Role of p38MAPK in palmitate-induced inflammation in C2C12 muscle cells
Résumé
The saturated fatty acid palmitate (PAL) is now recognized as an inducer of inflammation in many types of cells, including adipocytes and muscle
cells, whereas n-3 polyunsaturated fatty acids (n-3PUFA) have anti-inflammatory properties. Meanwhile, PAL induces muscle insulin resistance (IR) and n-3PUFA are suggested to reverse it. We investigated n-3PUFA effects on palmitate-induced inflammation and the potential link between inflammation, P38MAPK activation and IR in C2C12 myotubes. After 16 hours incubation with 500µM PAL without or with SB203580, a specific
inhibitor of p38MAPK, 50µM of alpha linolenic acid (ALA), eicosapentaenoic acid (EPA) or docosahexaenoic acid (DHA), myotubes were harvested and submitted to mRNA quantification or immunoblotting. IL-6, TNF-a and COX-2 mRNA levels were significantly increased by PAL treatment and reversed by EPA and DHA. Inhibition of p38MAPK significantly prevented the effect of PAL on these regulations although it had no significant effect on PAL-induced IR. Additional study should be performed to explore the involvement of NFKB signalling. Our results suggested that p38MAPK activation by PAL is crucial to induce inflammation in C212 muscle cells, independently of IR. Among n-3PUFA, only EPA and DHA reduced p38MAPK activation and improved IR. Additional studies are currently performed to explore the involvement of NFKB signalling in the effect of PAL on myotube inflammation and the impact of n-3 PUFA on this pathway
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