| 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 C18unsaturated fatty acids on fatty acid metabolism and the mechanism in mammary epithelial cells.The effects of C18unsaturated fatty acids on cell proliferation was tested by the method of MTT and C18UFA 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 of50-400μm/L,oleic acid promote the proliferation of CMECs,and higher oleic acid (800μm/L) inhibited the proliferation of CMECs. Linoleic acid with the concentration of25-100μm/L promote the proliferation of CMECs, however highter (200μm/L) inhibited. Linolenic acid with the concentration of0.5-1μm/L promote the proliferation of CMECs,however highter (2-8μm/L) inhibited. C18UFA stimulated the accumulation of triglyceride (TAG) in CMECs,and when the concentration of oleic acid was400μm/L,linoleic acid was100μm/L,linolenic acid was2μm/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 AC AC A and Stearoyl Co A desaturase (SCD) genes were inhibited by oleic acid with a dose response (P<0.01)Oleic acid with the concentration of50μmol/L upregulated the transcription of PPARG significantly. Linoleic acid upregulated the transcription of CD36significantly,and inhibited the FABP3,ACACA and SCD significantly. Higher linoleic acid inhibited the expression of mRNA for PPARG Linolenic acid upregulated the transcription of CD36significantly and promote the expression of mRNA for ACACA, The extent of linolenic acid concentration did not effect the transcriotion of PPARG and SCD. |
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