Cyclic helix B peptide protects HK-2 cells from oxidative stress by inhibiting ER stress and activating Nrf2 signalling and autophagy
文献类型：期刊论文
| 作者 | Li, Long4; Lin, Miao3; Zhang, Lexi2; Huang, Shang1; Hu, Chao4; Zheng, Long4; Li, Liping4; Zhang, Chao4; Yang, Cheng4; Long, Yaqiu5 |
| 刊名 | MOLECULAR MEDICINE REPORTS
 |
| 出版日期 | 2017-12 |
| 卷号 | 16期号:6页码:8055-8061 |
| ISSN号 | 1791-2997 |
| 关键词 | cyclic helix B peptide renal ischemia-reperfusion injury tubular epithelial cells oxidative stress endoplasmic reticulum stress autophagy |
| DOI | 10.3892/mmr.2017.7588 |
| 文献子类 | Article |
| 英文摘要 | Renal ischemia-reperfusion injury (IRI) is present in numerous diseases and is observed following certain treatments, including renal transplantation. Preventing tubular epithelial cells (TECs) from undergoing apoptosis is vital for treatment of renal IRI. Cyclic helix B peptide (CHBP) is a novel agent that has a protective effect on renal IRI in vivo. In the present study, the effect and underlying mechanism of CHBP on TECs was investigated. The HK-2 human renal proximal tubular epithelial cell line was treated with 500 mu mol/l H2O2 for 4 h prior to determining the effect of CHBP pretreatment for 1 h on cell viability, caspase 3 activity and expression levels, expression levels of oxidative stress markers, endoplasmic reticulum (ER) stress markers, NF-E2-related factor 2 (Nrf2), heme oxygenase-1 (HO-1) and autophagy markers. This was investigated using a Cell Counting kit 8, a terminal deoxynucleotidyl transferase-mediated dUTP nick-end labelling assay, western blotting, reverse transcription-quantitative polymerase chain reaction and immunocytochemistry. Results revealed that pretreatment with CHBP enhanced HK-2 cell viability, the glutathione/glutathione disulphide ratio, activation of Nrf2 and mRNA expression levels of HO-1 and the expression levels of beclin-1 and light chain 3 A/B-II/I. Conversely, CHBP pretreatment reduced the expression levels of reactive oxygen species, the activity and protein expression levels of capase-3, the mRNA and protein expression levels of C/EBP homologous protein and binding immunoglobulin protein, and the expression levels of phosphorylated (p) mechanistic target of rapamycin (mTOR) Ser2448 and p62 during oxidative stress. However, the expression of p-mTOR Ser2481 was enhanced after CHBP pretreatment. CHBP pretreatment reduced the expression levels of reactive oxygen species, the activity and protein expression levels of capase-3, the mRNA and protein expression levels of C/EBP homologous protein and binding immunoglobulin protein, and the expression levels of phosphorylated (p)-mechanistic target of rapamycin (mTOR) Ser2481, p62 and p-mTOR Ser 2448 during oxidative stress. In conclusion, CHBP pretreatment protected HK-2 cells from H2O2-induced injury, inhibited ER stress and proapoptotic pathways, and activated the Nrf2 signalling pathway and autophagy. These results provide a potential mechanism of how CHBP protects against renal IRI. |
| WOS关键词 | ISCHEMIA-REPERFUSION INJURY ; ENDOPLASMIC-RETICULUM STRESS ; ERYTHROPOIETIN ; DEGRADATION ; INDUCTION ; APOPTOSIS |
| 资助项目 | National Nature Science Foundation of China[81270833] ; National Nature Science Foundation of China[81300621] ; National Nature Science Foundation of China[81500568] ; National Health and Family Planning Commission Foundation of Shanghai[2014JQ008A] |
| WOS研究方向 | Oncology ; Research & Experimental Medicine |
| 语种 | 英语 |
| 出版者 | SPANDIDOS PUBL LTD |
| WOS记录号 | WOS:000418229200021 |
| 源URL | [http://119.78.100.183/handle/2S10ELR8/272365]  |
| 专题 | 药物化学研究室 |
| 通讯作者 | Rong, Ruiming; Zhu, Tongyu |
| 作者单位 | 1.Guangdong Acad Med Sci, Dept Urol, Guangdong Gen Hosp, Guangzhou 510080, Guangdong, Peoples R China; 2.Anhui Prov Hosp, Dept Urol, Hefei 230001, Anhui, Peoples R China; 3.Fudan Univ, Zhongshan Hosp, Dept Thorac Surg, Shanghai 200032, Peoples R China; 4.Fudan Univ, Zhongshan Hosp, Dept Urol, 180 Fenglin Rd, Shanghai 200032, Peoples R China; 5.Chinese Acad Sci, Shanghai Inst Mat Med, CAS Key Lab Receptor Res, Shanghai 201203, Peoples R China |
| 推荐引用方式 GB/T 7714 | Li, Long,Lin, Miao,Zhang, Lexi,et al. Cyclic helix B peptide protects HK-2 cells from oxidative stress by inhibiting ER stress and activating Nrf2 signalling and autophagy[J]. MOLECULAR MEDICINE REPORTS,2017,16(6):8055-8061. |
| APA | Li, Long.,Lin, Miao.,Zhang, Lexi.,Huang, Shang.,Hu, Chao.,...&Zhu, Tongyu.(2017).Cyclic helix B peptide protects HK-2 cells from oxidative stress by inhibiting ER stress and activating Nrf2 signalling and autophagy.MOLECULAR MEDICINE REPORTS,16(6),8055-8061. |
| MLA | Li, Long,et al."Cyclic helix B peptide protects HK-2 cells from oxidative stress by inhibiting ER stress and activating Nrf2 signalling and autophagy".MOLECULAR MEDICINE REPORTS 16.6(2017):8055-8061. |
入库方式： OAI收割
来源：上海药物研究所
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