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已发表论文
补肺益肾方III有效成分配伍通过VEGF165/P38 MAPK通路减轻COPD肺血管炎症
Authors Song Q , Cui L, Lu R, Shao X, Xu K, Tian Y
Received 17 February 2025
Accepted for publication 8 January 2026
Published 23 January 2026 Volume 2026:19 523270
DOI https://doi.org/10.2147/JIR.S523270
Checked for plagiarism Yes
Review by Single anonymous peer review
Peer reviewer comments 3
Editor who approved publication: Dr Cynthia Koziol-White
Qinghua Song,1,2 Lili Cui,1,2 Ruilong Lu,1,2 Xuejie Shao,1,2 Kexin Xu,1– 3 Yange Tian1,2,4
1Henan University of Chinese Medicine, Zhengzhou, Henan, 450046, People’s Republic of China; 2Collaborative Innovation Center for Chinese Medicine and Respiratory Diseases Co-Constructed by Henan Province and Education Ministry of People’s Republic of China, Zhengzhou, Henan, 450046, People’s Republic of China; 3First Affiliated Hospital of Henan University of Chinese Medicine, Zhengzhou, Henan, 450000, People’s Republic of China; 4Academy of Chinese Medical Sciences, Henan University of Chinese Medicine, Zhengzhou, Henan, 450046, People’s Republic of China
Correspondence: Yange Tian, Henan University of Chinese Medicine, Zhengzhou, Henan, 450046, People’s Republic of China, Tel +86-13783656761, Email yange0910@126.com
Purpose: Chronic inflammation of the lungs can affect pulmonary vascular remodeling in chronic obstructive pulmonary disease (COPD). The Bufei Yishen formula (BYF) and Effective-compound combination of BYF III (ECC-BYF III) ameliorate lung histopathological injury and remodeling, but the mechanism remains unclear. This study aimed to observe the effects of ECC-BYF III on pulmonary vascular inflammation in COPD and to elucidate its detailed mechanism.
Methods: In vivo, COPD rat model was established through cigarette smoke exposure (CSE) combined with repeated infections of Klebsiella pneumoniae. Rats were randomly treated with ECC-BYF III (5.5 mg/kg, once a day) or doxofylline (36 mg/kg, once a day) for eight weeks. In vitro, Human umbilical vein endothelial cells (HUVECs) and human monocyte leukemia cells (THP-1) were induced with 10 μg/mL LPS for 24h. The pulmonary function, histopathology, inflammatory factor levels, immunoblotting results were evaluated.
Results: Compared with the model group, ECC-BYF III significantly improved the lung function, alleviated pulmonary artery inflammation and relieved pulmonary vascular remodeling in COPD rats. At the molecular level, ECC-BYF III down-regulated VEGF165/P38 MAPK signaling pathway. In the inflammatory model of HUVEC induced by LPS, 35 and 70μg/mL ECC-BYF III significantly decreased the levels of tumor necrosis factor -α (TNF-α), interleukin-1β (IL-1β) and Endothelin-1 (ET-1) mRNA, and increased the expression of endothelial nitric oxide synthase (eNOS) mRNA. In addition, ECC-BYF III also inhibited VEGF165/P38 MAPK pathway in LPS-induced HUVEC and THP-1/HUVEC co-cultured inflammatory models.
Conclusion: Our findings demonstrate that ECC-BYF III can improve pulmonary vascular remodeling in COPD rats, and its key pharmacodynamic mechanism involves the inhibition of the VEGF165/P38 MAPK pathway, thereby reducing inflammatory infiltration.
Keywords: chronic obstructive pulmonary disease, Chinese medicine, pulmonary vascular inflammation, VEGF165/P38 MAPK pathway
1Henan University of Chinese Medicine, Zhengzhou, Henan, 450046, People’s Republic of China; 2Collaborative Innovation Center for Chinese Medicine and Respiratory Diseases Co-Constructed by Henan Province and Education Ministry of People’s Republic of China, Zhengzhou, Henan, 450046, People’s Republic of China; 3First Affiliated Hospital of Henan University of Chinese Medicine, Zhengzhou, Henan, 450000, People’s Republic of China; 4Academy of Chinese Medical Sciences, Henan University of Chinese Medicine, Zhengzhou, Henan, 450046, People’s Republic of China
Correspondence: Yange Tian, Henan University of Chinese Medicine, Zhengzhou, Henan, 450046, People’s Republic of China, Tel +86-13783656761, Email yange0910@126.com
Purpose: Chronic inflammation of the lungs can affect pulmonary vascular remodeling in chronic obstructive pulmonary disease (COPD). The Bufei Yishen formula (BYF) and Effective-compound combination of BYF III (ECC-BYF III) ameliorate lung histopathological injury and remodeling, but the mechanism remains unclear. This study aimed to observe the effects of ECC-BYF III on pulmonary vascular inflammation in COPD and to elucidate its detailed mechanism.
Methods: In vivo, COPD rat model was established through cigarette smoke exposure (CSE) combined with repeated infections of Klebsiella pneumoniae. Rats were randomly treated with ECC-BYF III (5.5 mg/kg, once a day) or doxofylline (36 mg/kg, once a day) for eight weeks. In vitro, Human umbilical vein endothelial cells (HUVECs) and human monocyte leukemia cells (THP-1) were induced with 10 μg/mL LPS for 24h. The pulmonary function, histopathology, inflammatory factor levels, immunoblotting results were evaluated.
Results: Compared with the model group, ECC-BYF III significantly improved the lung function, alleviated pulmonary artery inflammation and relieved pulmonary vascular remodeling in COPD rats. At the molecular level, ECC-BYF III down-regulated VEGF165/P38 MAPK signaling pathway. In the inflammatory model of HUVEC induced by LPS, 35 and 70μg/mL ECC-BYF III significantly decreased the levels of tumor necrosis factor -α (TNF-α), interleukin-1β (IL-1β) and Endothelin-1 (ET-1) mRNA, and increased the expression of endothelial nitric oxide synthase (eNOS) mRNA. In addition, ECC-BYF III also inhibited VEGF165/P38 MAPK pathway in LPS-induced HUVEC and THP-1/HUVEC co-cultured inflammatory models.
Conclusion: Our findings demonstrate that ECC-BYF III can improve pulmonary vascular remodeling in COPD rats, and its key pharmacodynamic mechanism involves the inhibition of the VEGF165/P38 MAPK pathway, thereby reducing inflammatory infiltration.
Keywords: chronic obstructive pulmonary disease, Chinese medicine, pulmonary vascular inflammation, VEGF165/P38 MAPK pathway