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目的研究松弛素(RLX)在过敏性紫癜(HSP)患儿血清及肾组织中的表达及其与临床、病理改变的相关关系,探讨RLX在HSP发病中的作用。方法收集2011年11月至2012年6月江西省儿童医院肾内科收治的具有完整随访资料的HSP患儿39例,根据临床有无尿改变分为无肾损害组(20例)、有肾损害组(19例),所有患儿均留取急性期与恢复期血标本,有肾损害组均进行肾活检,根据病理损害程度分为轻度病变组(5例,Ⅰ~Ⅱ级)、中度病变组(9例,Ⅲ级)和重度病变组(5例,Ⅳ级)。10例正常对照组血清来自于门诊健康体检儿童。3例对照肾组织取自肾肿瘤患儿切除肾脏远离肿瘤部分并经病理证实为正常肾组织。血清RLX浓度采用酶联免疫吸附法(ELISA)法检测;肾组织RLX蛋白表达采用免疫组织化学非生物素二步法检测。结果急性期HSP患儿血清RLX水平高于正常对照组;有肾损害组高于无肾损害组(P均<0.05);恢复期HSP患儿各组血清RLX均降低,无肾损害组低于有肾损害组(P<0.05)。免疫组化结果显示:HSPN患儿肾组织内RLX蛋白表达高于正常对照组(P<0.05),且随着肾脏病理损伤程度加重而递增(P<0.05)。相关分析显示,HSPN肾组织RLX蛋白表达与血清RLX浓度呈正相关(r=0.730,P<0.05);与24 h尿蛋白定量亦呈正相关(r=0.622,P<0.05)。结论 HSP患儿血及肾组织中RLX蛋白表达增加,且与疾病严重程度密切相关,提示RLX可能参与了HSP、HSPN的发病过程,RLX的保护性增加可能在延缓HSP、HSPN疾病进展中起防御作用。
Objective To investigate the expression of RLX in serum and kidney of children with Henoch-Schonlein Purpura (HSP) and its relationship with clinical and pathological changes, and to explore the role of RLX in the pathogenesis of HSP. Methods Thirty-nine HSP patients with complete follow-up data were collected from Department of Nephrology, Children’s Hospital of Jiangxi Province from November 2011 to June 2012. The patients were divided into no renal damage group (n = 20) (N = 19) .All children were enrolled in the acute and convalescent blood samples. All the patients with renal injury were examined by renal biopsy. According to the degree of pathological injury, they were divided into mild lesion group (5 cases, grade Ⅰ ~ Ⅱ) Degree of lesion group (9 cases, grade Ⅲ) and severe lesions group (5 cases, grade Ⅳ). 10 normal control serum from out-patient health examination of children. Three cases of control renal tissue were obtained from children with kidney neoplasms. The kidneys were removed from the tumor and confirmed by pathology as normal kidney tissue. Serum RLX concentration was detected by enzyme-linked immunosorbent assay (ELISA); Renal RLX protein expression was detected by immunohistochemical non-biotin two-step method. Results The serum levels of RLX in children with acute HSP were higher than those in normal control group. The levels of RLX in renal impairment group were higher than those without renal damage group (all P <0.05) Have kidney damage group (P <0.05). The results of immunohistochemistry showed that the expression of RLX protein in renal tissues of HSPN patients was higher than that of normal controls (P <0.05), and increased with the severity of renal pathological changes (P <0.05). Correlation analysis showed that there was a positive correlation between the expression of RLX protein and the concentration of serum RLX in HSPN kidney (r = 0.730, P <0.05), and positively correlated with 24 h urinary protein (r = 0.622, P <0.05). Conclusions The expression of RLX protein in blood and kidney tissues of HSP patients is increased and closely related to the severity of the disease, suggesting that RLX may be involved in the pathogenesis of HSP and HSPN. The protective effect of RLX may play a role in delaying the progress of HSP and HSPN diseases effect.