NF-κB p65通过miR-150/TRPC6信号通路改善肾缺血再灌注损伤  

NFκB p65 Improves Renal Ischemia-reperfusion Injury Through the miR-150/TRPC6 Signaling Pathway

作　　者：庞磊 李双宇 马秋波 马增伟 施莹 于晓艳 谷宝华 孙珊珊 于春磊 PANG Lei;LI Shuangyu;MA Qiubo;MA Zengwei;SHI Ying;YU Xiaoyan;GU Baohua;SUN Shanshan;YU Chunlei(Department of Nephrology,The Third Affiliated Hospital of Qiqihar Medical University,Qiqihar 161000,Heilongjiang,China;Research Institute of Medicine and Pharmacy,Qiqihar Medical University,Qiqihar 161000,Heilongjiang,China)

机构地区：[1]齐齐哈尔医学院附属第三医院肾内科,黑龙江齐齐哈尔161000 [2]齐齐哈尔医学院医药科学研究院,黑龙江齐齐哈尔161000

出　　处：《系统医学》2024年第15期1-4,共4页Systems Medicine

基　　金：黑龙江省卫生健康科研课题(20220202050966)。

摘　　要：目的 探究NF-κB(nuclear transcription factor-κB, NF-κB)p65通过miR-150/瞬时受体电位阳离子通道6(transient receptor potential cation channel 6, TRPC6)信号通路促进肾缺血再灌注损伤的作用。方法 选取2022年8月—2023年8月由齐齐哈尔医学院医药科学研究院购买的60只雄性大鼠作为研究对象,将体质量相似的大鼠按照随机数字表法随机分为3组:假手术实验组(Sham组,n=10)、缺血/再灌注(ischemic/reperfusion, I/R)I/R实验组(n=10)、慢病毒实验组(n=40),其中慢病毒实验组分为miR-150-mimic组(n=10)、I/R+miR-150-mimic组(n=10)、NF-κB p65-si组(n=10)、I/R+NF-κB p65-si组(n=10)。评估各组大鼠肾组织中血清肌酐(creatinine, Cr)和血尿素氮(blood urea nitrogen, BUN)、炎性因子、miR-150、NF-κB p65、TRPC6的水平。结果 I/R实验组与Sham组比较,NF-κB p65、miR-150蛋白水平降低(0.26±0.02 vs 0.79±0.03、0.34±0.08vs 1.46±0.12),TRPC6蛋白水平下降(0.35±0.04 vs. 1.08±0.15),差异有统计学意义(t=46.484、24.558、8.603,P均<0.05)。与I/R实验组相比,I/R+miR-150-mimic组TRPC6水平升高,而炎症因子水平更低,I/R+NF-κB p65-si组miR-150水平更高,炎症因子水平升高,差异有统计学意义(P均<0.05)。结论 NF-κB p65通过调节miR-150/TRPC6信号通路影响肾功能及炎症,改善肾缺血再灌注损伤。Objective Exploring the role of nuclear transcription factor-κB(NF-κB)p65 in promoting renal ischemia-reperfusion injury through the miR-150/transient receptor potential cation channel 6(TRPC6)signaling pathway.Methods A total of sixty male wistar rats purchased by the Research Institute of Medicine and Pharmacy of Qiqihar Medical College from August 2022 to August 2023 were selected as research subjects.Rat with similar body weight were randomly divided into three groups using a random number table method:sham surgery experimental group(Sham group,n=10),ischemia/in focusischemic/reperfusion(I/R)experimental group(n=10),and lentivirus ex⁃perimental group(n=40).The lentivirus experimental group was divided into miR-150-mimic group(n=10),I/R+miR-150-mimic group(n=10),NF-κB p65-si group(n=10),and I/R+NF-κB p65-si group(n=10).Evaluate the levels of serum creatinine(Cr),blood urea nitrogen(BUN),inflammatory factors,miR-150,NFκB p65,and TRPC6 in the renal tissues of rats in each group.Results Compared with the Sham group,the I/R experimental group showed a de⁃crease in NF-κB p65 and miR-150 protein levels(0.26±0.02 vs 0.79±0.03,0.34±0.08 vs 1.46±0.12),and an de⁃crease in TRPC6 protein levels(0.35±0.04 vs 1.08±0.15),the differences were statistically significant differences(t=46.484,24.558,8.603,all P<0.05).Compared with the I/R experimental group,the level of TRPC6 in the I/R+miR-150-mimic group increased,while the level of inflammatory factors decreased.The level of miR-150 in the I/R+NF-κB p65-si group was higher,and the level of inflammatory factors increased.The differences were statistically significant(all P<0.05).Conclusion NF-κB p65 affects renal function and inflammation by regulating the miR-150/TRPC6 signaling pathway,and improves renal ischemia-reperfusion injury.

关 键 词：NF-κB p65 miR-150 瞬时受体电位阳离子通道6 肾缺血再灌注损伤 

分 类 号：R33[医药卫生—人体生理学]