【摘要】：目的:探討與微炎癥狀態(tài)相應的C-反應蛋白(CRP)水平是否誘導腎小管上皮細胞凋亡。方法:以微炎癥狀態(tài)相應的CRP濃度刺激HK-2細胞。采用AnnexinⅤ-FITC、PI染色和流式細胞術檢測凋亡細胞的百分率。采用Hoechst 33258染色觀察腎小管上皮細胞凋亡的形態(tài)學改變。比色法檢測細胞caspase-3活性。Real-time PCR檢測促凋亡基因bax、抗凋亡基因bcl-2的mRNA表達。結果:CRP呈劑量和時間依賴性地誘導HK-2細胞凋亡,細胞凋亡在CRP濃度為10 mg/L時達高峰,在20 mg/L時則以晚期凋亡和壞死為主。Hoechst 33258細胞核染色顯示CRP作用的HK-2細胞呈現染色質濃縮、碎裂或染色質邊集等細胞凋亡的特點。CRP增高細胞caspase-3的酶活性、上調促凋亡基因bax的表達和下調抗凋亡基因bcl-2的表達。結論:CRP輕度增高可誘導腎小管上皮細胞凋亡。
[Abstract]:Aim: to investigate whether the level of C-reactive protein (CRP) associated with microinflammation can induce apoptosis of renal tubular epithelial cells. Methods: HK-2 cells were stimulated with the corresponding CRP concentration of microinflammatory state. The percentage of apoptotic cells was detected by Annexin 鈪，

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