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目的:观察CXC趋化因子配体16(CXCL16)在慢性肾脏病(CKD)患者和CDK动物模型中的表达情况,研究其与肾功能等因素的相关性,探讨CXCL16在CKD进展中的作用。方法:在临床研究方面,收集200例CKD患者[按肾小球滤过率(e GFR)分为CKD 1-2期组、CKD 3-4期组和CKD 5期组]和40例健康对照组的外周血标本,检测血清肌酐、尿素氮、血脂、e GFR等各项指标,并检测血清中CXCL16的含量。在动物实验方面,取雄性C57BL/6小鼠14只,随机分为普通对照组及普通模型组(各7只),雄性CXCL16基因敲除小鼠7只,随机分为基因敲除对照组(3只)及基因敲除模型组(4只)。4周后处死小鼠,检测小鼠血清尿素氮、肌酐、CXCL16等指标,观察肾组织病理改变。结果:健康对照组和CKD各期组患者之间年龄、性别、体质量指数(BMI)差异无统计学意义(P>0.05)。CKD 5期组患者血清CXCL16水平高于健康对照组和CKD 1-2期组、CKD3-4期组,差异均有统计学意义(P<0.05)。在校正了CKD患者的年龄、性别、BMI后,e GFR、C-反应蛋白(CRP)和脂联素与血浆CXCL-16独立相关。在动物实验中,CXCL基因敲除模型组与普通模型组相比,其血清尿素氮、肌酐及尿酸升高幅度偏低;肾脏病理提示基因敲除模型组小鼠肾脏损伤程度轻于普通模型组。结论:随着CKD的进展,血浆中CXCL-16的水平显著升高,并与肾功能的变化独立相关。
OBJECTIVE: To investigate the expression of CXCL16 in patients with chronic kidney disease (CKD) and animal models of CDK, and to investigate its correlation with renal function and to explore the role of CXCL16 in the progression of CKD. Methods: In clinical studies, 200 patients with CKD [divided into CKD stage 1-2, CKD stage 3-4 and CKD stage 5 by GFR] and 40 healthy controls Group of peripheral blood samples, serum creatinine, urea nitrogen, blood lipids, e GFR and other indicators, and the detection of serum CXCL16 content. In animal experiments, 14 male C57BL / 6 mice were randomly divided into normal control group and normal model group (7 mice each), 7 male CXCL16 knockout mice were randomly divided into control group ( 3) and knockout model group (4). After 4 weeks, the mice were sacrificed and the serum urea nitrogen, creatinine, CXCL16 and other indexes were detected to observe the pathological changes in the kidney. Results: There was no significant difference in age, sex and body mass index (BMI) between healthy controls and CKD groups (P> 0.05). The level of serum CXCL16 in CKD 5 group was significantly higher than that in healthy control group, CKD stage 1-2 group and CKD stage 3 - 4 group (P <0.05). EGFR, C-reactive protein (CRP), and adiponectin were independently associated with plasma CXCL-16 after adjusting for age, sex and BMI in CKD patients. In animal experiments, CXCL knockout model group compared with the normal model group, the serum urea nitrogen, creatinine and uric acid increased low; kidney pathology prompted knockout model mice kidney damage was lighter than the normal model group . CONCLUSIONS: With the progress of CKD, the level of CXCL-16 in plasma is significantly increased, which is independently related to the changes of renal function.