十八碳不饱与脂肪酸对乳腺上皮细胞脂肪代谢的影响及其机制研究.pdfVIP

Effects of C18 unsaturated fatty acids on lipid metabolism and its mechanisms in mammary epithelial cells Abstract Fatty acid is an important part of milk fat. Mammary epithelial cells is the direct components of fatty acid synthesis and transportation. We made mammary epithelial cells as a model to investigate the effects of C18 unsaturated fatty acids on fatty acid metabolism and the mechanism in mammary epithelial cells. The effects of C18 unsaturated fatty acids on cell proliferation was tested by the method of MTT and C18 UFA stimulated the accumulation of triglyceride (TAG) in CMECs, tested by Oil Red O stain. Using the RT-qPCR technique to detect the expression of mRNA for CD36,FABP3,ACACA,PPARG and SCD. The results shew that withing the increase of the concentration of 50-400μm/L,oleic acid promote the proliferation of CMECs,and higher oleic acid (800μm/L) inhibited the proliferation of CMECs. Linoleic acid with the concentration of 25-100μm/L promote the proliferation of CMECs, however highter (200μm/L) inhibited. Linolenic acid with the concentration of 0.5-1μm/L promote the proliferation of CMECs,however highter (2-8μm/L) inhibited. C18 UFA stimulated the accumulation of triglyceride (TAG) in CMECs,and when the concentration of oleic acid was 400μm/L,linoleic acid was 100 μm/L,linolenic acid was 2μm/L,the accumulation significantly. The extent of oleic acid concentration did not effect the transcriotion of CD36,but higher oleic acid downregulated the FABP3. The transcription level of ACACA and Stearoyl CoA desaturase (SCD) genes were inhibited by oleic acid with a dose response (P0.01)Oleic acid with the concentration of 50μmol/L upregulated the transcription of PPARG significantly. Linoleic acid upregulated the transcription of CD36 significantly,and inhibited th