Cholecalciferol pretreatment ameliorates ischemia/reperfusion-induced acute kidney injury through inhibiting ROS production, NF-KB pathway and pyroptosis

doi:10.1016/j.acthis.2022.151875

HFCAS OpenIR

	Cholecalciferol pretreatment ameliorates ischemia/reperfusion-induced acute kidney injury through inhibiting ROS production, NF-KB pathway and pyroptosis
	Wu, Wangyu 1; Liu, Dongyan 2,3; Zhao, Yuxiang 1; Zhang, Taotao 1; Ma, Jiaxing 1; Wang, Dengdian 1; Li, Jun 1; Qian, Weiwei 1; Zhang, Zhihui 1; Yu, Dexin 1; Zhang, Tao1
	2022-05-01
发表期刊	ACTA HISTOCHEMICA
ISSN	0065-1281
通讯作者	Zhang, Tao(zhangtao@ahmu.edu.cn)
摘要	Acute kidney injury (AKI) is a common complication in patients with potentially life-threatening diseases, and it is also usually associated with unacceptable morbidity and mortality rates. Therefore, new and efficient therapies are urgently required to relieve AKI. It is well known that, reactive oxygen species (ROS), the NF-KB signaling pathways and pyroptosis are involved in AKI induced by ischemia/reperfusion (I/R). The present study seeks to further confirm the internal relationship between vitamin D deficiency and I/R-induced AKI in patients, and to explore the underlying mechanisms of ROS, NF-KB signaling pathways and pyroptosis in the renal ischemiareperfusion injury, as well as investigating the protective role of cholecalciferol. Patients with vitamin D deficiency show worse renal function reflected by postoperative glomerular filtration rate (GFR) and more release of proinflammatory cytokine IL-18 and IL-18. Renal cell injury and renal dysfunction induced by I/R surgery were attenuated in the ICR mice administered with cholecalciferol. Cholecalciferol reduced ROS production, suppressed activated NF-KB signaling, and inhibited gasdermin D (GSDMD, a pyroptosis execution protein)-mediated pyroptosis. Cholecalciferol therefore has potential, as a clinical drug, to protect renal function in I/R-induced AKI through reducing ROS production, NF-KB activation and GSDMD-mediated pyroptosis.
关键词	Acute kidney injury Ischemia and reperfusion Cholecalciferol ROS NF-KB pathway Pyroptosis
DOI	10.1016/j.acthis.2022.151875
收录类别	SCI
语种	英语
资助项目	scientific research and Experiment Center of the Second Hospital of Anhui Medical University ; Doctoral Start-up Foundation of the Second Affiliated Hospital of Anhui Medical University[2018BSJJ012] ; Provincial Natural Science Foundation of Anhui, China[2008085MH290] ; Key projects of Provincial Natural Science Foundation of Colleges and Universities in Anhui, China[KJ2018A0209]
项目资助者	scientific research and Experiment Center of the Second Hospital of Anhui Medical University ; Doctoral Start-up Foundation of the Second Affiliated Hospital of Anhui Medical University ; Provincial Natural Science Foundation of Anhui, China ; Key projects of Provincial Natural Science Foundation of Colleges and Universities in Anhui, China
WOS研究方向	Cell Biology
WOS类目	Cell Biology
WOS记录号	WOS:000807362700001
出版者	ELSEVIER GMBH
引用统计	被引频次：10[WOS] [WOS记录] [WOS相关记录]
文献类型	期刊论文
条目标识符	http://ir.hfcas.ac.cn:8080/handle/334002/131232
专题	中国科学院合肥物质科学研究院
通讯作者	Zhang, Tao
作者单位	1.Anhui Med Univ, Dept Urol, Affiliated Hosp 2, Hefei 230601, Peoples R China 2.Chinese Acad Sci, Inst Hlth & Med Technol, Hefei Inst Phys Sci, Anhui Prov Key Lab Med Phys & Technol, Hefei 230031, Peoples R China 3.Univ Sci & Technol China, Hefei 230026, Peoples R China
推荐引用方式 GB/T 7714	Wu, Wangyu,Liu, Dongyan,Zhao, Yuxiang,et al. Cholecalciferol pretreatment ameliorates ischemia/reperfusion-induced acute kidney injury through inhibiting ROS production, NF-KB pathway and pyroptosis[J]. ACTA HISTOCHEMICA,2022,124.
APA	Wu, Wangyu.,Liu, Dongyan.,Zhao, Yuxiang.,Zhang, Taotao.,Ma, Jiaxing.,...&Zhang, Tao.(2022).Cholecalciferol pretreatment ameliorates ischemia/reperfusion-induced acute kidney injury through inhibiting ROS production, NF-KB pathway and pyroptosis.ACTA HISTOCHEMICA,124.
MLA	Wu, Wangyu,et al."Cholecalciferol pretreatment ameliorates ischemia/reperfusion-induced acute kidney injury through inhibiting ROS production, NF-KB pathway and pyroptosis".ACTA HISTOCHEMICA 124(2022).