Fuzheng Xuanfei Huashi prescription (扶正宣肺化湿方) suppresses inflammation in lipopolysaccharide-induced lung injury in mice via toll-like recptor 4/nuclear transcription factor κB and cyclooxygenase-2/prostaglandin E2 pathway

doi:10.19852/j.cnki.jtcm.2025.02.018

Journal of Traditional Chinese Medicine ›› 2025, Vol. 45 ›› Issue (2): 272-280.DOI: 10.19852/j.cnki.jtcm.2025.02.018

• Original articles • Previous Articles Next Articles

Fuzheng Xuanfei Huashi prescription (扶正宣肺化湿方) suppresses inflammation in lipopolysaccharide-induced lung injury in mice via toll-like recptor 4/nuclear transcription factor κB and cyclooxygenase-2/prostaglandin E2 pathway

HUANG Haiyang¹, ZHU Shumin², ZHONG Shaowen³, LIU Ying³, HOU Shaozhen³^,⁴, GAO Jie³, OU Jianzhao¹, DONG Mingguo¹(), NING Weimin¹()

1 Institute of Traditional Chinese Medicine, Dongguan Hospital of Traditional Chinese Medicine, Dongguan 523000, China
2 Department of Traditional Chinese Medicine, Guangdong Food and Drug Vocational College, Guangzhou 510520, China
3 School of Pharmaceutical Sciences, Guangzhou University of Chinese Medicine, Guangzhou 510006, China
4 Dongguan Institute of Guangzhou University of Chinese Medicine, Dongguan 523808, China

Received:2023-12-08 Accepted:2024-05-27 Online:2025-04-15 Published:2025-03-10
Contact: NING Weimin, Institute of Traditional Chinese Medicine, Dongguan Hospital of Traditional Chinese Medicine, Dongguan 523000, China. ningweiming11@126.com; DONG Mingguo, Institute of Traditional Chinese Medicine, Dongguan Hospital of Traditional Chinese Medicine, Dongguan 523000, China. dgdongmingguo@163.com, Telephone: +86-769-26385763
Supported by:
Emergency Corona Virus Disease 2019 (COVID-19) Response Project of Dongguan: Clinical Efficacy Observation and Mechanism Study of Fuzheng Xuanfei Huashi Formula in the Treatment of COVID-19 Based on the Lingnan Theory of Epidemic Diseases(202071715002124);National Natural Science Foundation of China: Study on the Mechanism of Lung Inflammatory Injury Induced by Gut-derived Lipopolysaccharide and Skatole in Spleen Deficiency Animals based on Pulmonary Alveolus Macrophage Heterogeneity(82274381);Guangdong Basic and Applied Basic Research Foundation: Development and Industrialization of Traditional Chinese Medicine Classic and Famous Prescription Compound Formulations(2021ZD006)

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Abstract

Abstract:

OBJECTIVE: To determine the effect of Traditional Chinese Medicine (TCM) Fuzheng Xuanfei Huashi prescription (扶正宣肺化湿方, FZXF) on lipopolysaccharide (LPS)-induced pneumonia in mice and identify the mechanism of FZXF in the treatment of LPS-induced lung inflammation.

METHODS: The pneumonia model was established by intraperitoneal injection of 5 mg/kg LPS in mice. Cytokines were detected by enzyme-linked immune-osorbent assay (ELISA), macrophages in lung tissue were determined by immunofluorescence, and pathway-related data were determined by quantitative real-time polymerase chain reaction (qPCR) and Western blot.

RESULTS: The liver, thymus, and spleen index values and the levels of aspartate aminotransferase (AST) and alanine aminotransferase (ALT) obviously increased in LPS-treated mice. FZXF decreased the white blood cell count and reduced the increase in the lung wet weight/dry weight ratio caused by LPS. The hematoxylin-eosin staining result showed that FZXF could maintain the integrity of lung tissue structure, alleviate interstitial oedema and alveolar wall thickening, and reduce inflammatory cell infiltration. Moreover, FZXF markedly reduced the expression of proinflammatory cytokines. FZXF also significantly reduced LPS-induced malondialdehyde production and increased superoxide dismutase level in the lung. By immunofluorescence, we found that FZXF could reduce macrophage infiltration.

The mRNA expression levels of cyclooxygenase-2 (COX-2), prostaglandin E2 (PGE2), toll-like receptor 4 (TLR4) and nuclear transcription factor κB (NF-κB) in the lung tissue of mice were decreased by treatment with FZXF. In addition, FZXF inhibited the protein expression of TLR4, p-p65 and COX-2. These results indicated that FZXF could inhibit the inflammatory response of LPS induced cytokine storm in mice through TLR4/NF-κB and COX-2/PGE2 signaling pathway.

CONCLUSION: These findings were suggested that FZXF prescription suppresses inflammation in LPS-induced pneumonia in mice via TLR4/NF-κB and COX-2/ PGE2 pathway.

Key words: pneumonia, lipopolysaccharides, toll-like receptor 4, NF-kappa B, cyclooxygenase 2, dinoprostone, signal transduction, Fuzheng Xuanfei Huashi prescription

HUANG Haiyang, ZHU Shumin, ZHONG Shaowen, LIU Ying, HOU Shaozhen, GAO Jie, OU Jianzhao, DONG Mingguo, NING Weimin. Fuzheng Xuanfei Huashi prescription (扶正宣肺化湿方) suppresses inflammation in lipopolysaccharide-induced lung injury in mice via toll-like recptor 4/nuclear transcription factor κB and cyclooxygenase-2/prostaglandin E2 pathway[J]. Journal of Traditional Chinese Medicine, 2025, 45(2): 272-280.

Figures/Tables 6

Table 1 The level of organ impairment in mice

Group	n	Liver index (%)	AST (U/L)	ALT (U/L)	Thymus index (%)	Spleen index (%)	WBC (10⁹/L)
NC	6	4.24±0.29	16.13±1.21	14.66±4.02	0.23±0.03	0.31±0.04	78.10±3.11
LPS	6	6.75±0.60^a	47.41±2.35^a	26.15±1.75^a	0.29±0.04	0.92±0.12^a	94.50±11.10^a
DEX	6	6.78±0.61	30.85±2.15^b	18.16±2.95^c	0.22±0.06	0.56±0.09^b	85.29±6.64^c
FZXFH	6	5.90±0.59^c	25.24±3.50^b	14.74±2.99^b	0.22±0.05	0.75±0.21	83.04±3.13^b
FZXFM	6	5.82±0.44^c	24.07±3.45^b	16.76±2.94^b	0.28±0.05	0.76±0.15	89.99±3.96
FZXFL	6	6.34±0.68	25.24±5.78^b	17.41±1.80^c	0.29±0.03	0.95±0.16	90.13±4.49

Figure 1 Histological injuries in the lungs of mice and W/D A-F: HE staining of mouse lung tissue (× 200); A: NC group; B: LPS group; C: DEX group; D: FZXFH group; E: FZXFM group; F: FZXFL group; G: the lungs of mice lung wet: dry weight ratio. NC: treated only with physiological saline; LPS: treated with lipopolysaccharide and physiological saline; DEX: treated with lipopolysaccharide and DEX of 0.25 mg/kg; FZXFH: treated with lipopolysaccharide and FZXF of 4.58 g/kg; FZXFM: treated with lipopolysaccharide and FZXF of 2.29 g/kg; FZXFL: treated with lipopolysaccharide and FZXF of 1.14 g/kg. W/D: lung wet weight∶dry weight; HE: hematoxylin-eosin; LPS: lipopolysaccharide and physiological saline; DEX: dexamethasone; FZXF: Fuzheng Xuanfei Huashi prescription; FZXFH: FZXF high; FZXFM: FZXF middle; FZXFL: FZXF low; ANOVA: analysis of variance. Data are expressed as mean ± standard deviation (n = 6). The difference among multiple groups was analyzed by one-way ANOVA statistical method. Compared with the NC group, aP < 0.01; compared with the LPS group, bP < 0.01.

Figure 2 FZXF attenuates inflammation and oxidative stress in LPS-induced mice A: level of TNF-α; B: level of IL-1β; C: level of IL-6; D: level of MCP-1; E: level of CRP; F: level of IL-10; G: level of MDA; H: level of SOD. NC: treated only with physiological saline; LPS: treated with lipopolysaccharide and physiological saline; DEX: treated with lipopolysaccharide and DEX of 0.25 mg/kg; FZXFH: treated with lipopolysaccharide and FZXF of 4.58 g/kg; FZXFM: treated with lipopolysaccharide and FZXF of 2.29 g/kg; FZXFL: treated with lipopolysaccharide and FZXF of 1.14 g/kg. TNF-α: necrosis factor-α; IL-1β: interleukin-1β; IL-6: interleukin-6; MCP-1: monocyte chemotactic protein-1; CRP: C-reactive protein; IL-10: interleukin-10; MDA: malondialdehyde; SOD: superoxide dismutase; LPS: lipopolysaccharide and physiological saline; DEX: dexamethasone; FZXF: Fuzheng Xuanfei Huashi prescription; FZXFH: FZXF high; FZXFM: FZXF middle; FZXFL: FZXF low; ANOVA: analysis of variance. Data are expressed as mean ± standard deviation (n = 6). The difference among multiple groups was analyzed by one-way ANOVA statistical method. Compared with the NC group, aP < 0.01; compared with the LPS group, bP < 0.01, cP < 0.05.

Figure 3 Immunofluorescence of lung macrophages (scale bar = 100 μm) A-F: expression of F4/80 (red) and cell nuclei (blue) in mouse lung tissue. G: relative expression level of F4/80. A1-F1: expression of F4/80 (red) in mouse lung tissue. A2-F2: The expression of cell nuclei (blue) in mouse lung tissue. A, A1, A2: NC group; B, B1, B2: LPS group; C, C1, C2: DEX group; D, D1, D2: FZXFH group; E, E1, E2: FZXFM group; F, F1, F2: FZXFL group. NC: treated only with physiological saline; LPS: treated with lipopolysaccharide and physiological saline; DEX: treated with lipopolysaccharide and DEX of 0.25 mg/kg; FZXFH: treated with lipopolysaccharide and FZXF of 4.58 g/kg; FZXFM: treated with lipopolysaccharide and FZXF of 2.29 g/kg; FZXFL: treated with lipopolysaccharide and FZXF of 1.14 g/kg. LPS: lipopolysaccharide and physiological saline; DEX: dexamethasone; FZXF: Fuzheng Xuanfei Huashi prescription; FZXFH: FZXF high; FZXFM: FZXF middle; FZXFL: FZXF low; ANOVA: analysis of variance. Data are expressed as mean±standard deviation (n = 3). The difference among multiple groups was analyzed by one-way ANOVA statistical method. Compared with the NC group, aP < 0.01; compared with the LPS group, bP < 0.01.

Table 2 The mRNA expression levels of TLR4, NF-κB, COX-2 and PGE2 in the lung

Group	n	mRNA TLR4	mRNA NF-κB	mRNA COX-2	mRNA PGE2
NC	6	0.96±0.20	1.22±0.14	1.34±0.14	1.01±0.11
LPS	6	3.21±0.08^a	2.57±0.14^a	4.44±0.89^a	3.68±0.44^a
DEX	6	1.50±0.19^b	1.59±0.06^b	1.96±0.32^b	1.76±0.31^b
FZXFH	6	1.71±0.15^b	1.54±0.28^b	2.66±0.23^c	1.75±0.46^b
FZXFM	6	2.19±0.48^b	2.14±0.30	3.02±0.72^c	3.30±0.13
FZXFL	6	2.54±0.32	2.41±0.36	3.99±0.96	3.51±0.09

Figure 4 Protein expression of the TLR4/NF-κB and COX-2/PGE2 signaling pathways in the lung A: Western blot bands of TLR4/ NF-κB signaling pathway; B: protein expression levels of TLR4; C: protein expression levels of p-p65/ p65; D: Western blot bands of COX-2/PGE2 signaling pathway; E: protein expression levels of COX-2; F: expression level of PGE2 in lung tissue. NC: treated only with physiological saline; LPS: treated with lipopolysaccharide and physiological saline; DEX: treated with lipopolysaccharide and DEX of 0.25 mg/kg; FZXFH: treated with lipopolysaccharide and FZXF of 4.58 g/kg; FZXFM: treated with lipopolysaccharide and FZXF of 2.29 g/kg; FZXFL: treated with lipopolysaccharide and FZXF of 1.14 g/kg. TLR4: toll-like receptor 4; p65: RelA, nuclear transcription factor κB3; p-p65: phosphorylated p65; COX-2: cyclooxygenase-2; GAPDH: glyceraldehyde-3-phosphate dehydrogenase; LPS: lipopolysaccharide and physiological saline; DEX: dexamethasone; FZXF: Fuzheng Xuanfei Huashi prescription; FZXFH: FZXF high; FZXFM: FZXF middle; FZXFL: FZXF low; ANOVA: analysis of variance. Data are expressed as mean ± standard deviation (n = 3). The difference among multiple groups was analyzed by one-way ANOVA statistical method. Compared with the NC group, aP < 0.01; compared with the LPS group, bP < 0.01, cP < 0.05.

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Fuzheng Xuanfei Huashi prescription (扶正宣肺化湿方) suppresses inflammation in lipopolysaccharide-induced lung injury in mice via toll-like recptor 4/nuclear transcription factor κB and cyclooxygenase-2/prostaglandin E2 pathway

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