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| Effect of Baicalin on chronic pulmonary infection of multidrug resistant Pseudomonas aeruginosa in rats |
| LI Lei1* WANG Jing2* CUI Lanfeng3* LYU Siyuan1 GUO Yufei1 QIN Xinxin1 WANG Chengxiang1 |
1.Department of Respiratory, Beijing University of Chinese Medicine Third Affiliated Hospital, Beijing 100029, China;
2.Office of Academic Affairs, Beijing University of Chinese Medicine, Beijing 100029;
3.Department of Traditional Chinese Medicine, Beijing Tsinghua Changgung Hospital Affiliated to Tsinghua University, Beijing 102218, China |
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Abstract Objective To study the effect of Baicalin on chronic pulmonary infection of multidrug resistant Pseudomonas aeruginosa (MDRPA) in rats. Methods Thirty-two SPF male SD rats (6-8 weeks old, weight 180-220 g) were randomly divided into blank group, model group, western medicine group, and Baicalin group, with eight rats in each group. Among them, the model group, western medicine group, and the Baicalin group were injected with MDRPA alginate coated body through ortracheal intubation to establish the rat model of MDRPA chronic pulmonary infection. The Baicalin group was given 0.8 g/(kg·d) Baicalin by gavage, and the western medicine group was given 0.8 g/(kg·d) Piperacillin Tazobactam Sodium intramuscular injection. The blank group and the model group were given the same amount of normal saline as the Baicalin group by gavage. After 14 days of intervention, serum and lung tissues of the four groups were collected, and the lung tissues were observed by hematoxylin-eosin staining. The levels of tumor necrosis factor-α (TNF-α) and interleukin-10 (IL-10) in serum were detected by enzyme-linked immunosorbent assay. The mRNA expressions of Toll-like receptor 4 (TLR4) and nuclear factor κB (p65 subunit) (NF-κB p65) in lung tissue were detected by quantitative polymerase chain reaction. Results The lung tissue of blank group was normal. In the model group, a large number of inflammatory cells were infiltrated and the alveolar wall was significantly thickened. In Baicalin group, there were fewer inflammatory cells and thinner alveolar wall in lung tissues. The levels of serum TNF-α and the levels of TLR4 and NF-κB p65 mRNA in lung tissues in the model group were higher than those in the blank group, and the level of serum IL-10 was lower than that in the blank group (P ＜ 0.05). The levels of serum TNF-α and the levels of TLR4 and NF-κB p65 mRNA in lung tissues in Baicalin group were lower than those in model group, and the level of serum IL-10 was higher than that in model group (P ＜ 0.05). Conclusion Baicalin can reduce the inflammatory injury of lung tissues in rats with MDRPA chronic lung infection, and the mechanism may be related to the inhibition of TLR4/NF-κB pathway activation.
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