Abstract：Objective: To investigate the role of macrophage mobile inhibitors in the inflammatory development of chronic obstructive pulmonary disease (COPD) rats. Methods: SD male rats were randomly divided into COPD models (n=20), ISO-1 (n=20), and healthy controls (n=20). The rat COPD model was prepared by using cigarette smoking alone, cigarette smoke mold was given to the COPD group and rats in ISO-1 were intraperitoneally injected with MIF inhibitor (ISO-1) one hour before each smoke at 0~30d,60~90d. Five individuals in each group were killed at 30d,60d and 90d, respectively, by HE staining for lung tissue inflammation, MIF (macrophage mobility inhibitory factor) and IL-6 levels in rat serum and lung tissue homogenates, and MIF protein expression was determined by immunohistochemical staining. Results: MIF was significantly highly expressed in serum and lung tissues in the COPD model group, but low in the ISO-1 group and statistically significant (P<0.05), while both rat serum and lung tissues were higher than in healthy controls (P<0.05). Lung tissue immunohistochemistry also showed higher MIF expression (except 30th d) in each time period model group than in the ISO-1 group as well as healthy controls, while the ISO-1 group was only higher than the healthy controls (P<0.05). The associated inflammatory factor, IL-6, is closely related to MIF, IL-6 expression in the ISO-1 group was significantly decreased in rat serum and lung tissue than in the model group. High expression was observed only in the unsuppressed model group (P<0.05). Lung histopathology showed a significant reduction in inflammation in group ISO-1. The COPD maturity was significantly reduced compared to the model group, showing that blocking MIF attenuated COPD inflammation in rats. Conclusion: MIF is significantly expressed in the development of COPD and is closely associated with inflammatory status, indicating that it plays an important role in the development of COPD inflammation, which can further reflect the inflammatory status of COPD and accelerate COPD disease progression, while inhibition of MIF can improve the inflammatory status of COPD rats, which provides a new idea for the treatment of clinical COPD patients.
钟莉, 李天浩, 王惠琴. MIF在香烟烟雾诱导的COPD大鼠炎症进展中的作用研究[J]. 河北医学, 2022, 28(5): 720-724.
ZHONG Li, LI Tianhao, WANG Huiqin. The Role of MIF in the Progression of Cigarette Smoke Induced Inflammation in Rats with COPD. HeBei Med, 2022, 28(5): 720-724.
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2022, Vol. 28 
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