Yinma Jiedu Granule attenuates LPS-induced acute lung injury in rats via suppressing inflammation level

• Published in: Journal of ethnopharmacology 2023-06, Vol.310, p.116292-116292, Article 116292
• Main Authors: Li, Gen, Ma, Jingwei, Yang, Yang, Zang, Caixia, Ju, Cheng, Yuan, Fangyu, Ning, Jingwen, Shang, Meiyu, Chen, Qiuzhu, Jiang, Yueqi, Li, Fangfang, Bao, Xiuqi, Mu, Degui, Zhang, Dan
• Format: Article
• Language: English
• Subjects: Acute lung injury; Acute Lung Injury - chemically induced; Acute Lung Injury - drug therapy; Acute Lung Injury - metabolism; Animals; Inflammation; Inflammation - pathology; JAK2/STAT1 signaling pathway; Lipopolysaccharide; Lipopolysaccharides - metabolism; Lipopolysaccharides - toxicity; Lung; Oxidative stress; Pulmonary Edema - metabolism; Rats; Tumor Necrosis Factor-alpha - metabolism; Yinma Jiedu Granule
• ISSN: 0378-8741; 1872-7573
• DOI: 10.1016/j.jep.2023.116292

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 2 h after the last administration, the rat model of ALI was induced by the intratracheal instillation of LPS. High performance liquid chromatography (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), lymphocytes (LYM), mononuclear cells (MON) and neutrophils (NEUT) in bronchoalveolar lavage fluid (BALF), reduced the concentration of tumor necrosis factor-α (TNF-α) and interleukin-1β (IL-1β) and inhibited inducible nitric oxide synthase (iNOS) and cyclooxygenase-2 (COX-2) expression in the lung tissue. Additionally, we found that YMJD could significantly increase the activity of superoxide dismutase (SOD) and reduce the malondialdehyde (MDA) level in the lung tissue. 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. [Display omitted] •Fingerprint analysis of YMJD was performed to verify its chemical constituents.•The protective effect of YMJD was investigated from the perspectives of inflammation and oxidative stress.•The lung protective effects of YMJD are associated with inhibition of JAK2/STAT1 activation.•YMJD is a potential drug to treat inflammatory pulmonary disease, such as ALI.