Barca Olga, Costoya José A, Señarís Rosa M, Arce Víctor M
Departamento de Fisioloxía, Facultade de Medicina, Universidade de Santiago de Compostela, 15782 Santiago de Compostela, Spain.
Exp Cell Res. 2008 Jul 1;314(11-12):2231-7. doi: 10.1016/j.yexcr.2008.04.005. Epub 2008 Apr 22.
Several large clinical trials have demonstrated that interferon-beta (IFN-beta) therapy is effective in the treatment of multiple sclerosis (MS) patients. However, the mechanisms underlying the beneficial effects of IFN-beta are not fully understood. Most of the effort in the study of the relevant mechanisms of IFN-beta has dealt with its immunomodulatory actions. However, the beneficial effects of IFN-beta in MS patients may also depend on non-immune mechanisms, including the modulation of astrocyte function. In the present work, we have found that IFN-beta treatment protects astrocytes against tumour necrosis factor-induced apoptosis via activation of p38 mitogen-activated protein kinase. We propose that this effect may be of importance to protect astrocytes against apoptosis within the demyelinated plaques of the MS.
多项大型临床试验表明,β-干扰素(IFN-β)疗法对治疗多发性硬化症(MS)患者有效。然而,IFN-β有益作用的潜在机制尚未完全明确。在研究IFN-β相关机制方面,大部分工作都集中在其免疫调节作用上。然而,IFN-β对MS患者的有益作用也可能取决于非免疫机制,包括对星形胶质细胞功能的调节。在本研究中,我们发现IFN-β治疗可通过激活p38丝裂原活化蛋白激酶来保护星形胶质细胞免受肿瘤坏死因子诱导的凋亡。我们认为,这一效应对于保护MS脱髓鞘斑块内的星形胶质细胞免于凋亡可能具有重要意义。