Li Li, Yan Jun, Ma Lin-Qin, Bi Wei, Wu Cai-Jun
Emergency Department, Dongzhimen Hospital, Beijing University of Chinese Medicine, Beijing 100700, China.
Institute of Sepsis, Beijing University of Chinese Medicine, Beijing 100029, China.
World J Emerg Med. 2022;13(1):32-37. doi: 10.5847/wjem.j.1920-8642.2022.023.
To investigate effects of Maxingloushi decoction on lung inflammation and programmed death markers (programmed death-1 [PD-1], programmed death-ligand 1 [PD-L1]) in the lung tissue, peripheral blood, and bronchoalveolar lavage fluid (BLF) in a mouse model of chronic obstructive pulmonary disease (COPD).
Thirty-six mature male BALB/C mice were randomly divided into normal group (group A, =6), COPD model group (group B, =10), Maxingloushi decoction + COPD group (group C, =10), and PD-1 inhibitor + COPD group (group D, =10). The COPD model was established by smoke inhalation combined with lipopolysaccharide (LPS). Levels of PD-1 and PD-L1 in plasma and BLF were measured by enzyme-linked immunosorbent assay (ELISA). Histopathological techniques were used to semi-quantitatively analyze the immuno-fluorescence optical density (IOD) value of the lung tissue.
In plasma and BLF, the expression of PD-1 in the group B was higher than that in the group A, and the expression of PD-L1 was lower than that in the group A. The expression of PD-1 and PD-L1 in the lung tissue was normalized in the group C in comparison with the group B (<0.05) and the group D (<0.05), and inflammatory cell infiltration in the lung tissue was also improved.
These findings reveal that COPD causes an immune imbalance in the peripheral blood and lung tissue, and that both Maxingloushi decoction and PD-1 inhibitor treatment can mitigate lung inflammation in COPD by reducing PD-1 expression and increasing PD-L1 expression. The treatment effect of Maxingloushi decoction may be superior to that of PD-1 inhibitor.
研究麻杏石甘汤对慢性阻塞性肺疾病(COPD)小鼠模型肺组织、外周血及支气管肺泡灌洗液(BALF)中肺部炎症和程序性死亡标志物(程序性死亡受体1 [PD-1]、程序性死亡配体1 [PD-L1])的影响。
将36只成年雄性BALB/C小鼠随机分为正常组(A组,n = 6)、COPD模型组(B组,n = 10)、麻杏石甘汤 + COPD组(C组,n = 10)和PD-1抑制剂 + COPD组(D组,n = 10)。通过吸入烟雾联合脂多糖(LPS)建立COPD模型。采用酶联免疫吸附测定(ELISA)法检测血浆和BALF中PD-1和PD-L1的水平。运用组织病理学技术对肺组织免疫荧光光密度(IOD)值进行半定量分析。
在血浆和BALF中,B组PD-1的表达高于A组,PD-L1的表达低于A组。与B组(P < 0.05)和D组(P < 0.05)相比,C组肺组织中PD-1和PD-L1的表达恢复正常,肺组织中的炎症细胞浸润也得到改善。
这些研究结果表明,COPD导致外周血和肺组织免疫失衡,麻杏石甘汤和PD-1抑制剂治疗均可通过降低PD-1表达和增加PD-L1表达减轻COPD肺部炎症。麻杏石甘汤的治疗效果可能优于PD-1抑制剂。