Key Laboratory of Neuropsychiatric Drug Research of Zhejiang Province, Hangzhou Medical College, Hangzhou, China.
Zhejiang Provincial Laboratory of Experimental Animal's & Nonclinical Laboratory Studies, Hangzhou Medical College, Hangzhou, China.
Biomed Res Int. 2022 Aug 22;2022:3510423. doi: 10.1155/2022/3510423. eCollection 2022.
Aurantiamide acetate (AA) is a dipeptide derivative with complex pharmacological activities and remarkable effects on preventing and treating various diseases. In the current study, we aimed to investigate whether AA can exert protective effects in a mouse model of ALI induced by LPS.
In this model, mice were given intranasal LPS for 3 days prior to receiving AA (2.5, 5, and 10 mg/kg) via oral gavage. An assessment of histopathological changes was performed by hematoxylin and eosin (HE). Proinflammatory cytokines were detected in bronchoalveolar lavage fluids (BALFs) by enzyme-linked immunosorbent assays (ELISAs). The effects of AA on protein expression of NF-B and PI3K/AKT signaling pathways were determined by Western blot. In addition, lung wet/dry (W/D) weight ratio, myeloperoxidase (MPO) activity, cell counts, and protein content were also measured.
According to results, AA pretreatment significantly reduced lung pathological changes, W/D ratio, MPO activity, and protein content. Additionally, AA resulted in a significant reduction in the number of total cells, neutrophils, and proinflammatory cytokines in the BALF after LPS stimulation. The subsequent study revealed that pretreatment with AA dose dependently suppressed LPS-induced activation of NF-B as well as PI3K/AKT phosphorylation.
The results indicated that the AA had a protective effect on LPS-induced ALI in mice and could be a potential drug for ALI.
醋酸橙皮酰胺（AA）是一种二肽衍生物，具有复杂的药理活性，对预防和治疗各种疾病有显著效果。在本研究中，我们旨在研究 AA 是否能对 LPS 诱导的 ALI 小鼠模型发挥保护作用。
在该模型中，小鼠先接受鼻内 LPS 处理 3 天，然后通过口服灌胃给予 AA（2.5、5 和 10mg/kg）。通过苏木精-伊红（HE）染色评估组织病理学变化。酶联免疫吸附试验（ELISA）检测支气管肺泡灌洗液（BALF）中的促炎细胞因子。Western blot 检测 AA 对 NF-B 和 PI3K/AKT 信号通路蛋白表达的影响。此外，还测量了肺湿/干（W/D）重量比、髓过氧化物酶（MPO）活性、细胞计数和蛋白含量。
AA 预处理显著减轻了 LPS 刺激后肺组织的病理变化、W/D 比、MPO 活性和蛋白含量。此外，AA 还导致 LPS 刺激后 BALF 中总细胞、中性粒细胞和促炎细胞因子的数量显著减少。进一步的研究表明，AA 预处理可剂量依赖性地抑制 LPS 诱导的 NF-B 激活以及 PI3K/AKT 磷酸化。
结果表明，AA 对 LPS 诱导的 ALI 小鼠具有保护作用，可能是 ALI 的潜在药物。
