Graduate School of Beijing University of Traditional Chinese Medicine, Beijing 100029, China.
Surgical Intensive Care Unit, China Japan Friendship Hospital, Beijing 100029, China.
J Healthc Eng. 2022 Mar 30;2022:8450673. doi: 10.1155/2022/8450673. eCollection 2022.
Inhalation of particles with a diameter of less than 2.5 m (PM2.5) among air pollutants may cause lung damage. Gu-Ben-Zhi-Ke-Zhong-Yao (GBZK) is a traditional Chinese medicine prescription that has a beneficial effect on the treatment of chronic obstructive pulmonary disease (COPD). However, the effect of GBZK on PM2.5-induced lung injury remains to be elucidated.
We constructed a mice lung injury model through PM2.5 stimulation and simultaneously performed GBZK gavage treatment. After 4 weeks, the lung tissues of the mice were collected for pathological staining to analyze the degree of damage. The activities of myeloperoxidase (MPO), malondialdehyde (MDA), and oxidative stress-related factors (superoxide dismutase, SOD; glutathione peroxidase, GSH-Px) were detected by commercial kit in lung tissue. Furthermore, the number of neutrophils and related inflammatory factors (interleukin-1, IL-1; tumor necrosis factor , TNF-; interleukin-6, IL-6) in bronchoalveolar lavage fluid (BALF) and serum were collected and tested to evaluate the effect of GBZK on inflammation. Masson staining was used to detect the level of lung fibrosis in mice. The activation of HMGB1 (high-mobility group protein 1) and NFBp65 (nucleus factor kappa B) in lung tissue was evaluated by immunohistochemistry and western blot.
The result revealed that PM2.5 induces lung damage, and GBZK gavage treatment could reduce the degree of injury in a concentration-dependent manner in mice. After GBZK treatment, the MPO activity, MDA content, and oxidative stress level in the lung tissues of mice decreased. And after GBZK treatment, the expression levels of inflammatory cytokines in BALF and blood were decreased. GBZK treatment also improved pulmonary fibrosis in mice. In addition, we also found that GBZK prevented the up-regulation of the HMGB1/NF-B axis in the lungs of mice.
These results indicated that GBZK might protect mice from PM2.5-induced lung injury by inhibiting the HMGB1/NFB pathway, thus repressing inflammation and pulmonary fibrosis.
空气中直径小于 2.5μm（PM2.5）的颗粒物吸入可能会导致肺部损伤。固本止咳中药（GBZK）是一种对治疗慢性阻塞性肺疾病（COPD）有有益效果的中药方剂。然而，GBZK 对 PM2.5 诱导的肺损伤的作用仍有待阐明。
我们通过 PM2.5 刺激构建了小鼠肺损伤模型，并同时进行了 GBZK 灌胃治疗。4 周后，收集小鼠的肺组织进行病理染色，分析损伤程度。采用商业试剂盒检测肺组织中髓过氧化物酶（MPO）、丙二醛（MDA）和氧化应激相关因子（超氧化物歧化酶，SOD；谷胱甘肽过氧化物酶，GSH-Px）的活性。此外，收集并检测支气管肺泡灌洗液（BALF）和血清中的中性粒细胞数量及相关炎症因子（白细胞介素-1，IL-1；肿瘤坏死因子-α，TNF-α；白细胞介素-6，IL-6），以评估 GBZK 对炎症的作用。采用 Masson 染色检测小鼠肺纤维化水平。通过免疫组织化学和 Western blot 评估肺组织中 HMGB1（高迁移率族蛋白 1）和 NFBp65（核因子 kappa B）的激活情况。
结果表明，PM2.5 可诱导肺损伤，GBZK 灌胃处理可在一定浓度范围内降低小鼠肺损伤程度。经 GBZK 处理后，小鼠肺组织中 MPO 活性、MDA 含量和氧化应激水平降低。经 GBZK 处理后，BALF 和血液中炎症细胞因子的表达水平降低。GBZK 处理还改善了小鼠的肺纤维化。此外，我们还发现，GBZK 可防止小鼠肺部 HMGB1/NF-B 轴的上调。
这些结果表明，GBZK 可能通过抑制 HMGB1/NFB 通路来保护小鼠免受 PM2.5 诱导的肺损伤，从而抑制炎症和肺纤维化。
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