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Ischemic postconditioning prevents renal ischemia reperfusion injury through the induction of heat shock proteins in rats.缺血后处理通过诱导大鼠热休克蛋白来预防肾缺血再灌注损伤。
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The heat-shock protein-70-induced renoprotective effect is partially mediated by CD4+ CD25+ Foxp3 + regulatory T cells in ischemia/reperfusion-induced acute kidney injury.热休克蛋白 70 诱导的肾保护作用部分是通过 CD4+ CD25+ Foxp3+调节性 T 细胞在缺血/再灌注诱导的急性肾损伤中介导的。
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Heat shock protein 90-binding agents protect renal cells from oxidative stress and reduce kidney ischemia-reperfusion injury.热休克蛋白90结合剂可保护肾细胞免受氧化应激,并减轻肾脏缺血再灌注损伤。
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慢性肾小球肾炎患者的热休克蛋白 70 及抗热休克蛋白 70 抗体。

Heat shock protein 70 and anti-heat shock protein 70 antibodies in patients with chronic glomerulonephritis.

机构信息

Tareev Clinic of Internal Diseases, Sechenov First Moscow State Medical University, Rossolimo 11/5, Moscow, Russia, 119435.

出版信息

Cell Stress Chaperones. 2018 Nov;23(6):1229-1235. doi: 10.1007/s12192-018-0928-8. Epub 2018 Jul 30.

DOI:10.1007/s12192-018-0928-8
PMID:30062391
原文链接:https://pmc.ncbi.nlm.nih.gov/articles/PMC6237676/
Abstract

We evaluated the heat shock system 70 (HSP70) in patients with chronic glomerulonephritis (CGN). Seventy-six patients with CGN patients were included in our study. Ten patients with mild proteinuria (median 0.48 [0.16-0.78] g/24 h) and ten healthy subjects served as positive and negative controls, respectively. Urinary levels of HSP70, interleukin-10, and serum levels of anti-HSP70 were measured by ELISA. The immunohistochemical peroxidase method was used to study the expression of HSP70 and Foxp3+ in kidney biopsies. Treg cells in the interstitium were determined morphometrically. Median urinary HSP70 levels in patients with nephrotic syndrome (NS) [6.57 (4.49-8.33) pg/mg] and subnephrotic range proteinuria [5.7 (4.12-6.9) pg/mg] were higher (p < 0.05) than in positive [3.7 (2.5-4.82) pg/mg] and negative [3.78 (2.89-4.84) pg/mg] controls. HSP70 expression index in tubular cells positively correlated with urinary HSP70 (Rs = 0.948, р < 0.05) and proteinuria (Rs = 0.362, p < 0.05). The number of Treg cells in the kidney interstitium and interleukin-10 excretion were lower in patients with NS. Anti-HSP70 antibody serum levels in patients with NS [21.1 (17.47-29.72) pg/ml] and subnephrotic range proteinuria [24.9 (18.86-30.92) pg/ml] were significantly higher than in positive [17.8 (12.95-23.03) pg/ml] and negative [18.9 (13.5-23.9) pg/ml] controls. In patients with CGN, increasing proteinuria was associated with higher HSP70 renal tissue and urinary levels. However, activation of HSP70 in patients with nephrotic syndrome did not lead to an increase in tissue levels of Treg cells or to the release of IL-10.

摘要

我们评估了慢性肾小球肾炎 (CGN) 患者的热休克系统 70 (HSP70)。我们的研究纳入了 76 例 CGN 患者。10 例轻度蛋白尿患者(中位数 0.48 [0.16-0.78] g/24 h)和 10 例健康受试者分别作为阳性和阴性对照。通过 ELISA 法检测尿 HSP70、白细胞介素-10 和血清抗 HSP70 水平。免疫组化过氧化物酶法研究肾脏活检中 HSP70 和 Foxp3+的表达。间质中 Treg 细胞通过形态计量学确定。肾病综合征 (NS) 患者[6.57 (4.49-8.33) pg/mg]和亚肾病范围蛋白尿患者[5.7 (4.12-6.9) pg/mg]的尿 HSP70 水平中位数较高(p<0.05)比阳性[3.7 (2.5-4.82) pg/mg]和阴性[3.78 (2.89-4.84) pg/mg]对照组。肾小管细胞中 HSP70 表达指数与尿 HSP70 呈正相关(Rs=0.948,p<0.05)和蛋白尿(Rs=0.362,p<0.05)。NS 患者肾间质 Treg 细胞数量和白细胞介素-10 排泄量较低。NS 患者血清抗 HSP70 抗体水平[21.1 (17.47-29.72) pg/ml]和亚肾病范围蛋白尿[24.9 (18.86-30.92) pg/ml]明显高于阳性[17.8 (12.95-23.03) pg/ml]和阴性[18.9 (13.5-23.9) pg/ml]对照组。在 CGN 患者中,蛋白尿增加与肾组织和尿 HSP70 水平升高相关。然而,肾病综合征患者 HSP70 的激活并没有导致组织中 Treg 细胞水平的增加或白细胞介素-10 的释放。