BAPTA-AM Nanoparticle for the Curing of Acute Kidney Injury Induced by Ischemia/Reperfusion | |
He, Zhiyu1,2,3,4; Tang, Haoyu5; You, Xinru4; Huang, Keqing4; Dhinakar, Arvind5; Kang, Yang2; Yu, Qiaoli3; Wu, Jun4 | |
刊名 | JOURNAL OF BIOMEDICAL NANOTECHNOLOGY |
2018-05-01 | |
卷号 | 14期号:5页码:868-883 |
关键词 | Acute Kidney Injury Calcium Ischemia-Reperfusion Anti-Apoptotic Nanoparticle |
ISSN号 | 1550-7033 |
DOI | 10.1166/jbn.2018.2532 |
产权排序 | 3 |
文献子类 | Article |
英文摘要 | Ischemia-reperfusion (I/R) is a major cause of acute kidney injury (AKI), which is associated with unacceptably high mortality rates in ICU. This research was designed to explore the therapeutic effect of BAPTA-AM (1,2-Bis(2-aminophenoxy)ethane-N, N, N, N-tetraacetic acid tetrakis(acetoxymethyl ester)) nanoparticle (BA-N) on AKI. BA-N was developed by liposome strategy and characterized by standard methods. The rat model was selected and the rats were randomly allocated into four groups: (1) Normal group; (2) Sham-operated group; (3) Model group (I/R+NS); (4) BA-N treatment group (I/R+BA-N). AKI model was established via clipping the bilateral renal artery with a microvascular clamp for 45 min. After reperfusion, serum cystatin C (Cys C), creatinine (Cr), blood urea nitrogen (BUN), lactate dehydrogenase (LDH) and caspase 3 levels were determined for the assessment of renal function. Kidney samples were then collected for the measurement of renal malondialdehyde (MDA) level and superoxide dismutase (SOD) activity. The assays of histological examination, ELISA, immunohistochemistry, western blot, TUNEL and RT-PCR were utilized for the detection of apoptosis. The results demonstrated that AKI model caused a significant decreasing in SOD activity, accompanied by a remarkable increase in Cys C, Cr, BUN, LDH, MDA, caspase 3 and cytochrome c (Cyt C) level, compared to the control group. BA-N (100 mu g/kg i.v.) significantly improved renal function and histopathological appearance, restored MDA level and SOD activity, decreased Bax/Bcl-2 ratio, caspase 3 activity, Cyt C release and TUNEL positive apoptotic cells. Our studies indicated that BA-N plays a renal-protective role, probably through antiapoptotic and antioxidant mechanisms. BA-N may regulate mitochondria pathway via decreasing Bax/Bcl-2 ratio, inhibiting caspase 3 expression and Cyt C release. Overall, BA-N may have potentials as an anti-AKI drug. |
学科主题 | Multidisciplinary |
URL标识 | 查看原文 |
WOS关键词 | ACUTE-RENAL-FAILURE ; EPITHELIAL-CELL INJURY ; DRUG-DELIVERY ; CANCER-THERAPY ; IN-VITRO ; POLYMERIC MICELLES ; BREAST-CANCER ; CALCIUM ; RELEASE ; PH |
WOS研究方向 | Science & Technology - Other Topics ; Materials Science |
语种 | 英语 |
出版者 | AMER SCIENTIFIC PUBLISHERS |
WOS记录号 | WOS:000432855600004 |
内容类型 | 期刊论文 |
源URL | [http://210.75.237.14/handle/351003/30257] |
专题 | 生物多样性与生态系统服务领域_中国科学院山地生态恢复与生物资源利用重点实验室 |
作者单位 | 1.Department of Materials Science and Engineering, and Institute for NanoBio Technology, Johns Hopkins University,Baltimore, MD 21218, USA; 2.Chinese Acad Sci, Chengdu Inst Biol, Key Lab Mt Ecol Restorat & Bioresource Utilizat, Chengdu 610041, Sichuan, Peoples R China; 3.Zhejiang Hosp, Dept Pharm, 12 Linying Rd, Hangzhou 310013, Zhejiang, Peoples R China; 4.Sun Yat Sen Univ, Sch Engn, Key Lab Sensing Technol & Biomed Instrument Guang, Guangzhou 510006, Guangdong, Peoples R China; 5.Univ Windsor, Windsor, ON N9B 3P4, Canada |
推荐引用方式 GB/T 7714 | He, Zhiyu,Tang, Haoyu,You, Xinru,et al. BAPTA-AM Nanoparticle for the Curing of Acute Kidney Injury Induced by Ischemia/Reperfusion[J]. JOURNAL OF BIOMEDICAL NANOTECHNOLOGY,2018,14(5):868-883. |
APA | He, Zhiyu.,Tang, Haoyu.,You, Xinru.,Huang, Keqing.,Dhinakar, Arvind.,...&Wu, Jun.(2018).BAPTA-AM Nanoparticle for the Curing of Acute Kidney Injury Induced by Ischemia/Reperfusion.JOURNAL OF BIOMEDICAL NANOTECHNOLOGY,14(5),868-883. |
MLA | He, Zhiyu,et al."BAPTA-AM Nanoparticle for the Curing of Acute Kidney Injury Induced by Ischemia/Reperfusion".JOURNAL OF BIOMEDICAL NANOTECHNOLOGY 14.5(2018):868-883. |
个性服务 |
查看访问统计 |
相关权益政策 |
暂无数据 |
收藏/分享 |
除非特别说明,本系统中所有内容都受版权保护,并保留所有权利。
修改评论