Morin attenuates sepsis-induced acute kidney injury by regulating inflammatory responses, oxidative stress and tubular regeneration (morin and sepsis-induced acute kidney injury)

IF 4.2 3区 环境科学与生态学 Q2 ENVIRONMENTAL SCIENCES
Aya M. Shehata , Nagui H. Fares , Basma H. Amin , Asmaa A. Mahmoud , Yomna I. Mahmoud
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Abstract

Sepsis-associated acute kidney injury (AKI) is a health complication, encompassing excessive inflammatory response, oxidative stress, and tubular necrosis; leading to kidney failure and death. Sepsis treatments are nonspecific and palliative. In this study, we evaluated the effect of morin, a flavonoid with known nephroprotective capabilities, on sepsis-induced AKI by dividing eighty male mice into: normal, morin-treated, septic, and septic mice treated with morin. Half of the groups were sacrified 3 days post sepsis induction, while the rest was sacrified on the 7th day. Treating septic mice with morin resulted in the amelioration of sepsis-associated pathophysiological renal alterations and the increase of the survival and recovery rates compared with those of septic control group. These findings indicate that morin has a therapeutic effect against sepsis-associated AKI via its anti-inflammatory, antioxidant and regenerative effects. Thus, it could be used as potential pharmacological intervention for preventing renal complications of sepsis.

Abstract Image

莫林通过调节炎症反应、氧化应激和肾小管再生减轻败血症诱发的急性肾损伤(莫林与败血症诱发的急性肾损伤)。
败血症相关急性肾损伤(AKI)是一种健康并发症,包括过度的炎症反应、氧化应激和肾小管坏死;导致肾衰竭和死亡。败血症的治疗是非特异性和姑息性的。在这项研究中,我们评估了吗啉(一种已知具有肾脏保护功能的类黄酮)对脓毒症诱发的 AKI 的影响,方法是将 80 只雄性小鼠分为:正常组、吗啉处理组、脓毒症组和吗啉处理组。其中一半的小鼠在败血症诱导后 3 天被处死,其余的在第 7 天被处死。与脓毒症对照组相比,用吗啉治疗脓毒症小鼠可改善脓毒症相关的肾脏病理生理改变,并提高存活率和康复率。这些研究结果表明,吗啉具有抗炎、抗氧化和再生作用,对脓毒症相关性 AKI 有治疗作用。因此,它可作为预防脓毒症肾脏并发症的潜在药物干预措施。
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来源期刊
CiteScore
7.00
自引率
4.70%
发文量
185
审稿时长
34 days
期刊介绍: Environmental Toxicology and Pharmacology publishes the results of studies concerning toxic and pharmacological effects of (human and veterinary) drugs and of environmental contaminants in animals and man. Areas of special interest are: molecular mechanisms of toxicity, biotransformation and toxicokinetics (including toxicokinetic modelling), molecular, biochemical and physiological mechanisms explaining differences in sensitivity between species and individuals, the characterisation of pathophysiological models and mechanisms involved in the development of effects and the identification of biological markers that can be used to study exposure and effects in man and animals. In addition to full length papers, short communications, full-length reviews and mini-reviews, Environmental Toxicology and Pharmacology will publish in depth assessments of special problem areas. The latter publications may exceed the length of a full length paper three to fourfold. A basic requirement is that the assessments are made under the auspices of international groups of leading experts in the fields concerned. The information examined may either consist of data that were already published, or of new data that were obtained within the framework of collaborative research programmes. Provision is also made for the acceptance of minireviews on (classes of) compounds, toxicities or mechanisms, debating recent advances in rapidly developing fields that fall within the scope of the journal.
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