Volume 10 Issue 4
Jul.  2019
Turn off MathJax
Article Contents
Article Navigation >  ORGAN TRANSPLANTATION  > 2019  >  10(4): 423-428
Fan Xuemei, Rong Song. Effect of protein kinase C β inhibitor on renal ischemia-reperfusion injury and expression level of macrophage subtypes in rat models[J]. ORGAN TRANSPLANTATION, 2019, 10(4): 423-428. doi: 10.3969/j.issn.1674-7445.2019.04.012
Citation: Fan Xuemei, Rong Song. Effect of protein kinase C β inhibitor on renal ischemia-reperfusion injury and expression level of macrophage subtypes in rat models[J]. ORGAN TRANSPLANTATION, 2019, 10(4): 423-428. doi: 10.3969/j.issn.1674-7445.2019.04.012
shu

Effect of protein kinase C β inhibitor on renal ischemia-reperfusion injury and expression level of macrophage subtypes in rat models

doi: 10.3969/j.issn.1674-7445.2019.04.012

  • Department of Urology, Affiliated Hospital of Zunyi Medical University, Zunyi 563000, China

More Information
  • Corresponding author: Rong Song, Email：1409843531@qq.com
  • Received Date: 2019-04-10
    Available Online: 2021-01-19
  • Publish Date: 2019-07-15
    Abstract
  •   Objective  To investigate the effect of protein kinase C (PKC) β inhibitor on the renal ischemia-reperfusion injury (RIRI) in rat models and detect the expression level of macrophage subtypes.  Methods  Eighteen healthy SD male rats were randomly divided into the Sham operation group (Sham group, n=6), RIRI group (n=6), PKCβ inhibitor +RIRI group (Inhibitor+RIRI group, n=6). Serum and left renal tissue samples were collected at postoperative 24 h. The contents of serum creatinine (Scr) and blood urea nitrogen (BUN) were detected by automatic biochemical analyzer. The infiltration of inflammatory cells and pathological injury in the renal tissues were observed by hematoxylin-eosin (HE) staining. The expression levels of CD68, inducible nitric oxide synthase (iNOS) and CD206 proteins in the renal tissues of rats in each group were assessed by immunohistochemistry and Western blot.  Results  The contents of serum Scr and BUN in the RIRI group were significantly higher than those in the Sham group (both P < 0.05). The contents of serum Scr and BUN in the Inhibitor+RIRI group were considerably lower than those in the RIRI group (both P < 0.05). No obvious renal injury was noted in the Sham group, whereas renal inflammatory cell infiltration and renal tubular structural damage were observed in the RIRI group. The renal inflammatory cell infiltration and renal tubular structural damage in the Inhibitor+RIRI group was slighter than that in the RIRI group. The protein expression levels of CD68, iNOS and CD206 in the renal tissue of rats in the RIRI group were significantly higher than those in the Sham group (all P < 0.05). The protein expression levels of CD68 and iNOS in the Inhibitor+RIRI group were remarkably lower than those in the RIRI group (all P < 0.05). The expression level of CD206 protein in the Inhibitor+RIRI group was significantly higher than that in the RIRI group (P < 0.05).  Conclusions  PKC β inhibitor can alleviate the RIRI in rat models to certain extent, which may be correlated with the role of PKC β inhibitor in mitigating inflammatory cell infiltration in ischemic renal tissues and promoting the expression of alternatively activated macrophage

     

    • FullText(HTML)
  • loading
    • References(23)
  • [1]
    CHOUCHANI ET, PELL VR, JAMES AM, et al.A unifying mechanism for mitochondrial superoxide production during ischemia-reperfusion injury[J]. Cell Metab, 2016, 23(2):254-263. DOI: 10.1016/j.cmet.2015.12.009.
    [2]
    ELTZSCHIG HK, ECKLE T. Ischemia and reperfusion--from mechanism to translation[J]. Nat Med, 2011, 17(11):1391-1401. DOI: 10.1038/nm.2507.
    [3]
    JAESCHKE H, WOOLBRIGHT BL. Current strategies to minimize hepatic ischemia-reperfusion injury by targeting reactive oxygen species[J]. Transplant Rev (Orlando), 2012, 26(2):103-114. DOI: 10.1016/j.trre.2011.10.006.
    [4]
    HAUSENLOY DJ, BOSTON-GRIFFITHS E, YELLON DM. Cardioprotection during cardiac surgery[J]. Cardiovasc Res, 2012, 94(2):253-265. DOI: 10.1093/cvr/cvs131.
    [5]
    KARUPPAGOUNDER V, BAJPAI A, MENG S, et al. Small molecule disruption of G protein βγ subunit signaling reprograms human macrophage phenotype and prevents autoimmune myocarditis in rats[J]. PLoS One, 2018, 13(7):e0200697. DOI: 10.1371/journal.pone.0200697.
    [6]
    CHEN J, LI M, YANG C, et al. Macrophage phenotype switch by sequential action of immunomodulatory cytokines from hydrogel layers on titania nanotubes[J]. Colloids Surf B Biointerfaces, 2018, 163:336-345. DOI: 10.1016/j.colsurfb.2018.01.007.
    [7]
    CHEN S, LI R, CHENG C, et al. Pseudomonas aeruginosa infection alters the macrophage phenotype switching process during wound healing in diabetic mice[J]. Cell Biol Int, 2018, 42(7):877-889. DOI: 10.1002/cbin.10955.
    [8]
    李春燕. PKCβ抑制剂对大鼠肾脏缺血再灌注损伤后M1及M2型巨噬细胞浸润的影响[D].遵义: 遵义医学院, 2017. http://cpfd.cnki.com.cn/Article/CPFDTOTAL-GZKX201811001100.htm
    [9]
    肖婷.肾缺血再灌注损伤中蛋白激酶C对巨噬细胞的影响[J].海南医学, 2017, 27(8):1302-1305.DOI: 10.3969/j.issn.1003-6350.2017.08.034.

    XIAO T. Influence of protein kinase C on macrophages in renal ischemia-reperfusion injury[J]. Hainan Med J, 2017, 27(8):1302-1305. DOI: 10.3969/j.issn.1003-6350.2017.08.034.
    [10]
    YONA S, KIM KW, WOLF Y, et al. Fate mapping reveals origins and dynamics of monocytes and tissue macrophages under homeostasis[J]. Immunity, 2013, 38(1):79-91. DOI: 10.1016/j.immuni.2012.12.001.
    [11]
    MALYSHEV I, MALYSHEV Y. Current concept and update of the macrophage plasticity concept: intracellular mechanisms of reprogramming and M3 macrophage "switch" phenotype[J]. Biomed Res Int, 2015:341308. DOI: 10.1155/2015/341308.
    [12]
    SUN YY, LI XF, MENG XM, et al. Macrophage phenotype in liver injury and repair[J]. Scand J Immunol, 2017, 85(3):166-174. DOI: 10.1111/sji.12468.
    [13]
    BUDHIRAJA S, SINGH J. Protein kinase C beta inhibitors: a new therapeutic target for diabetic nephropathy and vascular complications[J]. Fundam Clin Pharmacol, 2008, 22(3):231-240. DOI: 10.1111/j.1472-8206.2008.00583.x.
    [14]
    NOH H, KING GL. The role of protein kinase C activation in diabetic nephropathy[J]. Kidney Int Suppl, 2007, 106:S49-S53.DOI: 10.1038/sj.ki.5002386.
    [15]
    柯贵宝.蛋白激酶C-β抑制剂对大鼠移植肾脏的影响[D].遵义: 遵义医学院, 2013. http://d.wanfangdata.com.cn/Thesis/Y2341118
    [16]
    杨旸, 杨亦彬, 梁国标, 等.蛋白激酶C抑制剂对小鼠肾移植后炎性细胞浸润的影响[J].中华实验外科杂志, 2015, 32(1):204.DOI: 10.3760/cma.j.issn.1001-9030.2015.01.086.

    YANG Y, YANG YB, LIANG GB, et al. Effect of protein kinase C inhibitor on inflammatory cell infiltration after renal transplantation in mice[J].Chin J Exp Surg, 2015, 32(1):204. DOI: 10.3760/cma.j.issn.1001-9030.2015.01.086.
    [17]
    TSENG HC, KANAYAMA K, KAUR K, et al. Erratum: bisphosphonate-induced differential modulation of immune cell function in gingiva and bone marrow in vivo: role in osteoclast-mediated NK cell activation[J]. Oncotarget, 2015, 6(38):41398. DOI: 10.18632/oncotarget.6431.
    [18]
    CHO KY, MIYOSHI H, KURODA S, et al. The phenotype of infiltrating macrophages influences arteriosclerotic plaque vulnerability in the carotid artery[J]. J Stroke Cerebrovasc Dis, 2013, 22(7):910-918. DOI: 10.1016/j.jstrokecerebrovasdis.2012.11.020.
    [19]
    HUEN SC, HUYNH L, MARLIER A, et al. GM-CSF promotes macrophage alternative activation after renal ischemia/reperfusion injury[J]. J Am Soc Nephrol, 2015, 26(6):1334-1345. DOI: 10.1681/ASN.2014060612.
    [20]
    CURTIS BJ, BOE DM, SHULTS JA, et al. Effects of multi-day ethanol intoxication on post-burn inflammation, lung function, and alveolar macrophage phenotype[J]. Shock, 2018, 51(5):625-633. DOI: 10.1097/SHK.0000000000001188.
    [21]
    BONITO V, SMITS AIPM, GOOR OJGM, et al. Modulation of macrophage phenotype and protein secretion via heparin-IL-4 functionalized supramolecular elastomers[J]. Acta Biomater, 2018, 71:247-260. DOI: 10.1016/j.actbio.2018.02.032.
    [22]
    胡林昆, 陈城, 王卫珍, 等.抑炎因子IL-35与移植肾功能延迟恢复关系的研究[J].器官移植, 2018, 9(4):272-277.DOI: 10.3969/j.issn.1674-7445.2018.04.006.

    HU LK. CHEN C, WANG WZ, et al. Study on the relationship between anti-inflammatory cytokine IL-35and delayed renal graft function[J]. Organ Transplant, 2018, 9(4):272-277.DOI: 10.3969/j.issn.1674-7445.2018.04.006.
    [23]
    方羚, 陈晨, 康新梅, 等.小鼠脑实质注射水通道蛋白4抗体所致的病理损伤[J].中山大学学报(医学科学版), 2018, 39(2):207-214, 244. http://d.old.wanfangdata.com.cn/Periodical/zsykdxxb201802007

    FANG L, CHEN C, KANG XM, et al. Lesions caused by intracerebral injection of aquaporin-4 immunoglobulin G[J]. J Sun Yat-sen Univ(Med Sci), 2018, 39(2):207-214, 244. http://d.old.wanfangdata.com.cn/Periodical/zsykdxxb201802007
    • Relative Articles
    • Supplements(0)
    • Cited By
  • 加载中

Catalog

    通讯作者: 陈斌, bchen63@163.com
    • 1. 

      沈阳化工大学材料科学与工程学院 沈阳 110142

    1. 本站搜索
    2. 百度学术搜索
    3. 万方数据库搜索
    4. CNKI搜索

    Figures(3)

    Get Citation
    PDF
    XML

    Article Metrics

    Article views (112) PDF downloads(10) Cited by()
    Proportional views
    Related

    WeChat Subscription Account

    Wechat Service Account

    Contact Us
    • Tel：020-38736410
    • Email: organtranspl@163.com
    • Address：The Third Affiliated Hospital of Sun Yat-sen University, No. 600, Tianhe Road, Tianhe District, Guangzhou
    • Editorial Office of Organ Transplantation  粤ICP备2021030844号
    Links

    Supported by: Beijing Renhe Information Technology Co. Ltd    

    /

    DownLoad:  Full-Size Img  PowerPoint
    Return
    Return