Exposure to fine particulate matter with a diameter ≤2.5 μm (PM2.5) can cause a number of respiratory diseases. However, there is currently no safe treatment for PM2.5-induced lung damage. This study investigated the protective effect of IL-10 against lung injury and the possible involvement of AMPK/SIRT1/PGC-1α signaling. The mean diameter, particle size distribution, and zeta potential of PM2.5 samples were assessed using a Zetasizer Nano ZS90 analyzer. Thereafter, Wistar rats were exposed to PM2.5 (1.8, 5.4, or 16.2 mg/kg) alone or high-dose PM2.5 with recombinant rat IL-10 (rrIL-10; 5 μg/rat). Treatment with rrIL-10 ameliorated PM2.5-induced acute lung injury, reduced mitochondrial damage, and inhibited inflammation, oxidative stress, and apoptosis in the PM2.5-treated rats. Moreover, the mRNA and protein expression of AMPK, SIRT1, and PGC-1α were upregulated by rrIL-10 treatment. In conclusion, rrIL-10 protected lung tissues against PM2.5-induced inflammation by reducing oxidative stress and apoptosis via activating AMPK/SIRT1/PGC-1α signaling.

接触直径≤2.5 μm (PM2.5) 的细颗粒物会导致多种呼吸系统疾病。然而，目前没有针对 PM2.5 引起的肺损伤的安全治疗方法。本研究调查了 IL-10 对肺损伤的保护作用以及 AMPK/SIRT1/PGC-1α 信号传导的可能参与。使用 Zetasizer Nano ZS90 分析仪评估 PM2.5 样品的平均直径、粒度分布和 Zeta 电位。此后，Wistar 大鼠暴露于单独的 PM2.5（1.8、5.4 或 16.2 mg/kg）或高剂量 PM2.5 和重组大鼠 IL-10（rrIL-10；5 μg/大鼠）。rrIL-10 治疗改善了 PM2.5 诱导的急性肺损伤，减少了线粒体损伤，并抑制了 PM2.5 治疗大鼠的炎症、氧化应激和细胞凋亡。此外，AMPK、SIRT1、rrIL-10 处理使 PGC-1α 和 PGC-1α 上调。总之，rrIL-10 通过激活 AMPK/SIRT1/PGC-1α 信号传导减少氧化应激和细胞凋亡，从而保护肺组织免受 PM2.5 诱导的炎症。