Oraldi Manuela, Maggiora Marina, Paiuzzi Elena, Canuto Rosa A, Muzio Giuliana
Dipartimento di Medicina ed Oncologia Sperimentale, Università di Torino, Turin, Italy.
Lipids. 2013 Jan;48(1):29-38. doi: 10.1007/s11745-012-3734-6. Epub 2012 Nov 7.
Conjugated linoleic acid (CLA) is thought to have anti-proliferative and anti-inflammatory properties, but its effect on cancer cachexia is unknown. Two effects were here investigated: that of CLA on inflammatory mediator production in human lung cancer cells, and that of reduced mediators on the myogenic differentiation of murine muscle C2C12 cells. The latter cells were grown in medium conditioned by human lung cancer A427 cells, with or without CLA, to mimic only the effect of molecules released from the tumor "in vivo", excluding the effect of host-produced cachectic factors. The results obtained show that CLA was found to reduce the production of tumor necrosis factor-α, interleukin (IL)-1β and prostaglandin E2 (PGE2), but had no effect on IL-6 production. The mechanisms underlying the effect of CLA on cytokine or PGE2 release in A427 cells are probably mediated by activation of peroxisome proliferator-activated receptor (PPAR)α, which increased at 24 h CLA treatment. In turn, the reduced content of inflammatory mediators in medium conditioned by A427 cells, in the presence of CLA, allowed muscle cells to proliferate, again by inducing PPAR. The involvement of PPARα was demonstrated by treatment with the antagonist MK-886. The findings demonstrate the anti-inflammatory and myogenic action of CLA and point to its possible application as a novel dietary supplement and therapeutic agent in inflammatory disease states, such as cachexia.
共轭亚油酸(CLA)被认为具有抗增殖和抗炎特性,但其对癌症恶病质的影响尚不清楚。本文研究了CLA的两种作用:CLA对人肺癌细胞中炎症介质产生的影响,以及炎症介质减少对小鼠肌肉C2C12细胞成肌分化的影响。后一种细胞在由人肺癌A427细胞条件培养基中培养,添加或不添加CLA,以模拟肿瘤在“体内”释放分子的作用,排除宿主产生的恶病质因子的影响。获得的结果表明,CLA可降低肿瘤坏死因子-α、白细胞介素(IL)-1β和前列腺素E2(PGE2)的产生,但对IL-6的产生没有影响。CLA对A427细胞中细胞因子或PGE2释放的影响机制可能是由过氧化物酶体增殖物激活受体(PPAR)α的激活介导的,在CLA处理24小时后PPARα增加。反过来,在CLA存在的情况下,A427细胞条件培养基中炎症介质含量的降低,通过诱导PPAR,使肌肉细胞再次增殖。用拮抗剂MK-886处理证明了PPARα的参与。这些发现证明了CLA的抗炎和成肌作用,并指出其作为一种新型膳食补充剂和治疗剂在炎症性疾病状态(如恶病质)中的可能应用。