中文摘要：

腺苷酸活化蛋A激酶（AMP．activatedproteinkinase，AMPK）是参与调节细胞能量代谢的关键激酶，也可通过沉默信息调节因子1（silentinformationregulatoroftranscription1，SIRTl）依赖的途径发挥抗炎效应。AMPK激活SIRT1的机制在于AMPK促进了SIRTl的激活因子NAD＋的生成，并解除了DBCl对SIRTI活性及p53对SIRTl表达的抑制效应；而SIRTI则通过催化NF—KB、AP—1和组蛋A的去乙酰化反应而降低转录因子活性、恢复染色质致密构象，这可抑制炎症相关基因的转录。此外，AMPK激活剂及临床常用降糖药二甲双胍均可通过激活AMPK而在多种炎症相关性疾病模型中发挥有效保护作用。因而，AMPK—SIRTl通路有望成为抗炎治疗的新靶点。

英文摘要：

AMP-activated protein kinase （AMPK） is a crucial kinase involved in the modulation of cellular energy metabolism, and it also has SIRTl-dependent anti-inflammatory activity. The mechanisms through which AMPK activate SIRT1 include promoting the generation of SIRT1 activator NAD＋, relieving the suppressive effects on the activity of SIRT1 by DBC1 and on the expression of SIRT1 by p53. SIRT1 then modulates the inflammatory response through deacetylating nuclear factor kappa B （NF-κB）, activator protein 1 （AP-1） and histones, thus leading to suppressed transcriptional activities of transcription factors, altered conformation of chromatin, and eventually, transcriptional repression of inflammation-related genes. In addition, AMPK activator and the clinic antidiabetic metformin have protective benefits in various animal models with inflammation-related disorders through activating AMPK. Thus, AMPK-SIRTI pathway might become a novel target for anti-inflammatory therapy.