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目的:本研究旨在探讨LncRNA HCG18调控miR-185-5p/AGER轴对糖尿病肾病（diabetic nephropathy，DN）内质网应激和自噬的影响。方法:收集DN患者肾脏组织，建立高糖（high glucose，HG）诱导的足细胞损伤模型。检测DN患者肾组织与DN细胞模型中HCG18的表达。确定HCG18在细胞中的定位表达。证实HCG18与miR-185-5p、miR-185-5p与晚期糖基化终产物特异性受体（advanced glycosylation end-product specific receptor,AGER）的调控关系。qRT-PCR和western blot检测内质网应激相关因子（CHOP、XBP1）及自噬相关因子（Beclin-1、p62）的表达。结果:相对于非DN患者，DN患者肾组织中HCG18高表达（n P<0.05）。相对于正常糖（normal glucose，NG）组，HG模型中内质网应激相关因子（CHOP、XBP1）的mRNA和蛋白表达增加而自噬相关因子Beclin-1的mRNA和蛋白表达被抑制，p62的mRNA和蛋白表达增强（均n P<0.05）。HCG18通过调控miR-185-5p/AGER轴发挥生物学作用。敲低HCG18能减轻内质网应激，激活自噬并减少足细胞损伤，该作用被miR-185-5p抑制剂部分逆转。n 结论:HCG18调控miR-185-5p/AGER信号轴并通过调控内质网应激和自噬促进DN的发生。“,”Objective:To explore the effects of LncRNA HCG18 on endoplasmic reticulum stress and autophagy via regulating miR-185-5p/AGER axis in diabetic nephropathy (DN) .Methods:The kidney tissues of patients with DN were collected and the podocyte injury model induced by high glucose (HG) was established. The expression of HCG18 in renal tissue in DN patients and cell model was detected. The localization and expression of HCG18 in cells were determined. The regulatory relationship between HCG18 and miR-185-5p, miR-185-5p and AGER was testified. QRT-PCR and western blot were used to detect the expression of endoplasmic reticulum stress related factors (CHOP, XBP1) and autophagy related factors (Beclin-1, p62) .Results:Compared with non-DN patients, HCG18 was overexpressed in renal tissue of DN patients (n P<0.05) . Compared with normal glucose (NG) group, mRNA and protein expression of endoplasmic reticulum stress related factors (CHOP, XBP1) were overexpressed but mRNA and protein expression of autophagy related factors Beclin-1 were inhibited, p62 mRNA and protein expression were increased (alln P<0.05) . HCG18 regulated the miR-185-5p/AGER axis and played a biological role. Knocking down of HCG18 reduced endoplasmic reticulum stress, activated autophagy and reduced podocyte injury, but this effect can be partially reversed by miR-185-5p inhibitors.n Conclusion:HCG18 regulates the miR-185-5p/AGER signal axis and promotes DN progression through regulating endoplasmic reticulum stress and autophagy.