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芽菜提取物通过抑制氧化应激抑制对乙酰氨基酚诱导的小鼠肝毒性。

Extract of Sprouts Suppresses Acetaminophen-Induced Hepatotoxicity in Mice by Inhibiting Oxidative Stress.

机构信息

Department of Immunology, Institute of Medical Sciences, Medical School, Jeonbuk National University, Jeonju 54907, Korea.

Department of Health Administration, Kwangju Women's University, Kwangju 62396, Korea.

出版信息

Molecules. 2021 Oct 20;26(21):6336. doi: 10.3390/molecules26216336.

Abstract

Wheat ( L.) is the oldest known food crop, and many studies have reported that wheat shoots (i.e., wheatgrass) possess anti-cancer, anti-inflammatory, and antioxidant activities. However, the potentially ameliorative effect of wheat shoots on hepatotoxicity caused by high doses of -acetyl-para-aminophenol (acetaminophen, APAP) has yet to be reported. C57BL/6 mice received daily oral TAE (100 or 200 mg/kg), positive control (silymarin 100 mg/kg), or negative control (saline vehicle) treatments for 7 days prior to intraperitoneal APAP injection. Histological, serum (ELISA), Western blotting, and quantitative PCR analyses of excised liver tissues were then performed. Pre-treatment with TAE (100 or 200 mg/kg) ameliorated APAP-induced pathological damage (i.e., hepatotoxic lesions), reduced serum alanine aminotransferase (ALT) and aspartate aminotransferase (AST) levels, and also ameliorated APAP-induced increases in oxidative stress, thereby inhibiting oxidative liver damage and reducing the expression of inflammatory cytokines. In addition, TAE pre-treatment inhibited the expression of Cytochrome P4502E1 (CYP2E1), which is a key enzyme in the onset of APAP-induced hepatotoxicity, suppressed the expression of the target proteins regulated by the antioxidant enzyme Nrf2, and suppressed hepatocyte apoptosis. These findings suggest that TAE is an attractive therapeutic candidate that exhibits potential hepatoprotective activity by inhibiting oxidative stress, inflammation, apoptosis, and liver damage.

摘要

小麦(L.)是已知最古老的粮食作物,许多研究报告称,小麦芽(即小麦草)具有抗癌、抗炎和抗氧化活性。然而,小麦芽对大剂量-乙酰-对氨基酚(对乙酰氨基酚,APAP)引起的肝毒性的潜在改善作用尚未有报道。C57BL/6 小鼠在腹腔注射 APAP 前 7 天每天接受 TAE(100 或 200mg/kg)、阳性对照(水飞蓟素 100mg/kg)或阴性对照(盐水载体)处理。然后对切除的肝组织进行组织学、血清(ELISA)、Western blot 和定量 PCR 分析。TAE(100 或 200mg/kg)预处理可改善 APAP 诱导的病理损伤(即肝毒性病变),降低血清丙氨酸氨基转移酶(ALT)和天冬氨酸氨基转移酶(AST)水平,并改善 APAP 诱导的氧化应激增加,从而抑制氧化肝损伤并减少炎症细胞因子的表达。此外,TAE 预处理抑制了细胞色素 P4502E1(CYP2E1)的表达,CYP2E1 是 APAP 诱导肝毒性发生的关键酶,抑制了抗氧化酶 Nrf2 调节的靶蛋白的表达,并抑制了肝细胞凋亡。这些发现表明,TAE 是一种有吸引力的治疗候选物,通过抑制氧化应激、炎症、细胞凋亡和肝损伤显示出潜在的保肝活性。

https://cdn.ncbi.nlm.nih.gov/pmc/blobs/9938/8587876/0d915eb71560/molecules-26-06336-g001.jpg

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