Journal of Traditional Chinese Medicine ›› 2025, Vol. 45 ›› Issue (2): 281-290.DOI: 10.19852/j.cnki.jtcm.2025.02.022
• Original articles • Previous Articles Next Articles
Jinxin oral liquid (金欣口服液) reduced lung inflammation in influenza A virus infected mice through inhibiting NOD-like receptor protein 3 pathway
LI Tao1,2, WANG Xianzheng3, XIONG Yingcai2, DAI Qigang1, WANG Shouchuan1(
), JI Jianjian2()
- 1 Department of Pediatrics, Affiliated Hospital of Nanjing University of Chinese Medicine, Nanjing 210029, China
2 Jiangsu Key Laboratory of Children’s Health and Chinese Medicine, Nanjing University of Chinese Medicine, Nanjing 210023, China
3 Basic Medical College of Hebei University of Traditional Chinese Medicine, Shijiazhuang 050200, China
-
Received:2023-12-06Accepted:2024-05-15Online:2025-04-15Published:2025-03-10 -
Contact:Prof. JI Jianjian, Jiangsu Key Laboratory of Children’s Health and Chinese Medicine, Nanjing University of Chinese Medicine, Nanjing 210023, China. jijj@njucm.edu.cn; Prof. WANG Shouchuan, Department of Pediatrics, Affiliated Hospital of Nanjing University of Chinese Medicine, Nanjing 210029, China. wscnj@njucm.edu.cn, Telephone: +86-18260087292 -
Supported by:Young Elite Scientists Sponsorship Program by Chinese Association for Clinical Medicine(2021-QNRC2-B14);Colleges and universities in Jiangsu Province Natural Science Research: Investigating the Mechanism of Jinping Decoction Inhibiting the Differentiation of Myeloid-derived Suppressor Cells and Regulating Lipid Metabolism(22KJA360004);Jiangsu Graduate Practice Innovation Program: A Study on the Mechanism of Xiaofeng Xuanqiao Decoction in Treating Pediatric Rhinitis based on Interleukin-33/Suppression of Tumorigenicity 2(SJCX23_0803);Wuxi Health Commission Scientific Research Project: Observation on the Efficacy of Xiaofeng Xuanqiao Decoction in Treating Pediatric Rhinitis (Wind-Phlegm Obstructing Orifices Syndrome) and Its Influence on Serum IgE and Related Inflammatory Cytokine Levels(M202035);High-level Construction of Key Traditional Chinese Medicine (TCM) Disciplines, China: Research on Tic Disorders from the Perspective of the Five Viscera Syndrome Treatment(NZYEK004);High-level Construction of Key TCM Disciplines, China: Research on the Mechanism of Xiaofeng Xuanqiao Decoction in Treating Allergic Rhinitis based on the Interleukin-33/ST2 Axis(NZYEK006)
Cite this article
LI Tao, WANG Xianzheng, XIONG Yingcai, DAI Qigang, WANG Shouchuan, JI Jianjian. Jinxin oral liquid (金欣口服液) reduced lung inflammation in influenza A virus infected mice through inhibiting NOD-like receptor protein 3 pathway[J]. Journal of Traditional Chinese Medicine, 2025, 45(2): 281-290.
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Figure 1 JX showed protective effects response to H1N1 infection A: representative HE-stained lung tissue (middle lobe of right lung) from mice showed histologic differences group by HE staining (× 200) (n = 4); A1: normal control group; A2: H1N1 infected group; A3: ribavirin treatment group; A4: Jxin oral liquid high-dose group; A5: Jinxin oral liquid middle-dose group; A6: Jinxin oral liquid low-dose group. B: the body temperature was measured using thermometer (n = 5); C: the viral load in the lungs of mice was measured by viral N gene expression (n = 5); D: the weight of the lungs of mice was measured (n = 5); E: the albumin level in BALF was determined (n = 3). Normal control group: treated with normal diet and physiological saline; H1N1 infected group: H1N1, 106 PFU, 2 d; ribavirin treatment group: 46 mg·kg-1·d-1, 2 d; Jxin oral liquid high-dose group: 55.2 g·kg-1·d-1, 2 d, JX-H; Jinxin oral liquid middle-dose group: 27.6 g·kg-1·d-1, 2 d, JX-M; Jinxin oral liquid low-dose group: 13.8 g·kg-1·d-1, 2 d, JX-L. NLRP3: NOD-like receptor protein 3; HE: hematoxylin and eosin; BALF: bronchoalveolar lavage fluid; PFU: plaque formation unit; Control: normal control group; H1N1: influenza a virus; JX-H: Jinxin oral liquid high-dose group; JX-M: Jinxin oral liquid middle-dose group; JX-L: Jinxin oral liquid low-dose group; ANOVA: analysis of variance. All results are expressed as the mean ± standard deviation by one-way ANOVA with Dunnett’s post hoc tests for multiple comparisons. aP < 0.01, cP < 0.05, H1N1 group vs control group; bP < 0.01, dP < 0.05, vs H1N1 group.
Figure 1 JX showed protective effects response to H1N1 infection A: representative HE-stained lung tissue (middle lobe of right lung) from mice showed histologic differences group by HE staining (× 200) (n = 4); A1: normal control group; A2: H1N1 infected group; A3: ribavirin treatment group; A4: Jxin oral liquid high-dose group; A5: Jinxin oral liquid middle-dose group; A6: Jinxin oral liquid low-dose group. B: the body temperature was measured using thermometer (n = 5); C: the viral load in the lungs of mice was measured by viral N gene expression (n = 5); D: the weight of the lungs of mice was measured (n = 5); E: the albumin level in BALF was determined (n = 3). Normal control group: treated with normal diet and physiological saline; H1N1 infected group: H1N1, 106 PFU, 2 d; ribavirin treatment group: 46 mg·kg-1·d-1, 2 d; Jxin oral liquid high-dose group: 55.2 g·kg-1·d-1, 2 d, JX-H; Jinxin oral liquid middle-dose group: 27.6 g·kg-1·d-1, 2 d, JX-M; Jinxin oral liquid low-dose group: 13.8 g·kg-1·d-1, 2 d, JX-L. NLRP3: NOD-like receptor protein 3; HE: hematoxylin and eosin; BALF: bronchoalveolar lavage fluid; PFU: plaque formation unit; Control: normal control group; H1N1: influenza a virus; JX-H: Jinxin oral liquid high-dose group; JX-M: Jinxin oral liquid middle-dose group; JX-L: Jinxin oral liquid low-dose group; ANOVA: analysis of variance. All results are expressed as the mean ± standard deviation by one-way ANOVA with Dunnett’s post hoc tests for multiple comparisons. aP < 0.01, cP < 0.05, H1N1 group vs control group; bP < 0.01, dP < 0.05, vs H1N1 group.
Table 1 The chemical components identified in the JX
| No. | Compound name | Formula | Adduct | RT in STD | RTin JX | m/z | ppm |
|---|---|---|---|---|---|---|---|
| 1 | Ephedrine | C10H15NO | [M+H]+ | 2.96 | 3.01 | 166.12268 | 0.237 |
| 2 | Amygdalin | C20H27NO11 | [M+Na]+ | 4.39 | 4.41 | 480.14954 | 3.974 |
| 3 | Sinapine | C16H24NO5 | [M]+ | 4.60 | 4.60 | 310.16547 | 1.840 |
| 4 | Polydatin | C20H22O8 | [M+H]+ | 6.47 | 6.50 | 391.13983 | 2.776 |
| 5 | Baicalin | C21H18O11 | [M+H]+ | 8.26 | 8.26 | 447.09415 | 4.389 |
| 6 | Resveratrol | C14H12O3 | [M+H]+ | 8.83 | 8.82 | 229.08626 | 1.481 |
| 7 | Quercetin | C15H10O7 | [M+H]+ | 9.60 | 9.63 | 303.05054 | 2.016 |
| 8 | Emodin | C15H10O5 | [M+H]+ | 11.37 | 11.38 | 271.06082 | 2.656 |
| 9 | Praeruptorin | C24H28O7 | [M+H]+ | 20.63 | 20.60 | 429.19806 | 16.963 |
Table 1 The chemical components identified in the JX
| No. | Compound name | Formula | Adduct | RT in STD | RTin JX | m/z | ppm |
|---|---|---|---|---|---|---|---|
| 1 | Ephedrine | C10H15NO | [M+H]+ | 2.96 | 3.01 | 166.12268 | 0.237 |
| 2 | Amygdalin | C20H27NO11 | [M+Na]+ | 4.39 | 4.41 | 480.14954 | 3.974 |
| 3 | Sinapine | C16H24NO5 | [M]+ | 4.60 | 4.60 | 310.16547 | 1.840 |
| 4 | Polydatin | C20H22O8 | [M+H]+ | 6.47 | 6.50 | 391.13983 | 2.776 |
| 5 | Baicalin | C21H18O11 | [M+H]+ | 8.26 | 8.26 | 447.09415 | 4.389 |
| 6 | Resveratrol | C14H12O3 | [M+H]+ | 8.83 | 8.82 | 229.08626 | 1.481 |
| 7 | Quercetin | C15H10O7 | [M+H]+ | 9.60 | 9.63 | 303.05054 | 2.016 |
| 8 | Emodin | C15H10O5 | [M+H]+ | 11.37 | 11.38 | 271.06082 | 2.656 |
| 9 | Praeruptorin | C24H28O7 | [M+H]+ | 20.63 | 20.60 | 429.19806 | 16.963 |
Figure 2 JX reduces the expression of inflammatory cytokines and inhibits NLRP3 inflammasome activation in the lungs of H1N1-infected mice A: quantification of TNF-α in lungs from all groups of mice by qPCR (n = 6); B: quantification of IL-1β in lungs from all groups of mice by qPCR (n = 6); C: quantification of TNF-ɑ in BALF from all groups of mice by ELSIA (n = 4); D: quantification of IL-1β in BALF and serum from all groups of mice by ELISA (n = 4). Normal control group: treated with normal diet and physiological saline; H1N1 infected group: H1N1, 106 PFU, 2 d; ribavirin treatment group: 46 mg·kg-1·d-1, 2 d; Jxin oral liquid high-dose group: 55.2 g·kg-1·d-1, 2 d, JX-H; Jinxin oral liquid middle-dose group: 27.6 g·kg-1·d-1, 2 d, JX-M; Jinxin oral liquid low-dose group: 13.8 g·kg-1·d-1, 2 d, JX-L. NLRP3: nod-like receptor protein 3;TNF-α; tumor necrosis factor-α; IL-1β: interleukin-1β; qPCR: quantitative polymerase chain reaction; BALF; bronchoalveolar lavage fluid; PFU: plaque formation unit; ELISA: enzyme-linked immunosorbent assay; ANOVA: analysis of variance; Control: normal control group; H1N1: influenza a virus; JX-H: Jinxin oral liquid high-dose group; JX-M: Jinxin oral liquid middle-dose group; JX-L: Jinxin oral liquid low-dose group. All results are expressed as the mean ± standard deviation by one-way ANOVA with Dunnett’s post hoc tests for multiple comparisons. aP < 0.0001, eP < 0.001, H1N1 group vs control group; bP < 0.01, fP < 0.05, vs H1N1 group; cP < 0.001 dP < 0.0001, vs model group.
Figure 2 JX reduces the expression of inflammatory cytokines and inhibits NLRP3 inflammasome activation in the lungs of H1N1-infected mice A: quantification of TNF-α in lungs from all groups of mice by qPCR (n = 6); B: quantification of IL-1β in lungs from all groups of mice by qPCR (n = 6); C: quantification of TNF-ɑ in BALF from all groups of mice by ELSIA (n = 4); D: quantification of IL-1β in BALF and serum from all groups of mice by ELISA (n = 4). Normal control group: treated with normal diet and physiological saline; H1N1 infected group: H1N1, 106 PFU, 2 d; ribavirin treatment group: 46 mg·kg-1·d-1, 2 d; Jxin oral liquid high-dose group: 55.2 g·kg-1·d-1, 2 d, JX-H; Jinxin oral liquid middle-dose group: 27.6 g·kg-1·d-1, 2 d, JX-M; Jinxin oral liquid low-dose group: 13.8 g·kg-1·d-1, 2 d, JX-L. NLRP3: nod-like receptor protein 3;TNF-α; tumor necrosis factor-α; IL-1β: interleukin-1β; qPCR: quantitative polymerase chain reaction; BALF; bronchoalveolar lavage fluid; PFU: plaque formation unit; ELISA: enzyme-linked immunosorbent assay; ANOVA: analysis of variance; Control: normal control group; H1N1: influenza a virus; JX-H: Jinxin oral liquid high-dose group; JX-M: Jinxin oral liquid middle-dose group; JX-L: Jinxin oral liquid low-dose group. All results are expressed as the mean ± standard deviation by one-way ANOVA with Dunnett’s post hoc tests for multiple comparisons. aP < 0.0001, eP < 0.001, H1N1 group vs control group; bP < 0.01, fP < 0.05, vs H1N1 group; cP < 0.001 dP < 0.0001, vs model group.
Figure 3 NLRP3 pathway is necessary for the protective effects of JX against H1N1-induced A: representative HE-stained lung tissue (middle lobe of right lung) from mice showed histologic differences (n = 4). A1: Control group; A2: H1N1 infected group; A3: H1N1 infected and treated with Jinxin oral liquid high-dose group; A4: H1N1 infected and MCC950 Inhibitor group; A5: H1N1 infected group treated with Jinxin oral liquid middle-dose group and MCC950 inhibitor. HE staining, ×200; B: the protein levels of TNF-ɑ in BALF from all groups of mice was determined by ELISA at 24 h after H1N1 infection (n = 4). C: the expression of IL-1β in lungs from all groups of mice was determined by qPCR at 24 h after H1N1 infection (n = 4). D: the protein levels of IL1β in BALF from all groups of mice was determined by ELISA at 24 h after H1N1 infection (n = 4). Normal control group: treated with normal diet and physiological saline; H1N1 infected group: H1N1, 106 PFU, 2 d; Jxin oral liquid high-dose group: 55.2 g·kg-1·d-1, 2 d, JX-H; MCC950: H1N1 infected and mcc950 Inhibitor group; JX +MCC950: H1N1 infected group treated with Jinxin oral liquid middle-dose group and mcc950 inhibitor. HE: hematoxylin and eosin; TNF-α; tumor necrosis factor-α; IL-1β: interleukin-1β; BALF: bronchoalveolar lavage fluid; PFU: plaque formation unit; ELISA: enzyme-linked immunosorbent assay; qPCR: quantitative polymerase chain reaction; ANOVA: analysis of variance. All results are expressed as the mean ± standard deviation by one-way ANOVA with Dunnett’s post hoc tests for multiple comparisons, aP < 0.001, cP < 0.05, H1N1 group vs control group; bP < 0.01, dP < 0.05, vs H1N1 group.
Figure 3 NLRP3 pathway is necessary for the protective effects of JX against H1N1-induced A: representative HE-stained lung tissue (middle lobe of right lung) from mice showed histologic differences (n = 4). A1: Control group; A2: H1N1 infected group; A3: H1N1 infected and treated with Jinxin oral liquid high-dose group; A4: H1N1 infected and MCC950 Inhibitor group; A5: H1N1 infected group treated with Jinxin oral liquid middle-dose group and MCC950 inhibitor. HE staining, ×200; B: the protein levels of TNF-ɑ in BALF from all groups of mice was determined by ELISA at 24 h after H1N1 infection (n = 4). C: the expression of IL-1β in lungs from all groups of mice was determined by qPCR at 24 h after H1N1 infection (n = 4). D: the protein levels of IL1β in BALF from all groups of mice was determined by ELISA at 24 h after H1N1 infection (n = 4). Normal control group: treated with normal diet and physiological saline; H1N1 infected group: H1N1, 106 PFU, 2 d; Jxin oral liquid high-dose group: 55.2 g·kg-1·d-1, 2 d, JX-H; MCC950: H1N1 infected and mcc950 Inhibitor group; JX +MCC950: H1N1 infected group treated with Jinxin oral liquid middle-dose group and mcc950 inhibitor. HE: hematoxylin and eosin; TNF-α; tumor necrosis factor-α; IL-1β: interleukin-1β; BALF: bronchoalveolar lavage fluid; PFU: plaque formation unit; ELISA: enzyme-linked immunosorbent assay; qPCR: quantitative polymerase chain reaction; ANOVA: analysis of variance. All results are expressed as the mean ± standard deviation by one-way ANOVA with Dunnett’s post hoc tests for multiple comparisons, aP < 0.001, cP < 0.05, H1N1 group vs control group; bP < 0.01, dP < 0.05, vs H1N1 group.
Figure 4 JX inhibits the NLRP3 inflammasome activation in the AMs A: the expression of IL-1β in isolated AMs from all groups of mice was determined by qPCR at 24 h after H1N1 infection (n = 3); B: the expression of NLRP3 in isolated AMs from all groups of mice was determined by qPCR at 24 h after H1N1 infection (n = 3); C: the expression of NLRP3 in CD11c+ Siglec-F+ AMs from all groups of mice was determined by FACS at 24 h after H1N1 infection (n = 4); D: flow cytometry histograms for NLRP3+ (D1-D3) AMS in all groups. D1: Control Group; D2: H1N1 Group; D3: JX Group. E: the expression of caspase1 p20 in CD11c+ Siglec-F+ AMs from all groups of mice was determined by FACS at 24 h after H1N1 infection (n = 4). F: flow cytometry histograms for P20+ (F1-F3) AMS in all groups, F1: Control Group; F2: H1N1 Group; F3: JX Group. Normal control group: treated with normal diet and physiological saline; H1N1 infected group: H1N1, 106 PFU, 2 d; ribavirin treatment group: 46 mg·kg-1·d-1, 2 d; Jxin oral liquid high-dose group: 55.2 g·kg-1·d-1, 2 d, JX-H; Jinxin oral liquid middle-dose group: 27.6 g·kg-1·d-1, 2 d, JX-M; Jinxin oral liquid low-dose group: 13.8 g·kg-1·d-1, 2 d, JX-L. NLRP3: nod-like receptor protein 3; TNF-α; tumor necrosis factor-α; IL-1β:interleukin-1β; qPCR: quantitative polymerase chain reaction; BALF: bronchoalveolar lavage fluid; ELISA: enzyme-linked immunosorbent assay; PFU: plaque formation unit; ANOVA: analysis of variance; Ams: Alveolar macrophages; FACS: fluorescence-activated cell sorting; Control: normal control group; H1N1: influenza a virus; JX-H: Jinxin oral liquid high-dose group; JX-M: Jinxin oral liquid middle-dose group; JX-L: Jinxin oral liquid low-dose group. All results are expressed as the mean ± standard deviation by one-way ANOVA with Dunnett’s post hoc tests for multiple comparisons. aP < 0.01, eP < 0.0001, H1N1 group vs control group; bP < 0.01, cP < 0.001, dP < 0.05, vs H1N1 group.
Figure 4 JX inhibits the NLRP3 inflammasome activation in the AMs A: the expression of IL-1β in isolated AMs from all groups of mice was determined by qPCR at 24 h after H1N1 infection (n = 3); B: the expression of NLRP3 in isolated AMs from all groups of mice was determined by qPCR at 24 h after H1N1 infection (n = 3); C: the expression of NLRP3 in CD11c+ Siglec-F+ AMs from all groups of mice was determined by FACS at 24 h after H1N1 infection (n = 4); D: flow cytometry histograms for NLRP3+ (D1-D3) AMS in all groups. D1: Control Group; D2: H1N1 Group; D3: JX Group. E: the expression of caspase1 p20 in CD11c+ Siglec-F+ AMs from all groups of mice was determined by FACS at 24 h after H1N1 infection (n = 4). F: flow cytometry histograms for P20+ (F1-F3) AMS in all groups, F1: Control Group; F2: H1N1 Group; F3: JX Group. Normal control group: treated with normal diet and physiological saline; H1N1 infected group: H1N1, 106 PFU, 2 d; ribavirin treatment group: 46 mg·kg-1·d-1, 2 d; Jxin oral liquid high-dose group: 55.2 g·kg-1·d-1, 2 d, JX-H; Jinxin oral liquid middle-dose group: 27.6 g·kg-1·d-1, 2 d, JX-M; Jinxin oral liquid low-dose group: 13.8 g·kg-1·d-1, 2 d, JX-L. NLRP3: nod-like receptor protein 3; TNF-α; tumor necrosis factor-α; IL-1β:interleukin-1β; qPCR: quantitative polymerase chain reaction; BALF: bronchoalveolar lavage fluid; ELISA: enzyme-linked immunosorbent assay; PFU: plaque formation unit; ANOVA: analysis of variance; Ams: Alveolar macrophages; FACS: fluorescence-activated cell sorting; Control: normal control group; H1N1: influenza a virus; JX-H: Jinxin oral liquid high-dose group; JX-M: Jinxin oral liquid middle-dose group; JX-L: Jinxin oral liquid low-dose group. All results are expressed as the mean ± standard deviation by one-way ANOVA with Dunnett’s post hoc tests for multiple comparisons. aP < 0.01, eP < 0.0001, H1N1 group vs control group; bP < 0.01, cP < 0.001, dP < 0.05, vs H1N1 group.
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