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已发表论文
氧化苦参碱通过 KIT/PI3K 信号通路抑制肺上皮细胞凋亡以减轻急性肺损伤
Authors Qiao Z, Long K, Ding K, Zhang X, Gao X, Han S, Zheng N, Yang Y, Li J, Su Y, Zhang H , Li Y, Zhi W, Liu Y
Received 3 June 2025
Accepted for publication 11 September 2025
Published 23 September 2025 Volume 2025:19 Pages 8657—8674
DOI https://doi.org/10.2147/DDDT.S544479
Checked for plagiarism Yes
Review by Single anonymous peer review
Peer reviewer comments 2
Editor who approved publication: Dr Tuo Deng
Ziyao Qiao,1,* Kaihua Long,1,2,* Kairu Ding,1 Xiaoyan Zhang,2 Xiaoli Gao,1 Shanrong Han,1 Na Zheng,1 Yun Yang,1 Jingjing Li,1 Yaqiong Su,1 Hong Zhang,1,2 Ye Li,1,2 Wenbing Zhi,2 Yang Liu1,2
1College of Life Sciences, Northwest University, Xi’an, People’s Republic of China; 2Shaanxi Academy of Traditional Chinese Medicine (Shaanxi Traditional Chinese Medicine Hospital), Xi’an, People’s Republic of China
*These authors contributed equally to this work
Correspondence: Yang Liu, Shaanxi Academy of Traditional Chinese Medicine (Shaanxi Traditional Chinese Medicine Hospital), No. 421 Zhuque Street, Xi’an, Shaanxi, 710061, People’s Republic of China, Tel +86 02985395659, Email liuyang3111111@163.com Wenbing Zhi, Shaanxi Academy of Traditional Chinese Medicine (Shaanxi Traditional Chinese Medicine Hospital), No. 421 Zhuque Street, Xi’an, Shaanxi, 710061, People’s Republic of China, Tel +86 02985395659, Email zhiwenbing@163.com
Purpose: Acute lung injury (ALI) is an acute, diffuse, inflammatory lung injury caused by many factors. Oxysophocarpine (OSC), a quinoline alkaloid sourced from traditional Chinese herbs Sophora flavescens and Sophora davidii, possesses anti-inflammatory and antioxidant properties. However, its effects on ALI are still unclear. This study aims to investigate the role and potential mechanisms of OSC for the treatment of ALI.
Methods: The levels of TNF-α, IL-6, and IL-1β in bronchoalveolar lavage fluid (BALF) were measured with an enzyme-linked immunosorbent assay (ELISA). Lung tissue changes were examined through hematoxylin and eosin (HE) staining. Lung cell apoptosis was analyzed using the terminal deoxynucleotidyl transferase dUTP nick-end labeling (TUNEL) assay. Flow cytometry was utilized to detect neutrophil aggregation. Further, the network pharmacology and molecular docking was employed to predict the mechanisms. Key pathways and targets of OSC were confirmed using methods like immunohistochemistry (IHC), immunofluorescence (IF), real-time quantitative PCR (RT-qPCR), and Western blotting (WB).
Results: In vivo, OSC treatment significantly inhibited diffuse alveolar injury and interstitial edema compared to the LPS-induced model mice, reduced neutrophil infiltration, and lowered lung epithelial cell apoptosis. In vitro, OSC pretreatment enhanced lung epithelial cell viability and decreased LPS-induced apoptosis. Network pharmacology analysis suggested that OSC mainly targeted key proteins in the PI3K/AKT and apoptosis signaling pathways, such as KIT, PIK3CA, and Bcl-2. Molecular docking confirmed that OSC binds strongly to these targets. Further, PCR, WB, IF, and IHC assay demonstrated that OSC pretreatment elevated PI3K, KIT, and Bcl-2 expressions in BEAS-2B lung epithelial cells and lung tissues.
Conclusion: OSC reduced inflammatory cytokine production, neutrophil aggregation, and lung epithelial cell apoptosis via regulating the KIT/PI3K signaling pathway.
Keywords: pharmacological, inflammation, acute lung injury, KIT/PI3K signaling pathway, immunity
1College of Life Sciences, Northwest University, Xi’an, People’s Republic of China; 2Shaanxi Academy of Traditional Chinese Medicine (Shaanxi Traditional Chinese Medicine Hospital), Xi’an, People’s Republic of China
*These authors contributed equally to this work
Correspondence: Yang Liu, Shaanxi Academy of Traditional Chinese Medicine (Shaanxi Traditional Chinese Medicine Hospital), No. 421 Zhuque Street, Xi’an, Shaanxi, 710061, People’s Republic of China, Tel +86 02985395659, Email liuyang3111111@163.com Wenbing Zhi, Shaanxi Academy of Traditional Chinese Medicine (Shaanxi Traditional Chinese Medicine Hospital), No. 421 Zhuque Street, Xi’an, Shaanxi, 710061, People’s Republic of China, Tel +86 02985395659, Email zhiwenbing@163.com
Purpose: Acute lung injury (ALI) is an acute, diffuse, inflammatory lung injury caused by many factors. Oxysophocarpine (OSC), a quinoline alkaloid sourced from traditional Chinese herbs Sophora flavescens and Sophora davidii, possesses anti-inflammatory and antioxidant properties. However, its effects on ALI are still unclear. This study aims to investigate the role and potential mechanisms of OSC for the treatment of ALI.
Methods: The levels of TNF-α, IL-6, and IL-1β in bronchoalveolar lavage fluid (BALF) were measured with an enzyme-linked immunosorbent assay (ELISA). Lung tissue changes were examined through hematoxylin and eosin (HE) staining. Lung cell apoptosis was analyzed using the terminal deoxynucleotidyl transferase dUTP nick-end labeling (TUNEL) assay. Flow cytometry was utilized to detect neutrophil aggregation. Further, the network pharmacology and molecular docking was employed to predict the mechanisms. Key pathways and targets of OSC were confirmed using methods like immunohistochemistry (IHC), immunofluorescence (IF), real-time quantitative PCR (RT-qPCR), and Western blotting (WB).
Results: In vivo, OSC treatment significantly inhibited diffuse alveolar injury and interstitial edema compared to the LPS-induced model mice, reduced neutrophil infiltration, and lowered lung epithelial cell apoptosis. In vitro, OSC pretreatment enhanced lung epithelial cell viability and decreased LPS-induced apoptosis. Network pharmacology analysis suggested that OSC mainly targeted key proteins in the PI3K/AKT and apoptosis signaling pathways, such as KIT, PIK3CA, and Bcl-2. Molecular docking confirmed that OSC binds strongly to these targets. Further, PCR, WB, IF, and IHC assay demonstrated that OSC pretreatment elevated PI3K, KIT, and Bcl-2 expressions in BEAS-2B lung epithelial cells and lung tissues.
Conclusion: OSC reduced inflammatory cytokine production, neutrophil aggregation, and lung epithelial cell apoptosis via regulating the KIT/PI3K signaling pathway.
Keywords: pharmacological, inflammation, acute lung injury, KIT/PI3K signaling pathway, immunity