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水煎提取物的抗氧化特性及其对乙醇诱导的肝肾损伤的保护作用机制

Antioxidant Properties of Decoction Extract and Mechanism of Its Protective Effects on Ethanol-Induced Liver and Kidney Injuries.

作者信息

Jedidi Saber, Aloui Foued, Selmi Slimen, Selmi Houcine, Sammari Houcem, Ayari Ala, Abbes Chaabane, Sebai Hichem

机构信息

Unit of Functional Physiology and Valorization of Bio-Resources, Department of Animal Physiology, University of Jendouba, Higher Institute of Biotechnology of Beja, Beja, Tunisia.

Laboratory of Sylvo-Pastoral Resources, Department of Protection and Development of Resources and Agro-Forestry Areas, University of Jendouba, Sylvo-Pastoral Institute of Tabarka, Tabarka, Tunisia.

出版信息

J Med Food. 2022 May;25(5):546-556. doi: 10.1089/jmf.2021.0134. Epub 2022 Mar 22.

DOI:10.1089/jmf.2021.0134
PMID:35325568
Abstract

This study assessed the hepato- and nephroprotective effects of flowers decoction extract (SODE) against ethanol (EtOH)-induced oxidative stress in rats as well as the possible mechanism implicated in such protection. Animals were divided into four groups: control, EtOH, and EtOH+SODE. Wistar rats were pretreated with SODE (50, 100, and 200 mg/kg, body weight [b.w.], p.o.) for 15 days and intoxicated during 2 h by acute oral administration of EtOH (4 g/kg, b.w.) 60 min after the last dose of SODE. We found that SODE pretreatment, , protected against EtOH-induced liver and kidney injuries evident by plasma transaminases activity and preservation of the hepatic tissue structure. Compared with the control group, the animals treated with the SODE showed a significant decrease (68.81 ± 6.89-50.65 ± 3.97 UI/L) of alanine aminotransferase (ALT) and aspartate aminotransferase (AST; 144.38 ± 6.58-113.64 ± 8.03 UI/L) in a dose-dependent manner. By contrast, the plant extract significantly and dose dependently increased (0.175 ± 0.077-0.302 ± 0.011 mmol/L) the uric acid. The SODE counteracted EtOH-induced liver and kidney lipoperoxidation, preserved sulfhydryl groups (-SH) and glutathione reduced (GSH) contents. Our extract prevented the depletion of antioxidant enzyme activities such as superoxide dismutase (SOD), catalase (CAT), and glutathione peroxidase (GPx). We also showed that acute alcohol administration increased tissue and plasma hydrogen peroxide (HO), calcium and free iron levels. Of interest, SODE pretreatment reversed all EtOH-induced disturbances in intracellular mediators. More importantly, SODE treatment significantly protected against alcohol-induced inflammation by reducing C-reactive protein (CRP) and alkaline phosphatase (ALP) activities in plasma. It was concluded that the SODE exerted a potential protective effect against EtOH-induced inflammation and oxidative stress in the rat organs. This study recommends that the consumption of sage flowers is useful for patients who suffer from hepato- and nephrotoxicity.

摘要

本研究评估了鼠尾草花水煎液提取物(SODE)对乙醇(EtOH)诱导的大鼠氧化应激的肝保护和肾保护作用,以及这种保护作用可能涉及的机制。动物分为四组:对照组、乙醇组和乙醇+SODE组。将Wistar大鼠用SODE(50、100和200mg/kg体重,口服)预处理15天,并在最后一剂SODE给药60分钟后通过急性口服给予乙醇(4g/kg体重)使其在2小时内中毒。我们发现,SODE预处理可预防乙醇诱导的肝损伤和肾损伤,这可通过血浆转氨酶活性以及肝组织结构的保存得以证明。与对照组相比,用SODE处理的动物的丙氨酸转氨酶(ALT)和天冬氨酸转氨酶(AST)显著降低(68.81±6.89 - 50.65±3.97U/L),呈剂量依赖性(144.38±6.58 - 113.64±8.03U/L)。相比之下,该植物提取物显著且剂量依赖性地增加了尿酸(0.175±0.077 - 0.302±0.011mmol/L)。SODE可抵消乙醇诱导的肝和肾脂质过氧化,保留巯基(-SH)和还原型谷胱甘肽(GSH)含量。我们的提取物可防止抗氧化酶活性如超氧化物歧化酶(SOD)、过氧化氢酶(CAT)和谷胱甘肽过氧化物酶(GPx)的消耗。我们还表明,急性酒精给药会增加组织和血浆中的过氧化氢(HO)、钙和游离铁水平。有趣的是,SODE预处理可逆转所有乙醇诱导的细胞内介质紊乱。更重要的是,SODE处理可通过降低血浆中的C反应蛋白(CRP)和碱性磷酸酶(ALP)活性,显著预防酒精诱导的炎症。得出的结论是,SODE对乙醇诱导的大鼠器官炎症和氧化应激具有潜在的保护作用。本研究建议,食用鼠尾草花对患有肝毒性和肾毒性的患者有益。

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