中华劳动卫生职业病杂志
中華勞動衛生職業病雜誌
중화노동위생직업병잡지
CHINESE JOURNAL OF INDUSTRIAL HYGIENE AND OCCUPATIONAL DISEASES
2008年
6期
323-326
,共4页
杨学森%张伟%龚茜芬%余争平%张广斌%郝玉通
楊學森%張偉%龔茜芬%餘爭平%張廣斌%郝玉通
양학삼%장위%공천분%여쟁평%장엄빈%학옥통
辐射%有丝分裂素激活蛋白激酶类%细胞凋亡%PC12细胞
輻射%有絲分裂素激活蛋白激酶類%細胞凋亡%PC12細胞
복사%유사분렬소격활단백격매류%세포조망%PC12세포
Radiation%Mitogen-activated protein kinases%Apoptosis%PC12 cells
目的 探讨丝裂原活化蛋白激酶(MAPK)信号转导系统的差别激活与电磁辐射诱导PC12细胞凋亡的关系.方法 经MAPK特异性抑制剂SB203580、U0126预处理的PC12细胞接受65mW/cm2电磁波辐照20min,在辐照后3、24h2个观察时相点,采用蛋白质免疫印迹方法检测ERK1/2、JNK、P38 MAPK蛋白质磷酸化水平,采用Annexine-V-FITC标记流式细胞仪检测PC12细胞凋亡率.结果 电磁辐射后,PC12细胞ERK1/2的激活可以被U0126明显抑制,而SB203580对其无抑制作用.U0126和SB203580对辐照后JNK的活性无明显影响.SB203580可以明显抑制P38 MAPK的激活,而U0126对P38 MAPK激活的抑制作用不明显.SB203580可以明显减轻电磁辐射诱导的PC12细胞凋亡,而U0126预处理对细胞凋亡无明显影响.结论 电磁辐射诱导PC12细胞凋亡主要通过P38 MAPK信号通路的激活调控,而ERK通路对电磁辐射诱导的细胞凋亡无明显影响,JNK可能对辐照后早期的细胞凋亡有一定促进作用.
目的 探討絲裂原活化蛋白激酶(MAPK)信號轉導繫統的差彆激活與電磁輻射誘導PC12細胞凋亡的關繫.方法 經MAPK特異性抑製劑SB203580、U0126預處理的PC12細胞接受65mW/cm2電磁波輻照20min,在輻照後3、24h2箇觀察時相點,採用蛋白質免疫印跡方法檢測ERK1/2、JNK、P38 MAPK蛋白質燐痠化水平,採用Annexine-V-FITC標記流式細胞儀檢測PC12細胞凋亡率.結果 電磁輻射後,PC12細胞ERK1/2的激活可以被U0126明顯抑製,而SB203580對其無抑製作用.U0126和SB203580對輻照後JNK的活性無明顯影響.SB203580可以明顯抑製P38 MAPK的激活,而U0126對P38 MAPK激活的抑製作用不明顯.SB203580可以明顯減輕電磁輻射誘導的PC12細胞凋亡,而U0126預處理對細胞凋亡無明顯影響.結論 電磁輻射誘導PC12細胞凋亡主要通過P38 MAPK信號通路的激活調控,而ERK通路對電磁輻射誘導的細胞凋亡無明顯影響,JNK可能對輻照後早期的細胞凋亡有一定促進作用.
목적 탐토사렬원활화단백격매(MAPK)신호전도계통적차별격활여전자복사유도PC12세포조망적관계.방법 경MAPK특이성억제제SB203580、U0126예처리적PC12세포접수65mW/cm2전자파복조20min,재복조후3、24h2개관찰시상점,채용단백질면역인적방법검측ERK1/2、JNK、P38 MAPK단백질린산화수평,채용Annexine-V-FITC표기류식세포의검측PC12세포조망솔.결과 전자복사후,PC12세포ERK1/2적격활가이피U0126명현억제,이SB203580대기무억제작용.U0126화SB203580대복조후JNK적활성무명현영향.SB203580가이명현억제P38 MAPK적격활,이U0126대P38 MAPK격활적억제작용불명현.SB203580가이명현감경전자복사유도적PC12세포조망,이U0126예처리대세포조망무명현영향.결론 전자복사유도PC12세포조망주요통과P38 MAPK신호통로적격활조공,이ERK통로대전자복사유도적세포조망무명현영향,JNK가능대복조후조기적세포조망유일정촉진작용.
Objective To observe the effect of mitogen activated protein kinase (MAPK) signal transduction system on the apoptosis induced by electromagnetic exposure in PC12 cells. Methods After pretreated by SB203580 alone or together with U0126, PC12 cells were exposed to 65mW/cm2 electromagnetic wave for 20min. The phosphorylations of ERK1/2, JNK and P38 MAPK were tested by Western-blot at 3h and 24h after electromagnetic exposure. The apoptosis of PC12 cells were detected by Annexine-V-FITC flow cytometry. Results U0126, but not SB203580 could inhibit the activation of ERK1/2 induced by electromagnetic exposure. U0126 and SB203580 had no effects on the activation of JNK. SB203580 could inhibit the activation of P38 MAPK significantly. But U0126 had no such effect on the activation of P38 MAPK. After pretreated by SB203580 alone or together with U0126, the apoptosis of PC12 cells decreased. But the pretreatment by U0126 alone had no influence on the apoptosis of PC12 cells. Conclusion The P38 MAPK signa transduction modulate the apoptosis of PC12 cells induced by electromagnetic exposure. ERK signal transduction has no effect on the apoptosis of PC12 cells. JNK signal transduction may promote the apoptosis of PC12 cells in the early stage after electromagnetic exposure.