Ma Yuanhong, Chen Yifan, Li Yan, Liu Yan, Kong Yurong, Zou Qiao, Guo Zhengguang, Li Xin, Chu Yan, Wang Qian
Beijing University of Chinese Medicine, Beijing 100029, China.
Third Affiliated Hospital of Beijing University of Chinese Medicine, Beijing 10029, China.
Evid Based Complement Alternat Med. 2022 Feb 18;2022:3051797. doi: 10.1155/2022/3051797. eCollection 2022.
This study discusses the anti-inflammatory mechanism of Yiqi Huayu Jiedu decoction (YQHYJD) and studies the intervening effect of YQHYJD on the inflammatory cytokines in acute respiratory distress syndrome (ARDS) rats by inhibiting the TLR4/NLRP3 signal pathway. The aim of the probe is to provide evidence to support the identification of therapeutic targets in Chinese medicine treatment, which broadens the alternatives for the treatment of ARDS.
A lipopolysaccharide (LPS)-induced ARDS model group is established on rats by tail vein injection. A medicine group is established on ARDS rats by prophylactic administration using YQHYJD. Materials are collected, and tests are conducted according to experimental processes.
The rats in the medicine group gained weight compared with those in the ARDS model group. Pathological sections from the medicine group indicated improved condition in terms of pulmonary and interstitial edema in the lung tissues of rats compared with that from the ARDS model group. The percentage of neutrophil of the medicine group was significantly brought down compared with that of the ARDS model group ( < 0.001). Enzyme-linked immunosorbent assay (ELISA) was used to detect the changes in the level of inflammatory cytokines. It was observed that the levels of IL-1 and IL-18 in serum of the medicine group significantly decreased ( < 0.001 and < 0.01), the contents of TLR4 and NLRP3 in bronchoalveolar lavage fluid (BALF) of the medicine group decreased, and the contents of TLR4 and NLRP3 in lung tissue homogenate of the medicine group significantly decreased ( < 0.05, < 0.001, < 0.01, and < 0.05). In further mass spectrum identification of the proteins from the same animal groups, it was observed that the expressions of inflammatory proteins TNFRSF1, LBP, and NOS2 of the medicine group were reduced. The differences were statistically significant.
The pharmacological action of YQHYJD's anti-inflammatory mechanism is closely associated with the regulation of inflammatory cytokines TLR4, NLRP3, IL-1, IL-18, TNFRSF1, LBP, and NOS2 on the TLR4/NLRP3 signal pathway.
本研究探讨益气化瘀解毒汤（YQHYJD）的抗炎机制，并通过抑制TLR4/NLRP3信号通路研究YQHYJD对急性呼吸窘迫综合征（ARDS）大鼠炎症细胞因子的干预作用。本探索的目的是为中医治疗中治疗靶点的确定提供证据，拓宽ARDS治疗的选择。
通过尾静脉注射建立脂多糖（LPS）诱导的大鼠ARDS模型组。采用YQHYJD对ARDS大鼠进行预防性给药，建立药物组。按照实验流程收集材料并进行检测。
与ARDS模型组相比，药物组大鼠体重增加。药物组的病理切片显示，与ARDS模型组相比，大鼠肺组织的肺和间质水肿情况有所改善。与ARDS模型组相比，药物组中性粒细胞百分比显著降低（<0.001）。采用酶联免疫吸附测定（ELISA）检测炎症细胞因子水平的变化。观察到药物组血清中IL-1和IL-18水平显著降低（<0.001和<0.01），药物组支气管肺泡灌洗液（BALF）中TLR4和NLRP3含量降低，药物组肺组织匀浆中TLR4和NLRP3含量显著降低（<0.05、<0.001、<0.01和<0.05）。在对同一动物组蛋白质的进一步质谱鉴定中，观察到药物组炎症蛋白TNFRSF1、LBP和NOS2的表达降低。差异具有统计学意义。
YQHYJD抗炎机制的药理作用与TLR4/NLRP3信号通路中炎症细胞因子TLR4、NLRP3、IL-1、IL-18、TNFRSF1、LBP和NOS2的调节密切相关。
