银麻解毒颗粒（YMJD）是一种传统的中成药，已被证明具有抗炎效果并对阻塞性肺疾病具有治疗作用。本研究的目的是确定YMJD是否能减轻脂多糖（LPS）诱导的急性肺损伤（ALI）大鼠模型并研究其潜在机理。大鼠连续14天接受YMJD或药剂，最后一次给药后两小时，通过气管插管的方式诱导ALI模型。采用HPLC指纹图谱分析YMJD的功效和分子机制。结果表明，YMJD可以改善大鼠的一般状态，减少体重损失和血清乳酸（LA）水平，减轻肺水肿和肺组织的病理损伤。此外，我们发现YMJD可以有效减少支气管肺泡灌洗液中白细胞（WBC）、淋巴细胞（LYM）、单核细胞（MON）和中性粒细胞（NEUT）的浸润，并减少肺中肿瘤坏死因子-α（TNF-α）和白细胞介素-1β（IL-1β）的浓度，抑制诱导型一氧化氮合酶（iNOS）和环氧合酶2（COX-2）的表达。我们还发现YMJD能够提高大鼠肺组织的超氧化物歧化酶（SOD）活性和降低丙二醛（MDA）水平。通过RNA测序，我们确定JAK2/STAT1是与YMJD肺部保护有关的重要通路，并进一步进行了西方印迹实验证实YMJD可以有效抑制JAK2/STAT1通路的激活。YMJD可以通过抑制炎症和氧化应激来减轻LPS诱导的大鼠肺损伤，与抑制JAK2/STAT1活化有关。这些发现为YMJD在治疗ALI等炎性肺部疾病方面的临床应用提供了证据。版权所有©2023 Elsevier B.V.

Yinma Jiedu Granule (YMJD) is a traditional Chinese patent medicine (CPM), which has been proved to have anti-inflammatory effects and therapeutical effects on obstructive pulmonary disease.The purpose of the current investigation is to find out if YMJD can alleviate acute lung injury (ALI) induced by lipopolysaccharide (LPS) in rats and its underlying mechanisms.Rats were treated with either vehicle or YMJD for 14 consecutive days, and two hours after the last administration, the rat model of ALI was induced by the intratracheal instillation of LPS. HPLC was applied for the fingerprint analysis of YMJD. The efficacy and molecular mechanisms were investigated.The results showed that treatment with YMJD improved the general state of rats, reduced weight loss and serum lactate (LA) levels, attenuated pulmonary edema and pathological damage of the lung tissue. Moreover, we found that YMJD effectively decreased the infiltration of white blood cells (WBC), lymphocyte (LYM), mononuclear cells (MON) and neutrophils (NEUT) in bronchoalveolar lavage fluid (BALF), reduced the concentrations of tumor necrosis factor-α (TNF-α) and interleukin-1β (IL-1β) in the lung and inhibited inducible nitric oxide synthase (iNOS) and cyclooxygenase 2 (COX-2) expression. We also found that YMJD could increase the activity of superoxide dismutase (SOD) and reduce the malondialdehyde (MDA) level in the lung tissue of rats. By employing RNA-sequencing, we have identified that JAK2/STAT1 is an important pathway that is involved in the lung protection of YMJD, and further western blot assay verified that YMJD could effectively inhibit the activation of the JAK2/STAT1 pathway.YMJD could attenuate LPS-induced ALI through suppressing inflammation and oxidative stress in the lung tissue of rats, associating with the inhibition of JAK2/STAT1 activation. These findings provide evidence for the clinical use of YMJD for treatment of inflammatory pulmonary diseases like ALI.Copyright © 2023. Published by Elsevier B.V.