Alleviating penicillin-resistant Streptococcus pneumoniae‑induced lung epithelial cell injury: mechanistic insights into effects of the optimized combination of main components from Yinhuapinggan granules

被引:0
作者
Jiangbo Lv [1 ]
Haofang Wan [2 ]
Daojun Yu [1 ]
Huifen Zhou [2 ]
Wenba Wang [3 ]
Haitong Wan [1 ]
机构
[1] College of Chinese Medicine for Cardiovascular-Cranial Disease, Zhejiang Chinese Medical University, Hangzhou
[2] Zhejiang Key Laboratory of Chinese Medicine for Cardiovascular and Cerebrovascular Disease, Hangzhou
[3] Hangzhou First People’s Hospital, Hangzhou
[4] Academy of Chinese Medical Sciences, Henan University of Chinese Medicine, Henan Province, Zhengzhou
基金
中国国家自然科学基金;
关键词
Drug resistance; Inflammation; Lung injury; Streptococcus pneumoniae; Yinhuapinggan granules;
D O I
10.1186/s12879-025-10951-1
中图分类号
学科分类号
摘要
Objective: Penicillin-resistant Streptococcus pneumoniae (PRSP), for which novel treatment medicines are required, has expanded extensively due to the overuse of antibiotics. This study aimed to detect the optimal ratio of the combination of the main components based on Yinhuapinggan granules (YHPG) to generate novel treatment concepts for PRSP-induced lung injury. Methods: Three representative main components: chlorogenic acid (C), amygdalin (A), and puerarin (P) were selected, and the optimal combination of these three components was determined by an orthogonal experiment. Investigations were conducted on the potential mechanisms underlying the protective effect of this optimized combination against PRSP-induced lung epithelial cell damage. Meanwhile, the bacteriostatic effect was further explored through the optimized combination of these natural products combined with penicillin G (PG). Results: The optimized combination CAP (C: 16 µg/mL, A: 24 µg/mL, P: 24 µg/mL) screened by the orthogonal experimental design reduced cell damage in a model of human lung epithelial cells infected by PRSP, and the combination of CAP and PG had a synergistic effect. At the cellular level, CAP attenuated lung epithelial cell injury by modulating the TLRs/MyD88 inflammatory pathway. At the bacterial level, CAP modulated the virulence and drug resistance of PRSP, resulting in enhanced bacterial inhibition by the combination of CAP and PG. Conclusion: Taken together, our results suggest that CAP can modulate or synergize with PG to modulate the TLRs/MyD88 pathway and attenuate PRSP-induced lung injury, and can be used as a potential drug for treating PRSP infection. © The Author(s) 2025.
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