| 陈 钊,田李芳,马晓桃,马芳霞,姚 恬,王 莉.缺血预处理通过激活自噬保护肾缺血-再灌注损伤[J].现代生物医学进展英文版,2019,19(23):4421-4424. |
| 缺血预处理通过激活自噬保护肾缺血-再灌注损伤 |
| Ischemic Preconditioning Protects ischemia-reperfusion-induced acute Kidney Injury and Renal Fibrosis by Activating Autophagy |
| Received:June 06, 2019 Revised:June 30, 2019 |
| DOI：10.13241/j.cnki.pmb.2019.23.005 |
| 中文关键词: 缺血预处理 自噬 肾损伤 肾功能 |
| 英文关键词: Ischemic preconditioning Autophagy Renal injury Renal function |
| 基金项目:陕西省社会发展科技攻关项目(2016SF-176) |
| Author Name | Affiliation | E-mail | | CHEN Zhao | Department of nephrological, The Second Affiliated Hospital of Xi'an Jiaotong University, Xi'an, Shaanxi, 710000, China | chenzz0681@163.com | | TIAN Li-fang | Department of nephrological, The Second Affiliated Hospital of Xi'an Jiaotong University, Xi'an, Shaanxi, 710000, China | | | MA Xiao-tao | Department of nephrological, The Second Affiliated Hospital of Xi'an Jiaotong University, Xi'an, Shaanxi, 710000, China | | | MA Fang-xia | Department of nephrological, The Second Affiliated Hospital of Xi'an Jiaotong University, Xi'an, Shaanxi, 710000, China | | | YAO Tian | Department of nephrological, The Second Affiliated Hospital of Xi'an Jiaotong University, Xi'an, Shaanxi, 710000, China | | | WANG Li | Department of nephrological, The Second Affiliated Hospital of Xi'an Jiaotong University, Xi'an, Shaanxi, 710000, China | |
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| 中文摘要: |
| 摘要 目的：探讨缺血预处理对缺血-再灌注所致急性肾损伤的保护作用与可能机制。方法：将健康雄性SD大鼠18只随机分为三组：假手术组(Sham组)、肾缺血组(I/R组)、实验组，Sham组大鼠开腹后游离左侧肾蒂血管，不夹闭，观察60 min关闭腹部。I/R组大鼠开腹后切除右肾，左肾蒂血管分离，观察15 min后用无损伤动脉夹持续夹闭左肾蒂血管45 min后，关闭腹部，恢复左肾血流。实验组开腹后切除切除右肾，左肾蒂血管分离，行4个循环夹闭左肾蒂血管1 min/再灌注4 min预处理后，无损伤动脉持续夹闭45 min，关闭腹部，恢复左肾血流。比较各组大鼠术后尿素氮值(Burea nitrogen，BUN)与肌酐值(Serum creatinine，SCR)水平，肾组织病理学评分及微管相关蛋白轻链3(Microtubule-associated protein l light chain 3，LC3)和自噬基因Beclin-1的表达。结果：所有大鼠在实验过程无死亡。I/R组、实验组再灌注后4 h、24 h的BUN与SCr值显著高于Sham组(P<0.05)，肾脏组织病理学评分显著高于Sham组(P<0.05)，实验组以上指标均显著低于I/R组(P<0.05)；I/R组LC3-Ⅱ/LC3-Ⅰ比值、Beclin-1相对表达量显著高于Sham组(P<0.05)，实验组以上指标均显著低于I/R组(P<0.05)。实验组大鼠再灌注后24h LC3-Ⅱ/LC3-Ⅰ比值、Beclin-1相对表达量与肾组织病理学评分、BUN、SCr值呈显著相关性(P<0.05)。结论：缺血预处理可能通过激活自噬，减轻缺血-再灌注所致急性肾损伤，并改善肾功能。 |
| 英文摘要: |
| ABSTRACT Objective: To investigate the protective effect and possible mechanism of Ischemic preconditioning on acute kidney injury induced by ischemia-reperfusion. Methods: 18 healthy male Sprague-Dawley rats were randomly divided into three groups: sham operation group (Sham group), renal ischemia group (I/R group), and experimental group. The rats in the Sham group were freed from the left renal pedicle after laparotomy, without clipping, and the abdomen was observed for 60 min. In the I/R group, the right kidney was excised after laparotomy, and the left renal pedicle was separated. After 15 minutes, the left renal pedicle was continuously clamped with a non-injured artery clip for 45 min, then the abdomen was closed and the left renal blood flow was restored. In the experimental group, the right kidney was removed after laparotomy, and the left renal pedicle was separated. After 4 cycles of clamping the left renal pedicle for 1 min/reperfusion for 4 min, the injured artery was continuously clamped for 45 min, and the abdomen was closed and restored. Left renal blood flow. The levels of BUN and SCR, renal histopathology score and expression of LC3 and Beclin-1 were compared between the groups. Results: All rats did not die during the course of the experiment. The BUN and SCr values in the I/R group and the experimental group were significantly higher than those in the Sham group at 4 h and 24 h after reperfusion (P<0.05). The histopathological scores of the kidneys were significantly higher than those in the Sham group (P<0.05). The indicators were significantly lower than the I/R group (P<0.05). The ratio of LC3-II/LC3-I and the relative expression of Beclin-1 were significantly higher than Sham group (P<0.05). The above indexes in the experimental group were significantly lower than those in the I/R group (P<0.05). At 24 h after reperfusion, the LC3-II/LC3-I ratio and the relative expression of Beclin-1 in the experimental group were significantly correlated with renal histopathological scores, BUN and SCr values (P<0.05). Conclusion: Ischemic preconditioning may attenuate acute renal injury and induced by ischemia-reperfusion and improve renal function by activating autophagy. |
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