CAJ | 학술논문

目的：检测缺氧条件下肾癌细胞斯钙素蛋白1（STC1）及线粒体膜电势稳定指标的变化，结合细胞增殖和Ca2+水平，初步探讨肾癌细胞可能的抗乏氧机制。方法分别使用50μmol/L、100μmol/L、150μmol/L的CoCl2干预细胞培养基构建化学性缺氧模型；MTT法检测细胞生长情况，荧光分光光度法检测细胞内Ca2+水平和线粒体膜电位（ΔΨm），紫外分光光度计测MPTP，RT-PCR检测STC1、HIF-1α的基因表达情况。结果与对照组相比，缺氧能显著抑制细胞增殖，促进细胞内Ca2+水平上升（P<0.05）；缺氧可使MPTP开放度增加、?Ψm减低（P<0.05），且此时细胞内STC1、HIF-1α的基因表达升高（P<0.05）；以上变化均随着缺氧程度的加剧而逐渐增大。结论缺氧条件下STC1、HIF-1α对Ca2+的负调控可能有利于肾癌细胞线粒体膜电势稳定，对肾癌细胞起保护作用。
목적：검측결양조건하신암세포사개소단백1（STC1）급선립체막전세은정지표적변화，결합세포증식화Ca2+수평，초보탐토신암세포가능적항핍양궤제。방법분별사용50μmol/L、100μmol/L、150μmol/L적CoCl2간예세포배양기구건화학성결양모형；MTT법검측세포생장정황，형광분광광도법검측세포내Ca2+수평화선립체막전위（ΔΨm），자외분광광도계측MPTP，RT-PCR검측STC1、HIF-1α적기인표체정황。결과여대조조상비，결양능현저억제세포증식，촉진세포내Ca2+수평상승（P<0.05）；결양가사MPTP개방도증가、?Ψm감저（P<0.05），차차시세포내STC1、HIF-1α적기인표체승고（P<0.05）；이상변화균수착결양정도적가극이축점증대。결론결양조건하STC1、HIF-1α대Ca2+적부조공가능유리우신암세포선립체막전세은정，대신암세포기보호작용。
Objective Detecting the change of mitochondrial membrane potential and stanniocalcin 1 (STC1) in renal carcinoma cell under hypoxic conditions, combined with cell proliferation and Ca2+ levels, this preliminary study aim to explore the possible mechanisms of anti-hypoxia in renal cancer cells. Methods CoCl2 at the concentrations of 50μmol/L, 100μmol/L, 150μmol/L were added to the mediums of renal cancer cells, and cells proliferation, expressions of HIF-1α, STC1, levels of Ca2+, mitochondrial membrane potential and mitochondrial permeability transition pore (MPTP) were detected by MTT, RT-PCR, fluorescence spectrophotometer and ultraviolet spectrophotometer, respectively. Results Compared with the control group, hypoxia could inhibit cell proliferation significantly and increase intracellular Ca2+ levels (P <0.05). Hypoxia could increase mitochondrial MPTP opening, reduce ΔΨm (P <0.05), and increase the expressions of HIF-1α, STC1 (P <0.05). The above changes were intensified with the degree of hypoxia increases gradually. Conclusion Ca2+ negatively regulated by STC1, HIF-1α may be beneficial renal carcinoma stable mitochondrial membrane potential under hypoxic conditions.