Journal of Traditional Chinese Medicine ›› 2025, Vol. 45 ›› Issue (5): 1048-1058.DOI: 10.19852/j.cnki.jtcm.2025.05.011
• Original Articles • Previous Articles Next Articles
Jianpi Yifei Tongluo recipe (健脾益肺通络方剂) attenuates inflammation by promoting the expression of interferon regulatory factor 4 in the rat model of chronic obstructive pulmonary disease
WANG Wei, LONG Qi, FU Ling, WU Haiqiao(
)
- Department of respiratory and critical care medicine, Chongqing Traditional Chinese Medicine Hospital, Chongqing 400038, China
-
Received:2024-03-22Accepted:2024-06-18Online:2025-10-15Published:2025-09-15 -
Contact:WU Haiqiao, Department of respiratory and critical care medicine, Chongqing Traditional Chinese Medicine Hospital, Chongqing 400038, China. Wuhaiqiao20571380@163.com,Telephone: +86-13896033821 -
Supported by:National Science Foundation for Distinguished Young Scholars of China to Intestinal Microflora-Mediated Regulation of Breast Regression Protein 39/chitinase-3-like Protein 1 Signaling pathway in the Intervention of Chronic Obstructive Pulmonary Disease by Invigorating Spleen Supplementing Lung and Relaxing Collaterals Method(81804074)
Cite this article
WANG Wei, LONG Qi, FU Ling, WU Haiqiao. Jianpi Yifei Tongluo recipe (健脾益肺通络方剂) attenuates inflammation by promoting the expression of interferon regulatory factor 4 in the rat model of chronic obstructive pulmonary disease[J]. Journal of Traditional Chinese Medicine, 2025, 45(5): 1048-1058.
share this article
Figure 1 Effect of JYTR on pulmonary function and Histological examination A: TV; B: MV; C: PEF; D: representative histological images of lung tissue (HE staining, × 100). D1: Control group; D2: Model group; D3: Model + Budesonide group; D4: Model + Synbiotics group; D5: Model + JYTR (low dose); D6: Model + JYTR (medium dose); D7: Model + JYTR (high dose). E: Quantification of lung injury scores; F: MLI; G: MAN. The COPD model was established via daily CS exposure combined with intratracheal LPS administration on days 7 and 21 in the model, Western medicine, and JYTR groups. Apart from LPS administration days, rats were continuously exposed to cigarette smoke for 12 weeks. Control and model group rats received normal saline by gavage at 10 mL/kg once daily. The medium dose of JYTR and the dose of Western medicine were calculated based on the equivalent adult human dose, adjusted for body surface area. The low and high JYTR doses were set at 0.5 × and 2 × the medium dose, respectively. The Budesonide group received once-daily inhalation of nebulized budesonide, and the Synbiotics group received Synbiotics at 1.17 × 101? CFU·kg?1·d?1. JYTR was administered by gavage at 10 mL·kg?1·d?1 according to body weight in each respective dose group. JYTR: Jianpi Yifei Tongluo recipe; TV: tidal volume; MV: minute ventilation; PEF: peak expiratory flow; HE: hematoxylin-eosin; MLI: mean linear intercepts; MAN: mean alveolar number; COPD: chronic obstructive pulmonary disease; CS: cigarette smoke; LPS: lipopolysaccharide; ANOVA: analysis of variance. Statistical analysis was performed using one-way ANOVA followed by the least significant difference post hoc test. Data are presented as mean ± standard deviation (n = 3). aP < 0.05 vs Control group; bP < 0.05 and cP > 0.05 vs Model group.
Figure 1 Effect of JYTR on pulmonary function and Histological examination A: TV; B: MV; C: PEF; D: representative histological images of lung tissue (HE staining, × 100). D1: Control group; D2: Model group; D3: Model + Budesonide group; D4: Model + Synbiotics group; D5: Model + JYTR (low dose); D6: Model + JYTR (medium dose); D7: Model + JYTR (high dose). E: Quantification of lung injury scores; F: MLI; G: MAN. The COPD model was established via daily CS exposure combined with intratracheal LPS administration on days 7 and 21 in the model, Western medicine, and JYTR groups. Apart from LPS administration days, rats were continuously exposed to cigarette smoke for 12 weeks. Control and model group rats received normal saline by gavage at 10 mL/kg once daily. The medium dose of JYTR and the dose of Western medicine were calculated based on the equivalent adult human dose, adjusted for body surface area. The low and high JYTR doses were set at 0.5 × and 2 × the medium dose, respectively. The Budesonide group received once-daily inhalation of nebulized budesonide, and the Synbiotics group received Synbiotics at 1.17 × 101? CFU·kg?1·d?1. JYTR was administered by gavage at 10 mL·kg?1·d?1 according to body weight in each respective dose group. JYTR: Jianpi Yifei Tongluo recipe; TV: tidal volume; MV: minute ventilation; PEF: peak expiratory flow; HE: hematoxylin-eosin; MLI: mean linear intercepts; MAN: mean alveolar number; COPD: chronic obstructive pulmonary disease; CS: cigarette smoke; LPS: lipopolysaccharide; ANOVA: analysis of variance. Statistical analysis was performed using one-way ANOVA followed by the least significant difference post hoc test. Data are presented as mean ± standard deviation (n = 3). aP < 0.05 vs Control group; bP < 0.05 and cP > 0.05 vs Model group.
Figure 2 Effect of JYTR on CS-mediated expression of IRF4, Arg1, CD206, iNOS, CD86, IKB-α, and P65 in vivo and vitro A: Western blot analysis was performed to detect protein expression levels of IRF4, Arg 1, iNOS, CD86, CD206, and Actin B in rat lung tissue. B: Western blot quantification results of each group; B1: gray analysis of the protein levels of IRF4; B2: gray analysis of the protein levels of Arg1; B3: gray analysis of the protein levels of iNOS; B4: gray analysis of the protein levels of CD86; B5: gray analysis of the protein levels of CD206; C: Western blot analysis and gray analysis of the protein levels of p-IκB-α and IκB-α; D: Western blot analysis and gray analysis of the protein levels of p-P65,and P65; E: in vitro effects of JYTR on CS-induced IRF4 protein expression; F: flow cytometric analysis of CD86 and CD206 expression in NR8383 cells. F1, F6: Control group; F2, F7: 15% CSE group; F3, F8: JYTR (10 μM) + 15% CSE group; F4, F9: JYTR (50 μM) + 15% CSE group; F5, F10: JYTR (100 μM) + 15% CSE group. The model was established via daily exposure to CS, combined with intratracheal LPS instillation on days 7 and 21 in the model group, Western medicine group, and each JYTR dose group. Except for LPS administration days, rats were exposed to CS continuously for 12 weeks. Control and model groups received normal saline by gavage at 10 mL·kg?1·d?1. The medium dose of JYTR and the Western medicine dose were adjusted from human adult equivalents based on body surface area. Low and high JYTR doses corresponded to × 0.5 and × 2 the medium dose, respectively. The budesonide grouP received daily nebulized budesonide, while the Synbiotics grouP received Synbiotics at 1.17 × 101? CFU·kg?1·d?1. JYTR was administered orally at 10 mL·kg?1·d?1 according to body weight. NR8383 cells were treated with either 0% (control) or 15% CSE. For the treatment groups, cells were pretreated with JYTR at 10, 50, or 100 μM for 24 h, followed by 15% CSE exposure for an additional 4 h. IRF4: interferon regulatory factor 4; Arg1: arginase 1; iNOS: inducible nitric oxide synthase; CD: cluster of differentiation; IκB-α: nuclear factor of kappa light polypeptide gene enhancer in B-cells inhibitor alpha; CS: cigarette smoke; LPS: lipopolysaccharide; JYTR: Jianpi Yifei Tongluo recipe; CSE: cigarette smoke extract; ANOVA: analysis of variance. Statistical analysis was performed using one-way ANOVA followed by the least significant difference post hoc test. Data are presented as mean ± standard deviation (n = 3). aP < 0.05 and eP > 0.05 vs control group; bP < 0.05, cP < 0.01, and dP > 0.05 vs model group; fP < 0.05 vs 15% CSE group.
Figure 2 Effect of JYTR on CS-mediated expression of IRF4, Arg1, CD206, iNOS, CD86, IKB-α, and P65 in vivo and vitro A: Western blot analysis was performed to detect protein expression levels of IRF4, Arg 1, iNOS, CD86, CD206, and Actin B in rat lung tissue. B: Western blot quantification results of each group; B1: gray analysis of the protein levels of IRF4; B2: gray analysis of the protein levels of Arg1; B3: gray analysis of the protein levels of iNOS; B4: gray analysis of the protein levels of CD86; B5: gray analysis of the protein levels of CD206; C: Western blot analysis and gray analysis of the protein levels of p-IκB-α and IκB-α; D: Western blot analysis and gray analysis of the protein levels of p-P65,and P65; E: in vitro effects of JYTR on CS-induced IRF4 protein expression; F: flow cytometric analysis of CD86 and CD206 expression in NR8383 cells. F1, F6: Control group; F2, F7: 15% CSE group; F3, F8: JYTR (10 μM) + 15% CSE group; F4, F9: JYTR (50 μM) + 15% CSE group; F5, F10: JYTR (100 μM) + 15% CSE group. The model was established via daily exposure to CS, combined with intratracheal LPS instillation on days 7 and 21 in the model group, Western medicine group, and each JYTR dose group. Except for LPS administration days, rats were exposed to CS continuously for 12 weeks. Control and model groups received normal saline by gavage at 10 mL·kg?1·d?1. The medium dose of JYTR and the Western medicine dose were adjusted from human adult equivalents based on body surface area. Low and high JYTR doses corresponded to × 0.5 and × 2 the medium dose, respectively. The budesonide grouP received daily nebulized budesonide, while the Synbiotics grouP received Synbiotics at 1.17 × 101? CFU·kg?1·d?1. JYTR was administered orally at 10 mL·kg?1·d?1 according to body weight. NR8383 cells were treated with either 0% (control) or 15% CSE. For the treatment groups, cells were pretreated with JYTR at 10, 50, or 100 μM for 24 h, followed by 15% CSE exposure for an additional 4 h. IRF4: interferon regulatory factor 4; Arg1: arginase 1; iNOS: inducible nitric oxide synthase; CD: cluster of differentiation; IκB-α: nuclear factor of kappa light polypeptide gene enhancer in B-cells inhibitor alpha; CS: cigarette smoke; LPS: lipopolysaccharide; JYTR: Jianpi Yifei Tongluo recipe; CSE: cigarette smoke extract; ANOVA: analysis of variance. Statistical analysis was performed using one-way ANOVA followed by the least significant difference post hoc test. Data are presented as mean ± standard deviation (n = 3). aP < 0.05 and eP > 0.05 vs control group; bP < 0.05, cP < 0.01, and dP > 0.05 vs model group; fP < 0.05 vs 15% CSE group.
Figure 3 Effect of interference with IRF4 on the efficacy of traditional Chinese medicine on COPD in rats A: TV; B: PEF; C: MV; D: representative histopathological images of lung tissue (HE staining, × 100); D1: control group; D2: model group; D3: JYTR medium-dose group ("Middle group"); D4: Middle + sh-NC group; D5: Middle + sh-IRF4 group; E: quantification of lung injury scores; F: MLI; G: MAN. COPD model Group: Induced by daily CS exposure combined with intratracheal LPS administration on days 7 and 21. Rats were exposed to CS for 12 consecutive weeks, excluding LPS injection days; JYTR medium-dose group (“Middle group”): Model rats were treated with a medium dose of JYTR; Middle + sh-NC group: Six hours after LPS injection, rats were injected with an adenovirus carrying a non-targeting shRNA control (sh-NC; 60 μL, 6 × 1013 GC/mL) via the tail vein, followed by JYTR medium-dose treatment; Middle + sh-IRF4 group: Six hours after LPS injection, rats received a tail vein injection of an adenovirus expressing shRNA targeting IRF4 (sh-IRF4; 60 μL, 6 × 1013 GC/mL), followed by JYTR medium-dose treatment. IRF4: interferon regulatory factor 4; TV: tidal volume; PEF: peak expiratory flow; MV: minute ventilation; HE: hematoxylin-eosin; COPD: chronic obstructive pulmonary disease; CS: cigarette smoke; LPS: lipopolysaccharide; JYTR: Jianpi Yifei Tongluo recipe; MLI: mean linear intercepts; MAN: mean alveolar number; ANOVA: analysis of variance. Data are presented as mean ± standard deviation (n = 3). Statistical analysis was performed using one-way ANOVA followed by the least significant difference post hoc test. aP < 0.05 vs control group; bP < 0.05 and cP > 0.05 vs model group.
Figure 3 Effect of interference with IRF4 on the efficacy of traditional Chinese medicine on COPD in rats A: TV; B: PEF; C: MV; D: representative histopathological images of lung tissue (HE staining, × 100); D1: control group; D2: model group; D3: JYTR medium-dose group ("Middle group"); D4: Middle + sh-NC group; D5: Middle + sh-IRF4 group; E: quantification of lung injury scores; F: MLI; G: MAN. COPD model Group: Induced by daily CS exposure combined with intratracheal LPS administration on days 7 and 21. Rats were exposed to CS for 12 consecutive weeks, excluding LPS injection days; JYTR medium-dose group (“Middle group”): Model rats were treated with a medium dose of JYTR; Middle + sh-NC group: Six hours after LPS injection, rats were injected with an adenovirus carrying a non-targeting shRNA control (sh-NC; 60 μL, 6 × 1013 GC/mL) via the tail vein, followed by JYTR medium-dose treatment; Middle + sh-IRF4 group: Six hours after LPS injection, rats received a tail vein injection of an adenovirus expressing shRNA targeting IRF4 (sh-IRF4; 60 μL, 6 × 1013 GC/mL), followed by JYTR medium-dose treatment. IRF4: interferon regulatory factor 4; TV: tidal volume; PEF: peak expiratory flow; MV: minute ventilation; HE: hematoxylin-eosin; COPD: chronic obstructive pulmonary disease; CS: cigarette smoke; LPS: lipopolysaccharide; JYTR: Jianpi Yifei Tongluo recipe; MLI: mean linear intercepts; MAN: mean alveolar number; ANOVA: analysis of variance. Data are presented as mean ± standard deviation (n = 3). Statistical analysis was performed using one-way ANOVA followed by the least significant difference post hoc test. aP < 0.05 vs control group; bP < 0.05 and cP > 0.05 vs model group.
Figure 4 Effect of interference with IRF4 on Cytokines and Protein Expression of traditional Chinese medicine on COPD in rats A: cytokine levels of TGF-β in serum and lung tissues; B: cytokine levels of TNF-α in serum; C: cytokine levels of IL-6 in serum; D: cytokine levels of IL-10 in serum; E: cytokine levels of TGF-β in serum; F: cytokine levels of TNF-α in lung tissues; G: cytokine levels of IL-6 in lung tissues; H: cytokine levels of IL-10 in lung tissues; I: Western blot analysis was performed to detect protein expression levels of IRF4, Arg1, iNOS, p-IKB-α, p-P65 (J5) and ActinB in the rat lung tissues; J1: gray analysis of the protein levels of IRF4; J2: gray analysis of the protein levels of Arg1; J3: gray analysis of the protein levels of iNOS; J4: gray analysis of the protein levels of p-IKB-α; J5: gray analysis of the protein levels of p-P65. COPD model was induced by daily CS exposure combined with intratracheal LPS administration on days 7 and 21. Rats were exposed to CS for 12 consecutive weeks, excluding LPS injection days. JYTR medium-dose group ("Middle group"): Model rats were treated with a medium dose of JYTR. Middle + sh-NC group: Six hours after LPS injection, rats were injected with an adenovirus carrying a non-targeting shRNA control (sh-NC; 60 μL, 6 × 1013 GC/mL) via the tail vein, followed by JYTR medium-dose treatment. Middle + sh-IRF4 group: Six hours after LPS injection, rats received a tail vein injection of an adenovirus expressing shRNA targeting IRF4 (sh-IRF4; 60 μL, 6 × 1013 GC/mL), followed by JYTR medium-dose treatment. IRF4: interferon regulatory factor 4; TGF-β: transforming growth factor-β; TNF-α: tumor necrosis factor-α; IL: interleukin; Arg1: arginase 1; iNOS: inducible nitric oxide synthase; CD: cluster of differentiation; IκB-α: nuclear factor of kappa light polypeptide gene enhancer in B-cells inhibitor alpha; COPD: chronic obstructive pulmonary disease; CS: cigarette smoke; LPS: lipopolysaccharide; JYTR: Jianpi Yifei Tongluo recipe; ANOVA: analysis of variance. Statistical analysis was performed using one-way ANOVA followed by the least significant difference post hoc test. Data are presented as mean ± standard deviation (n = 3). aP < 0.05 and bP < 0.01 vs control group; cP < 0.05 and dP > 0.05 vs model group.
Figure 4 Effect of interference with IRF4 on Cytokines and Protein Expression of traditional Chinese medicine on COPD in rats A: cytokine levels of TGF-β in serum and lung tissues; B: cytokine levels of TNF-α in serum; C: cytokine levels of IL-6 in serum; D: cytokine levels of IL-10 in serum; E: cytokine levels of TGF-β in serum; F: cytokine levels of TNF-α in lung tissues; G: cytokine levels of IL-6 in lung tissues; H: cytokine levels of IL-10 in lung tissues; I: Western blot analysis was performed to detect protein expression levels of IRF4, Arg1, iNOS, p-IKB-α, p-P65 (J5) and ActinB in the rat lung tissues; J1: gray analysis of the protein levels of IRF4; J2: gray analysis of the protein levels of Arg1; J3: gray analysis of the protein levels of iNOS; J4: gray analysis of the protein levels of p-IKB-α; J5: gray analysis of the protein levels of p-P65. COPD model was induced by daily CS exposure combined with intratracheal LPS administration on days 7 and 21. Rats were exposed to CS for 12 consecutive weeks, excluding LPS injection days. JYTR medium-dose group ("Middle group"): Model rats were treated with a medium dose of JYTR. Middle + sh-NC group: Six hours after LPS injection, rats were injected with an adenovirus carrying a non-targeting shRNA control (sh-NC; 60 μL, 6 × 1013 GC/mL) via the tail vein, followed by JYTR medium-dose treatment. Middle + sh-IRF4 group: Six hours after LPS injection, rats received a tail vein injection of an adenovirus expressing shRNA targeting IRF4 (sh-IRF4; 60 μL, 6 × 1013 GC/mL), followed by JYTR medium-dose treatment. IRF4: interferon regulatory factor 4; TGF-β: transforming growth factor-β; TNF-α: tumor necrosis factor-α; IL: interleukin; Arg1: arginase 1; iNOS: inducible nitric oxide synthase; CD: cluster of differentiation; IκB-α: nuclear factor of kappa light polypeptide gene enhancer in B-cells inhibitor alpha; COPD: chronic obstructive pulmonary disease; CS: cigarette smoke; LPS: lipopolysaccharide; JYTR: Jianpi Yifei Tongluo recipe; ANOVA: analysis of variance. Statistical analysis was performed using one-way ANOVA followed by the least significant difference post hoc test. Data are presented as mean ± standard deviation (n = 3). aP < 0.05 and bP < 0.01 vs control group; cP < 0.05 and dP > 0.05 vs model group.
| 1. |
Adeloye D, Song P, Zhu Y, Campbell H, Sheikh A, Rudan I. Global, regional, and national prevalence of, and risk factors for, chronic obstructive pulmonary disease (COPD) in 2019: a systematic review and modelling analysis. Lancet Respir Med 2022; 10: 447-58.
DOI PMID |
| 2. |
Prevalence and attributable health burden of chronic respiratory diseases, 1990-2017: a systematic analysis for the global burden of disease study 2017. Lancet Respir Med 2020; 8: 585-96.
DOI PMID |
| 3. |
Varmaghani M, Dehghani M, Heidari E, Sharifi F, Moghaddam SS, Farzadfar F. Global prevalence of chronic obstructive pulmonary disease: systematic review and Meta-analysis. East Mediterr Health J 2019; 25: 47-57.
DOI PMID |
| 4. |
Corhay JL, Bonhomme O, Heinen V, Moermans C, Louis R. Chronic obstructive pulmonary disease. A chronic inflammatory disease. Rev Med Liege 2022; 77: 295-301.
PMID |
| 5. |
Rhee CK. Chronic obstructive pulmonary disease research by using big data. Clin Respir J 2021; 15: 257-63.
DOI PMID |
| 6. |
Ritchie AI, Wedzicha JA. Definition, causes, pathogenesis, and consequences of chronic obstructive pulmonary disease exacerbations. Clin Chest Med 2020; 41: 421-38.
DOI PMID |
| 7. |
Zhang H, Li J, Yu X, et al. Effects of chinese medicine on patients with acute exacerbations of copd: study protocol for a randomized controlled trial. Trials 2019; 20: 735.
DOI PMID |
| 8. | Burge AT, Cox NS, Abramson MJ, Holland AE. Interventions for promoting physical activity in people with chronic obstructive pulmonary disease (COPD). Cochrane Database Syst Rev 2020; 4: Cd012626. |
| 9. | Chan KH, Tsoi YYS, Mccall M. The effectiveness of Traditional Chinese Medicine (TCM) as an adjunct treatment on stable COPD patients: a systematic review and Meta-analysis. Evid Based Complement Alternat Med 2021; 2021: 5550332. |
| 10. | Yu XQ, Wang MH, Li JS, et al. Effect of comprehensive therapy based on Chinese medicine patterns on self-efficacy and effectiveness satisfaction in chronic obstructive pulmonary disease patients. Chin J Integr Med 2019; 25: 736-42. |
| 11. | Wang H, Hou Y, Ma X, et al. Multi-omics analysis reveals the mechanisms of action and therapeutic regimens of Traditional Chinese Medicine, Bufei Jianpi granules: implication for copd drug discovery. Phytomedicine 2022; 98: 153963. |
| 12. | Wang S, Xiong LL, Ren W, Zhu CD, Li CY, Zhou Q. Effect of yifei jianpi recipe on airway inflammation and airway mucus hypersecretion of chronic obstructive pulmonary disease model rats. Zhong Guo Zhong Xi Yi Jie He Za Zhi 2015; 35: 993-99. |
| 13. |
Jefferies CA. Regulating IRFs in ifn driven disease. Front Immunol 2019; 10: 325.
DOI PMID |
| 14. | Chen M, Wen X, Gao Y, et al. IRF-4 deficiency reduces inflammation and kidney fibrosis after folic acid-induced acute kidney injury. Int Immunopharmacol 2021; 100: 108142. |
| 15. | Zhang X, Artola-Boran M, Fallegger A, et al. IRF 4 expression is required for the immunoregulatory activity of conventional type 2 dendritic cells in settings of chronic bacterial infection and cancer. J Immunol 2020; 205: 1933-43. |
| 16. | Ngwa C, Mamun AA, Xu Y, Sharmeen R, Liu F. Phosphorylation of microglial IRF5 and IRF4 by IRAK4 regulates inflammatory responses to ischemia. Cells 2021: 10. |
| 17. | Bae S, Park PSU, Lee Y, et al. Myc-mediated early glycolysis negatively regulates proinflammatory responses by controlling IRF 4 in inflammatory macrophages. Cell Rep 2021; 35: 109264. |
| 18. | Song Y, Cui D, Mao P. A study on pathological changes and the potential role of growth factors in the airway wall remodeling of copd rat models. Zhong Hua Jie He He Hu Xi Za Zhi 2001; 24: 283-7. |
| 19. | Hu YX, Cui H, Fan L, et al. Resveratrol attenuates left ventricular remodeling in old rats with copd induced by cigarette smoke exposure and lps instillation. Can J Physiol Pharmacol 2013; 91: 1044-54. |
| 20. | Vernooy JH, Dentener MA, Van Suylen RJ, Buurman WA, Wouters EF. Long-term intratracheal lipopolysaccharide exposure in mice results in chronic lung inflammation and persistent pathology. Am J Respir Cell Mol Biol 2002; 26: 152-9. |
| 21. | Mao J, Li Y, Li S, et al. Bufei jianpi granules reduce quadriceps muscular cell apoptosis by improving mitochondrial function in rats with chronic obstructive pulmonary disease. Evid Based Complement Alternat Med 2019; 2019: 1216305. |
| 22. |
Hao D, Li Y, Shi J, Jiang J. Baicalin alleviates chronic obstructive pulmonary disease through regulation of hsp72-mediated JNK pathway. Mol Med 2021; 27: 53.
DOI PMID |
| 23. | Ma J, Tian Y, Li J, et al. Effect of bufei yishen granules combined with electroacupuncture in rats with chronic obstructive pulmonary disease via the regulation of TLR-4/NF-κB signaling. Evid Based Complement Alternat Med 2019; 2019: 6708645. |
| 24. | Fan Y, Wen X, Zhang Q, et al. Effect of Traditional Chinese Medicine Bufei granule on stable chronic obstructive pulmonary disease: a systematic review and Meta-analysis based on existing evidence. Evid Based Complement Alternat Med 2020; 2020: 3439457. |
| 25. | Tang CY, Tang SL, Huang KF, Xu J, Yu H, Lin L. Jian-pi-yi-fei granule suppresses airway inflammation in mice induced by cigarette smoke condensate and lipopolysaccharide. Indian J Pharmacol 2019; 51: 263-8. |
| 26. |
Xi C, Li F, Cheng W, et al. Application of Traditional Chinese and Western Medicine combined with chronic disease management in pulmonary rehabilitation and evaluation of efficacy. Am J Transl Res 2021; 13: 6372-81.
PMID |
| 27. | Duffy SP, Criner GJ. Chronic obstructive pulmonary disease: evaluation and management. Med Clin North Am 2019; 103: 453-61. |
| 28. |
Barnes PJ. Inflammatory mechanisms in patients with chronic obstructive pulmonary disease. J Allergy Clin Immunol 2016; 138: 16-27.
DOI PMID |
| 29. | Rodrigues SO, Cunha C, Soares GMV, Silva PL, Silva AR, Gonçalves-De-Albuquerque CF. Mechanisms, pathophysiology and currently proposed treatments of chronic obstructive pulmonary disease. Pharmaceuticals (Basel) 2021; 14: 979-1002. |
| 30. |
Brassington K, Selemidis S, Bozinovski S, Vlahos R. Chronic obstructive pulmonary disease and atherosclerosis: common mechanisms and novel therapeutics. Clin Sci (Lond) 2022; 136: 405-23.
DOI PMID |
| 31. | Jin F, Zhang L, Chen K, et al. Effective-component compatibility of Bufei Yishen formula Ⅲ combined with electroacupuncture suppresses inflammatory response in rats with chronic obstructive pulmonary disease via regulating SIRT1/NF-κB signaling. Biomed Res Int 2022; 2022: 3360771. |
| 32. |
Silva BSA, Lira FS, Ramos D, et al. Severity of COPD and its relationship with IL-10. Cytokine 2018; 106: 95-100.
DOI PMID |
| 33. |
Takiguchi H, Yang CX, Yang CWT, et al. Macrophages with reduced expressions of classical M1 and M2 surface markers in human bronchoalveolar lavage fluid exhibit pro-inflammatory gene signatures. Sci Rep 2021; 11: 8282.
DOI PMID |
| 34. | Bazzan E, Turato G, Tinè M, et al. Dual polarization of human alveolar macrophages progressively increases with smoking and COPD severity. Respir Res 2017; 18: 40. |
| 35. |
Arora S, Dev K, Agarwal B, Das P, Syed MA. Macrophages: their role, activation and polarization in pulmonary diseases. Immunobiology 2018; 223: 383-96.
DOI PMID |
| 36. | Yamasaki K, Eeden SFV. Lung macrophage phenotypes and functional responses: Role in the pathogenesis of COPD. Int J Mol Sci 2018; 19: 1449-65. |
| 37. | Zhou F, Mei J, Han X, et al. Kinsenoside attenuates osteoarthritis by repolarizing macrophages through inactivating NF-κB/MAPK signaling and protecting chondrocytes. Acta Pharm Sin B 2019; 9: 973-85. |
| 38. | Liu L, Guo H, Song A, et al. Progranulin inhibits lps-induced macrophage M1 polarization via NF-кB and MAPK pathways. BMC Immunol 2020; 21: 32. |
| 39. | Fan L, Chen R, Li L, et al. Protective effect of Jianpiyifei Ⅱ granule against chronic obstructive pulmonary disease via NF-κB signaling pathway. Evid Based Complement Alternat Med 2018; 2018: 4265790. |
| 40. | Ferrante CJ, Leibovich SJ. Regulation of macrophage polarization and wound healing. Adv Wound Care (New Rochelle) 2012; 1: 10-6. |
| 41. |
Chistiakov DA, Myasoedova VA, Revin VV, Orekhov AN, Bobryshev YV. The impact of interferon-regulatory factors to macrophage differentiation and polarization into M1 and M2. Immunobiology 2018; 223: 101-11.
DOI PMID |
| 42. |
Zhu Y, Yang G. Molecular identification and functional characterization of IRF4 from common carp (cyprinus carpio. L) in immune response: a negative regulator in the IFN and NF-κB signalling pathways. BMC Vet Res 2022; 18: 106.
DOI PMID |
| Viewed | ||||||
|
Full text |
|
|||||
|
Abstract |
|
|||||
