice.

机构信息

School of Basic Medicine, Hebei University of Chinese Medicine, Shijiazhuang 050200, China.

College of Nursing, Hebei University of Chinese Medicine, Shijiazhuang 050200, China.

出版信息

Toxicol Appl Pharmacol. 2021 Aug 1;424:115596. doi: 10.1016/j.taap.2021.115596. Epub 2021 May 24.

DOI:10.1016/j.taap.2021.115596
PMID:34044072
Abstract

Excessive iron deposition can produce toxicity. Liver, as the main storage site of iron, is more vulnerable to excessive iron than other organs. Many studies have found that Resveratrol (RES) can effectively eliminate oxygen free radicals and resist lipid peroxide damage. However, studies investigating the mechanism of how RES prevents liver injury induced by iron overload are few. This study aims to observe the protective effect of RES on liver injury induced by iron overload in mice. Mice, except for the control group, received an intraperitoneal injection of iron dextran (50 mg/kg) every morning. The L-RES and H-RES groups received intragastric administration of low- and high-concentration RES solutions (20 or 50 mg/kg). The deferoxamine (DFO) group was intraperitoneally injected with DFO (50 mg/kg), while the control and iron overload groups were intraperitoneally injected with the same amount of normal saline every afternoon. Two weeks after continuous administration, iron-overloaded mice treated with high and low doses of RES significantly improved liver injury (GOT and GPT) and decreased LDH activity and MDA content and increased SOD and GSH activities (P < 0.01). Morphological tests showed that RES treatment can reduce liver iron deposition and improve liver pathological changes in iron-overloaded mice. Furthermore, RES treatment caused a significant decrease in Ft expression (P < 0.01). In conclusion, RES can alleviate liver injury in iron-overloaded mice. The mechanism may be related to improve the antioxidant capacity and reduce excess iron in the liver.

摘要

过量的铁沉积会产生毒性。肝脏作为铁的主要储存场所,比其他器官更容易受到过量铁的影响。许多研究发现,白藜芦醇(RES)可以有效清除氧自由基,抵抗脂质过氧化损伤。然而,研究 RES 如何预防铁过载引起的肝损伤的机制的研究较少。本研究旨在观察 RES 对铁过载诱导的小鼠肝损伤的保护作用。除对照组外,所有小鼠每天早上均接受腹腔注射右旋糖酐铁(50mg/kg)。L-RES 和 H-RES 组分别给予低浓度和高浓度 RES 溶液(20 或 50mg/kg)灌胃。DFO 组腹腔注射 DFO(50mg/kg),而对照组和铁过载组每天下午均腹腔注射等量生理盐水。连续给药 2 周后,高、低剂量 RES 处理的铁过载小鼠的肝损伤(GOT 和 GPT)明显改善,LDH 活性和 MDA 含量降低,SOD 和 GSH 活性增加(P<0.01)。形态学测试表明,RES 治疗可减少肝铁沉积并改善铁过载小鼠的肝病理变化。此外,RES 治疗导致 Ft 表达显著降低(P<0.01)。综上所述,RES 可减轻铁过载小鼠的肝损伤。其机制可能与提高抗氧化能力和减少肝脏内多余的铁有关。

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