Deng Jinfang, He Zhenpeng, Li Xiuru, Chen Wei, Yu Ziwen, Qi Ting, Xu Shuangyi, Xu Zhengxin, Fang Lei
Department of Pathlogy, First Medical Center of PLA General Hospital, Beijing 100853, China.
Institute of Translational Medicine, Medical College, Yangzhou University, Yangzhou 225009, China.
Evid Based Complement Alternat Med. 2021 Sep 22;2021:6626483. doi: 10.1155/2021/6626483. eCollection 2021.
Huangkui capsule (HKC) comprises the total flavonoid extract of flowers of (L.) Medicus. This study aimed to explore the effects of HKC on lipopolysaccharide- (LPS-) induced acute lung injury (ALI) in mice and LPS-stimulated RAW 264.7 cells.
Enzyme-linked immunosorbent assay, histopathology, spectrophotometry, and quantitative real-time polymerase chain reaction were used for the assessments. Statistical analysis was performed using a one-way analysis of variance.
LPS significantly increased lung inflammation, neutrophil infiltration, and oxidative stress and downregulated lung miR-451 expression. Treatment with HKC dramatically, reduced the total cell count in the bronchoalveolar lavage fluid (BALF), and inhibited myeloperoxidase activity in the lung tissues 24 h after LPS challenge. Histopathological analysis demonstrated that HKC attenuated LPS-induced tissue oedema and neutrophil infiltration in the lung tissues. Additionally, the concentrations of tumour necrosis factor- (TNF-) and interleukin- (IL-) 6 in BALF and IL-6 in the plasma reduced after HKC administration. Moreover, HKC could enhance glutathione peroxidase and catalase activities and upregulate the expression of miR-451 in the lung tissues. In vitro experiments revealed that HKC inhibited the production of nitric oxide, TNF-, and IL-6 in LPS-induced RAW 264.7 cells and mouse primary peritoneal macrophages. Additionally, HKC downregulated LPS-induced transcription of TNF and IL-6 in RAW 264.7 cells.
These findings suggest that HKC has anti-inflammatory and antioxidative effects that may protect mice against LPS-induced ALI and macrophage activation.
黄葵胶囊（HKC）由（L.）Medicus花的总黄酮提取物组成。本研究旨在探讨HKC对脂多糖（LPS）诱导的小鼠急性肺损伤（ALI）和LPS刺激的RAW 264.7细胞的影响。
采用酶联免疫吸附测定、组织病理学、分光光度法和定量实时聚合酶链反应进行评估。使用单向方差分析进行统计分析。
LPS显著增加肺部炎症、中性粒细胞浸润和氧化应激，并下调肺miR-451表达。HKC治疗显著降低了支气管肺泡灌洗液（BALF）中的总细胞计数，并在LPS攻击后24小时抑制了肺组织中的髓过氧化物酶活性。组织病理学分析表明，HKC减轻了LPS诱导的肺组织水肿和中性粒细胞浸润。此外，HKC给药后，BALF中肿瘤坏死因子（TNF）-和白细胞介素（IL）-6以及血浆中IL-6的浓度降低。此外，HKC可增强肺组织中谷胱甘肽过氧化物酶和过氧化氢酶的活性，并上调miR-451的表达。体外实验表明，HKC抑制LPS诱导的RAW 264.7细胞和小鼠原代腹腔巨噬细胞中一氧化氮、TNF-和IL-6的产生。此外，HKC下调LPS诱导的RAW 264.7细胞中TNF和IL-6的转录。
这些发现表明，HKC具有抗炎和抗氧化作用，可能保护小鼠免受LPS诱导的ALI和巨噬细胞活化。
