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为观察低密度脂蛋白（ＬＤＬ）对肾上管上皮细胞的影响及涉及的相关信号传导机制，以人近曲行小管上皮细胞系（ＨＫ－２）为对象，采用３Ｈ－ＴｄＲ掺入与细胞计数测定增殖；特异性底物磷酸化法测定细胞外信号调节激酶（Ｅｎｇ）活性；凝胶迁移率法检测转录活化因于（ＡＰ－１）ＤＮＡ结合活性。发现ＬＤＬ１００～５００ｕｇ／ｍＬ刺激ＨＫ－２细胞７２ｈ可促进其增殖：加入ＬＤＬ２５０ｕｇ／ｍＬ后２～６０ｍｉｎ内可使该细胞ＥＲＫ活性明显增加，１０ｍｉｎ时达高峰；不同剂量（５０～５００ｕｇ／ｍＬ）刺激时，ＥＲＫ活性分别较对照组增加１．５６～２．１９倍。ＬＤＬ促使核内转录因子ＡＰ－１结合活性增加。ＥＩＵＬ特异性阻断剂ＰＤ（５０ｕｍｏｌ／Ｌ）可以分别阻断ＬＤＬ刺激的ＨＫ－２细胞ＥＲＫ活性和ＤＮＡ合成。ＲＭＡ阻断ＰＫＣ信号途径后，ＬＤＬ对于ＥＲＫ的活化效应明显减弱。
To observe the effect of low density lipoprotein (LDL) on renal epithelial cells and related signal transduction mechanisms, 3H-TdR incorporation into human tubular epithelial cell line (HK-2) The activity of extracellular signal-regulated kinase (Eng) was determined by specific substrate phosphorylation assay. The transcriptional activation of (AP-1) was detected by gel mobility shift assay. The results showed that stimulation of LDL100 ~ 500 ug / mL for 72 h promoted the proliferation of HK-2 cells: ERK activity increased significantly at 2 ~ 60 min after adding LDL 250 ug / mL and reached the peak at 10 min; ERK activity increased by 1.56 ~ 2.19 times compared with the control group respectively. LDL promotes the increase of nuclear transcription factor AP-1 binding activity. EIUL specific inhibitor PD (50umol / L) could block ERK activity and DNA synthesis in HK-2 cells stimulated by LDL. After RMA blocks PKC signaling pathway, the activation effect of LDL on ERK is obviously weakened.