Literature DB >> 33865225

Dl-3-n-butylphthalide pretreatment attenuates renal ischemia/reperfusion injury.

Yang Dong1, Jianyong Yin1, Teng Chen2, Jiejun Wen1, Qunzi Zhang1, Xiaomei Li1, Wenjun Lin1, Feng Liu3, Ying Fan4, Niansong Wang5.   

Abstract

BACKGROUND: Renal ischemia reperfusion injury (IRI) has become a growing concern in clinical practice with high morbidity and mortality rates. There is currently no effective prophylactic regimen available to prevent its occurrence and to improve its clinical prognosis. Dl-3-n-butylphthalide (NBP) has been used for stroke treatment in China for years. Little is known about its role in preventing kidney injury.
METHODS: The kidneys of male C57BL/6J mice were subjected to 33 min of ischemia followed by 24 h of reperfusion. NBP was administered by gavage prior to surgery. The reno-protective effect of NBP was evaluated by serum creatinine, kidney injury markers and renal pathological changes. Furthermore, the inflammation, oxidative stress, and apoptosis markers in kidney tissue were examined. In vitro, HK2 cells were treated prophylactically with NBP and then exposed to hypoxia/reoxygenation (H/R). Cell viability and apoptosis related protein were quantified to verify the protective effect of NBP. Pro-inflammation genes expression as well as ROS generation were further investigated also.
RESULTS: NBP pretreatment significantly improved renal dysfunction and alleviated pathological injury, renal inflammation response, oxidative stress and cell apoptosis. Consistently, NBP attenuated H/R induced increases in ROS, pro-inflammatory genes expression, apoptosis and cleaved caspase-3 levels in HK2 cells.
CONCLUSION: Our promising results validated for the first time that NBP could ameliorate renal IRI via attenuating inflammation, oxidative stress, and apoptosis, which indicated that NBP might be a good candidate against AKI.
Copyright © 2021 The Authors. Published by Elsevier Inc. All rights reserved.

Entities:  

Keywords:  Acute kidney injury (AKI); Apoptosis; Dl-3-n-butylphthalide (NBP); Inflammation; Ischemia reperfusion injury (IRI); Oxidative stress

Year:  2021        PMID: 33865225     DOI: 10.1016/j.bbrc.2021.04.006

Source DB:  PubMed          Journal:  Biochem Biophys Res Commun        ISSN: 0006-291X            Impact factor:   3.575


  1 in total

1.  Dl-3-n-butylphthalide attenuates myocardial ischemia reperfusion injury by suppressing oxidative stress and regulating cardiac mitophagy via the PINK1/Parkin pathway in rats.

Authors:  Dongqin Zhang; Nan Zheng; Xiaoli Fu; Jian Shi; Jun Zhang
Journal:  J Thorac Dis       Date:  2022-05       Impact factor: 3.005

  1 in total

北京卡尤迪生物科技股份有限公司 © 2022-2023.