Pharmacological advances of alkaloids from Traditional Chinese Medicine against pulmonary fibrosis: focus on anti-inflammatory mechanisms

doi:10.19852/j.cnki.jtcm.2026.05.023

Journal of Traditional Chinese Medicine ›› 2026, Vol. 46 ›› Issue (5): 1307-1322.DOI: 10.19852/j.cnki.jtcm.2026.05.023

Pharmacological advances of alkaloids from Traditional Chinese Medicine against pulmonary fibrosis: focus on anti-inflammatory mechanisms

DONG Jiamei¹^,², ZHONG Jieren³, YANG Mingqi⁴^,⁵, YU Jiangkun⁶, ZHOU Zhuoling⁷, LUO Yuhong², WANG Ruiqi², YANG Yang², YANG Haikui², LIU Yanyan⁸, XU Jiehua¹^,⁶(), WU Qibiao¹^,⁹()

¹ Faculty of Chinese Medicine and State Key Laboratory of Mechanism and Quality of Chinese Medicine, Macau University of Science and Technology, Macau 999078, China
² Department of Pharmacy, Zhuhai People's Hospital (The Affiliated Hospital of Beijing Institute of Technology, Zhuhai Clinical Medical College of Jinan University), Zhuhai 519000, China
³ Department of Radiation Oncology, Zhuhai Clinical Medical College of Jinan University (Zhuhai People's Hospital, The Affiliated Hospital of Beijing Institute of Technology), Zhuhai 519000, China
⁴ Faculty of Medicine, Macau University of Science and Technology, Macau 999078, China
⁵ Outpatient Department, Zhuhai People's Hospital (the Affiliated Hospital of Beijing Institute of Technology, Zhuhai Clinical Medical College of Jinan University), Zhuhai 519000, China
⁶ Department of Nuclear Medicine, Zhuhai People's Hospital (The Affiliated Hospital of Beijing Institute of Technology, Zhuhai Clinical Medical College of Jinan University), Zhuhai 519000, China
⁷ School of Pharmaceutical Sciences, Southern Medical University, Guangzhou 510515, China
⁸ Guangdong Provincial Key Laboratory of Tumor Interventional Diagnosis and Treatment, Zhuhai People's Hospital (The Affiliated Hospital of Beijing Institute of Technology, Zhuhai Clinical Medical College of Jinan University), Zhuhai 519000, China
⁹ Zhuhai M.U.S.T. Science and Technology Research Institute, Guangdong-Macao In-Depth Cooperation Zone in Hengqin, Zhuhai 519000, China

Received:2025-12-12 Accepted:2026-04-13 Online:2026-10-15 Published:2026-10-09
Contact: Prof. WU Qibiao, Faculty of Chinese Medicine and State Key Laboratory of Mechanism and Quality of Chinese Medicine, Macau University of Science and Technology, Macau 999078, China; Zhuhai M.U.S.T. Science and Technology Research Institute, Guangdong-Macao In-Depth Cooperation Zone in Hengqin, Zhuhai 519000, China, qbwu@must.edu.mo,Telephone: +853-88972261; Prof. XU Jiehua, Faculty of Chinese Medicine and State Key Laboratory of Mechanism and Quality of Chinese Medicine, Macau University of Science and Technology, Macau 999078, China; Department of Nuclear Medicine, Zhuhai People's Hospital (The Affiliated Hospital of Beijing Institute of Technology, Zhuhai Clinical Medical College of Jinan University), Zhuhai 519000, China. xujhgz3@163.com,Telephone: +86-15992459188
About author:
DONG Jiamei and ZHONG Jieren are co-first authors and contributed equally to this work
Supported by:
Science and Technology Development Fund, Macau Special Administrative Region: the Molecular Mechanisms of High Metastasis Propensity in Colorectal Cancer with Spleen Deficiency, Damp-Heat, and Blood Stasis Syndrome and the Preventive Role of Xianlian Jiedu Decoction in Preventing Metastasis(0048/2023/AFJ);Science and Technology Development Fund, Macau Special Administrative Region: Identification of the Anti-Depressive Mechanism of Ginsenoside by Exploring Its Interaction with Kynurenine 3-Monooxygenase and Effects on the Kynurenine Pathway(0164/2023/RIA3);Zhuhai People’s Hospital: Positron Emission Tomography/Computed Tomography Scintigraphy of Hepatocellular Carcinoma with Aptamer JHIT2e And Its Targeted Molecular(2021KYQD-03);Beijing Dadi Medical Charity Foundation: Population Pharmacokinetics of Meropenem in Patients with SevereInfections(DDYL-A-KT-20250519-0058);Basic and Applied Basic Research Project of Guangdong Province: Application Research of Multiple Biomarker Detection Based on Electrode Array and Electrochemiluminescence Technology in Early Diagnosis of Liver Cancer(2024A1515220042);Science and Technology Planning Project of Guangzhou: the Role and Mechanism of Asproin in Liver Fibrosis Associated with Non-Alcoholic Fatty Liver Disease(2024A03J0377);National Natural Science Foundation of China: Asporin Promotes Hepatic Fibrosis by Activating Cyclin-dependent Kinase 1 Related Mitochondrial Homeostasis Imbalance of Hepatic Stellate Cells(82304589)

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Abstract

Abstract:

Pulmonary fibrosis (PF) is a fatal respiratory disease characterized by abnormal repair of the pulmonary interstitium and scar formation. Currently, only nintedanib and pirfenidone are approved for clinical use, but their efficacy is limited, and they have significant side effects. The sustained inflammatory microenvironment promotes fibroblast activation and collagen deposition via unresolved inflammation, representing a central pathological mechanism in PF progression. Therefore, anti-inflammatory effects are key in relieving and treating PF. Alkaloids derived from Chinese herbal medicine have become a new hotspot in anti-PF research because of their good anti-inflammatory properties and advantages in multitarget and multipathway approaches. This review elucidates that PF is triggered by multiple factors, such as genetics, the environment, drugs, and infection, and reveals the core mechanism of its pathogenesis from the perspective of the roles of various cell types involved in PF. In this review, we focus on the experimental efficacy and mechanisms of alkaloid drugs that mitigate pulmonary fibrosis through anti-inflammatory actions. We review the research progress of experimental models and signaling pathway regulatory mechanisms to provide a reference for subsequent research. Finally, this review analyzes the transformation bottlenecks faced by alkaloids when applied to PF, such as low active ingredient content, poor target selectivity, and insufficient toxicological and clinical data. Strategies such as structural optimization, nanodelivery, multiomics validation, and real-world research are proposed to overcome these challenges, providing a reference for the development of highly efficient and low-toxicity anti-PF drugs.

Key words: pulmonary fibrosis, inflammation, traditional Chinese medicinal alkaloids, antifibrosis, mechanism of action, review

DONG Jiamei, ZHONG Jieren, YANG Mingqi, YU Jiangkun, ZHOU Zhuoling, LUO Yuhong, WANG Ruiqi, YANG Yang, YANG Haikui, LIU Yanyan, XU Jiehua, WU Qibiao. Pharmacological advances of alkaloids from Traditional Chinese Medicine against pulmonary fibrosis: focus on anti-inflammatory mechanisms[J]. Journal of Traditional Chinese Medicine, 2026, 46(5): 1307-1322.

Figures/Tables 5

Figure 1 Multifaceted etiology of PF and the role of various cell types involved in PF PF: pulmonary fibrosis; AT1 cell: alveolar type I cell; AT2 cell: alveolar type II cell; EMT: epithelial-mesenchymal transition; SASP: senescence-associated secretory phenotype; TGF-β1: transforming growth factor-beta 1; MMPs: matrix metalloproteinases; PDGF: platelet-derived growth factor; EndMT: endothelial-to-mesenchymal transition; VEGF: vascular endothelial growth factor; ECM: extracellular matrix; FMT: fibroblast-to-myofibroblast transition; TNF-α: tumor necrosis factor alpha. Created using BioRender (BioRender.com Inc., Toronto, Canada).

Figure 2 Mechanism of action of the active alkaloid components in TCM against PF TCM: Traditional Chinese Medicine; PF: pulmonary fibrosis; DDR: DNA damage response; TGF-β: transforming growth factor-beta; NF-κB: nuclear factor kappa B; α-SMA: α-smooth muscle actin; IL-1β: interleukin-1 beta; TNF-α: tumor necrosis factor alpha; IL-6: interleukin-6; ROS: reactive oxygen species; MDA: malondialdehyde; MPO: myeloperoxidase; TGF-β1: transforming growth factor-beta 1; SOD: superoxide dismutase; GSH-Px: glutathione peroxidase; CAT: catalase; M2: alternatively activated macrophage; ECM: extracellular matrix; MMPs: matrix metalloproteinases; TIMPs: tissue inhibitors of metalloproteinases; AEC: alveolar epithelial cell; ERS: endoplasmic reticulum stress; UPR: unfolded protein response; SASP: senescence-associated secretory phenotype; EMT: epithelial-mesenchymal transition; FMT: fibroblast-to-myofibroblast transition. Created using BioRender (BioRender.com Inc., Toronto, Canada).

Figure 3 Thirteen Traditional Chinese Medicinal alkaloids involved in anti-inflammatory mechanisms and structural formulas for improving PF PF: pulmonary fibrosis; NTS: neotuberostemonine; TS: tuberostemonine; CAE: citrus alkaline extracts; TET: tetrandrine; CEP: cepharanthine; COP: coptisine. Created using BioRender (BioRender.com Inc., Toronto, Canada).

Table 1 Details of the in vivo experimental model and dose of alkaloid natural products derived from TCM involved in improving the anti-inflammatory mechanism of PF

Name	Experimental model in vivo	Dosage	Reference
Berberine	BLM-induced PF in male wistar albino rats	The rats were treated continuously according to the dosage of 200 mg/kg for the first 14 d and the following 14 d	95
Berberine	BLM-induced PF in albino male mice	Mice were treated with berberine at a dosage of 5 mg/kg from days 15 to 28 after BLM induction	96
Berberine hydrochloride	PM2.5-induced PF in male C57BL/6 mice	Mice were treated continuously according to the dosage of 50 mg/kg for 45 d	98
CEP	BLM-induced PF in male C57BL/6 mice	The mice were treated continuously according to the dosage of 10 mg/kg for 7 d	106
Neferine	Amiodarone- induced PF in adult male Kunming mice	The rats were treated continuously according to the dosage of 20 mg/kg twice a day for 14 d	107
Neferine	BLM-induced PF in Kunming mice	The rats were treated continuously according to the dosage of 20 mg/kg for 7, 14, and 21 d	111
Tetrandrine	BLM-induced male C57BL/ 6 mice	The mice were treated continuously according to the dosage of 20 mg/kg for 14 d	114
Tetrandrine	BLM-induced IPF in male C57BL/6 mice	The mice were treated with TET-LIPs via intratracheal atomization at a dose of 2.5 mg/kg, once every two days for three weeks	116
Citrus alkaline extracts	BLM-induced PF in male Sprague-Dawley rats	The rats were treated continuously according to the dosage of 8, 16, and 32 mg·kg^-1·d^-1 for 28 d	117
Evodiamine	LPS-induced PF in male BALB/c mice	Mice were treated continuously according to the dosage of 10 mg/kg for 7 d	66
Vincamine	BLM-induced PF in male C57BL/6J mice	The mice were treated continuously according to the dosage of 15, 30 mg/kg for 20 d	123
Extract of Arenaria kansuensis (Part 1)	BLM-induced PF in adult male and female Kunming mice	The rats were treated continuously according to the dosage of 50, 100 and 150 mg/kg for 15 d	124
Peiminine	BLM-induced PF in acute lung injury in Sprague-Dawley rats	The rats were treated with peiminine at a dosage of 5 mg/kg for 28 consecutive days	128
Peimine	BLM-induced PF in male C57BL/6 mice	Mice were treated with Peimine at dosages of 2.5 or 5 mg/kg for 14 d starting for 15 d	130
Peimine	BLM-induced PF in Sprague-Dawley rats	The rats were treated with peimine at a dosage of 0.24 mg/kg orally for 14 d	129
Neotuberostemonine and tuberostemonine	BLM-induced PF in male ICR mice	The mice were orally administered with NTS (30 mg/kg) and TS (30 mg/kg) once a day	131

Table 1 Details of the in vivo experimental model and dose of alkaloid natural products derived from TCM involved in improving the anti-inflammatory mechanism of PF

Name	Experimental model in vivo	Dosage	Reference
Berberine	BLM-induced PF in male wistar albino rats	The rats were treated continuously according to the dosage of 200 mg/kg for the first 14 d and the following 14 d	95
Berberine	BLM-induced PF in albino male mice	Mice were treated with berberine at a dosage of 5 mg/kg from days 15 to 28 after BLM induction	96
Berberine hydrochloride	PM2.5-induced PF in male C57BL/6 mice	Mice were treated continuously according to the dosage of 50 mg/kg for 45 d	98
CEP	BLM-induced PF in male C57BL/6 mice	The mice were treated continuously according to the dosage of 10 mg/kg for 7 d	106
Neferine	Amiodarone- induced PF in adult male Kunming mice	The rats were treated continuously according to the dosage of 20 mg/kg twice a day for 14 d	107
Neferine	BLM-induced PF in Kunming mice	The rats were treated continuously according to the dosage of 20 mg/kg for 7, 14, and 21 d	111
Tetrandrine	BLM-induced male C57BL/ 6 mice	The mice were treated continuously according to the dosage of 20 mg/kg for 14 d	114
Tetrandrine	BLM-induced IPF in male C57BL/6 mice	The mice were treated with TET-LIPs via intratracheal atomization at a dose of 2.5 mg/kg, once every two days for three weeks	116
Citrus alkaline extracts	BLM-induced PF in male Sprague-Dawley rats	The rats were treated continuously according to the dosage of 8, 16, and 32 mg·kg^-1·d^-1 for 28 d	117
Evodiamine	LPS-induced PF in male BALB/c mice	Mice were treated continuously according to the dosage of 10 mg/kg for 7 d	66
Vincamine	BLM-induced PF in male C57BL/6J mice	The mice were treated continuously according to the dosage of 15, 30 mg/kg for 20 d	123
Extract of Arenaria kansuensis (Part 1)	BLM-induced PF in adult male and female Kunming mice	The rats were treated continuously according to the dosage of 50, 100 and 150 mg/kg for 15 d	124
Peiminine	BLM-induced PF in acute lung injury in Sprague-Dawley rats	The rats were treated with peiminine at a dosage of 5 mg/kg for 28 consecutive days	128
Peimine	BLM-induced PF in male C57BL/6 mice	Mice were treated with Peimine at dosages of 2.5 or 5 mg/kg for 14 d starting for 15 d	130
Peimine	BLM-induced PF in Sprague-Dawley rats	The rats were treated with peimine at a dosage of 0.24 mg/kg orally for 14 d	129
Neotuberostemonine and tuberostemonine	BLM-induced PF in male ICR mice	The mice were orally administered with NTS (30 mg/kg) and TS (30 mg/kg) once a day	131

Figure 4 Overview of target signaling pathways involved in the antipulmonary fibrosis effects of thirteen bioactive alkaloids derived from TCM TCM: Traditional Chinese Medicine; COP: coptisine; CEP: cepharanthine; TET: tetrandrine; CAE: Citrus alkaline extracts; NTS: neotuberostemonine; TS: tuberostemonine; Nrf2: nuclear factor erythroid 2-related factor 2; NF-κB: nuclear factor kappa B; iNOS: inducible nitric oxide synthase; A2aR: A2a receptor; SDF-1: stromal cell-derived factor-1; CXCR4: C-X-C chemokine receptor type 4; TNF-α: tumor necrosis factor alpha; EMT: epithelial-mesenchymal transition; HO-1: heme oxygenase-1; ROS: reactive oxygen species; FMT: fibroblast-to-myofibroblast transition; M2: alternatively activated macrophage; ECM: extracellular matrix; Th1: type 1 helper T cell; Th2: type 2 helper T cell; IFN-γ: interferon-gamma; IL-6: interleukin-6; PINK1: PTEN-induced putative kinase 1; AECs: alveolar epithelial cells; SAβ-gal: senescence-associated beta-galactosidase; P21: cyclin-dependent kinase inhibitor 1A; P16: cyclin-dependent kinase inhibitor 2A; SASP: senescence-associated secretory phenotype; Bip: binding immunoglobulin protein; PEPK: protein kinase RNA-like endoplasmic reticulum kinase; ER Stress: endoplasmic reticulum stress; MMP-9: matrix metalloproteinase-9; TIMP-1: tissue inhibitor of metalloproteinase-1; HYP: hydroxyproline; CCL17: C-C motif chemokine ligand 17; GPR40: G protein-coupled receptor 40; NLRP3: NOD-like receptor family, pyrin domain containing 3; IL-1β: interleukin-1 beta; ASC: apoptosis-associated speck-like protein containing a CARD; EGF: epidermal growth factor; P65: transcription factor p65; TGF-β1: transforming growth factor-beta 1; α-SMA: α-smooth muscle actin; CTGF: connective tissue growth factor; P38: p38 mitogen-activated protein kinase; MAPK: mitogen-activated protein kinase; p-AKt: phosphorylated protein kinase B; p-STAT6: phosphorylated signal transducer and activator of transcription 6; PI3K: phosphoinositide 3-kinase; HIF1α: hypoxia-inducible factor-1 alpha; CoL: collagen; FN: fibronectin. Created using BioRender (BioRender.com Inc., Toronto, Canada).

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Pharmacological advances of alkaloids from Traditional Chinese Medicine against pulmonary fibrosis: focus on anti-inflammatory mechanisms

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