CAJ | 학술논문

目的探讨小白菊内酯（PTL）对高糖诱导的大鼠肾小球系膜细胞（MC）增殖、核因子-κB（NF-κB）活性和单核细胞趋化蛋白-1（MCP-1）表达的影响。方法采用正常葡萄糖组（糖浓度为5.6 mmol/L）和高糖组（糖浓度为30 mmol/L）、高糖+PTL组，分别体外培养大鼠肾小球MC，MTT法检测MC的增殖，ELISA法检测培养液上清中MCP-1的浓度，Western Blot法检测IκBα反映NF-κB的活性，EMSA法检测NF-κB的活性。结果高糖诱导后MC增殖、MCP-1表达和NF-κB活性明显增强，NF-κB结合蛋白IκBα明显降解；应用PTL干预后，MC增殖、MCP-1表达和NF-κB活性均明显降低，IκBα降解被抑制。结论PTL能抑制高糖诱导的肾小球MC NF-κB活化及MCP-1的表达，从而为PTL用于临床防治糖尿病肾病提供了一定的理论依据。
목적탐토소백국내지（PTL）대고당유도적대서신소구계막세포（MC）증식、핵인자-κB（NF-κB）활성화단핵세포추화단백-1（MCP-1）표체적영향。방법채용정상포도당조（당농도위5.6 mmol/L）화고당조（당농도위30 mmol/L）、고당+PTL조，분별체외배양대서신소구MC，MTT법검측MC적증식，ELISA법검측배양액상청중MCP-1적농도，Western Blot법검측IκBα반영NF-κB적활성，EMSA법검측NF-κB적활성。결과고당유도후MC증식、MCP-1표체화NF-κB활성명현증강，NF-κB결합단백IκBα명현강해；응용PTL간예후，MC증식、MCP-1표체화NF-κB활성균명현강저，IκBα강해피억제。결론PTL능억제고당유도적신소구MC NF-κB활화급MCP-1적표체，종이위PTL용우림상방치당뇨병신병제공료일정적이론의거。
Objective To explore the effects of parthenolide (PTL) on high glucose-stimulated cell proliferation, NF-κB activation and monocyte chemoattractant protein-1 (MCP-1) expression in rat mesangial cells (MCs). Methods MCs were cultured in normal glucose (5.6 mmol/L), high glucose (30 mmol/L), or high glucose with PTL. MTT assay was used to detect the cell proliferation. MCP-1 content in the supernatant was measured by ELISA, and the level of IκBα was detected by Western blotting to reflect NF-κB activity. EMSA method was used to measure the activation of NF-κB. Results MC proliferation, MCP-1 expression and NF-κB activation were significantly enhanced and the expression of NF-κB-binding protein IκBα was obviously reduced in cells cultured in high glucose. Application of PTL obviously abolished the effects of high glucose. Conclusion PTL can suppress high glucose-stimulated NF-κB activation and MCP-1 expression in rat MC. These data provide a theoretical basis for the clinical application of PTL in prevention and control of diabetic nephropathy.