Pan Yue, Zhang Hanxu, Liu Qiannan, Wu Hao, Du Siqi, Song Wuqi, Zhang Fengmin, Liu Hailiang
Department of Microbiology, Wu Lien-Teh Institute, Harbin Medical University, Harbin, P.R. China.
Departments of Laboratory Diagnosis, Daqing Oilfield General Hospital, Daqing, China.
Photobiomodul Photomed Laser Surg. 2024 Feb;42(2):148-158. doi: 10.1089/photob.2023.0034. Epub 2024 Feb 2.
Sepsis-induced acute lung injury (ALI) is a clinical syndrome characterized by excessive uncontrolled inflammation. Photobiomodulation such as light-emitting diode (LED) irradiation has been used to attenuate inflammatory disease. The protective effect of 630 nm LED irradiation on sepsis-induced ALI remains unknown. The purpose of this study was to investigate the role of 630 nm LED irradiation in sepsis-induced ALI and its underlying mechanism. C57BL/6 mice were performed cecal ligation and puncture (CLP) for 12 h to generate experimental sepsis models. Histopathology analysis showed that alveolar injury, inflammatory cells infiltration, and hemorrhage were suppressed in CLP mice after 630 nm LED irradiation. The ratio of wet/dry weigh of lung tissue was significantly inhibited by irradiation. The number of leukocytes was reduced in bronchoalveolar lavage fluid. Reverse transcription-quantitative polymerase chain reaction (RT-qPCR) results and enzyme-linked immunosorbent assay showed that 630 nm LED irradiation significantly inhibited the mRNA and protein levels of M1 macrophage-related genes in the lung of CLP-induced septic mice. Meanwhile, LED irradiation significantly inhibited signal transducer and activator of transcription 1 (STAT1) phosphorylation in the lung of septic mice. experiments showed that 630 nm LED irradiation significantly inhibited M1 genes mRNA and protein expression in THP-1-derived M1 macrophages without affecting the cell viability. LED irradiation also significantly inhibited the level of STAT1 phosphorylation in THP-1-derived M1 macrophages. We concluded that 630 nm LED is promising as a treatment against ALI through inhibiting M1 macrophage polarization, which is associated with the downregulation of STAT1 phosphorylation.
脓毒症诱导的急性肺损伤(ALI)是一种以过度失控性炎症为特征的临床综合征。光生物调节,如发光二极管(LED)照射,已被用于减轻炎症性疾病。630 nm LED照射对脓毒症诱导的ALI的保护作用尚不清楚。本研究的目的是探讨630 nm LED照射在脓毒症诱导的ALI中的作用及其潜在机制。对C57BL/6小鼠进行盲肠结扎和穿刺(CLP)12小时以建立实验性脓毒症模型。组织病理学分析表明,630 nm LED照射后,CLP小鼠的肺泡损伤、炎性细胞浸润和出血受到抑制。照射显著抑制了肺组织湿/干重比。支气管肺泡灌洗液中的白细胞数量减少。逆转录-定量聚合酶链反应(RT-qPCR)结果和酶联免疫吸附测定表明,630 nm LED照射显著抑制了CLP诱导的脓毒症小鼠肺中M1巨噬细胞相关基因的mRNA和蛋白水平。同时,LED照射显著抑制了脓毒症小鼠肺中信号转导和转录激活因子1(STAT1)的磷酸化。实验表明,630 nm LED照射显著抑制THP-1来源的M1巨噬细胞中M1基因的mRNA和蛋白表达,而不影响细胞活力。LED照射还显著抑制THP-1来源的M1巨噬细胞中STAT1的磷酸化水平。我们得出结论,630 nm LED有望通过抑制M1巨噬细胞极化来治疗ALI,这与STAT1磷酸化的下调有关。