低功率激光调节脂肪细胞内ERK与Akt促进甘油三酯的合成  

Triglyceride Biosynthesis Induced by Low-Power Laser Irradiation via Regulation of ERK and Akt in Adipocytes

作　　者：蒋笑笑 巩龙龙 黄磊[1] 

机构地区：[1]华南师范大学生物光子学研究院激光生命科学研究所暨激光生命科学教育部重点实验室,广东广州510631

出　　处：《中国激光》2013年第12期113-117,共5页Chinese Journal of Lasers

基　　金：国家973计划(2011CB910402;2010CB732602);教育部'长江学者与创新团队计划'创新团队项目(IRT0829);国家自然科学基金(81101741)

摘　　要：低功率激光照射(LPLI)可以激活细胞内多种信号途径促进细胞增殖、迁移、分化等,但是LPLI能否调节脂肪细胞内胞外信号调节激酶(ERK)和蛋白激酶B(Akt)促进甘油三酯的合成却尚未见报道。利用LPLI刺激前脂肪细胞和成熟脂肪细胞并结合蛋白质免疫印迹法分析处理后细胞内ERK和Akt活性的变化。研究结果表明LPLI处理后前脂肪细胞内ERK和Akt的活性增高,而LPLI处理成熟脂肪细胞后ERK活性下降而Akt活性增高,说明LPLI在脂肪细胞内可以差异性调节ERK和Akt的活性。此外,LPLI能通过抑制ERK、激活Akt而增加胰岛素抵抗脂肪细胞内甘油三酯的含量。该结果暗示LPLI可能通过调节ERK与Akt信号缓解脂代谢紊乱造成的胰岛素抵抗。Low-power laser irradiation （LPLI） can promote cell proliferation, migration and differentiation through activation of multiple signaling pathways. However, it is unclear whether LPLI can promote triglyceride biosynthesis in adipocytes via regulation of extracellular signal-regulated kinase （ERK） and protein kinase B （PKB, also named Akt）. In the present study, the changes of the ERK and Akt activity in 3T3-L1 pre-adipocytes and mature adipocytes upon LPLI stimulations is investigated using western blot analysis. The findings indicate that the activity of ERK and Akt is significantly elevated in 3T3-L1 pre-adipocytes under LPLI treatment. In contrast, the activity of ERK is dramatically reduced in mature adipocytes, but the activity of Akt is significantly elevated under LPLI treatment, suggesting that LPLI can differentially regulate the activity of ERK and Akt. Furthermore, the concentration of triglyceride in insulin resistant adipocytes is increased which is induced by LPLI through inhibition of ERK and activation of Akt. These results imply that LPLI can improve lipid metabolic disorders-induced insulin resistance through regulation of ERK and Akt.

关 键 词：生物光学 低功率激光照射 蛋白质免疫印迹 脂肪细胞 胞外信号调节激酶 蛋白激酶B 

分 类 号：O436[机械工程—光学工程]