The Ethical Kampo Formulation Sho-Seiryu-To (TJ-19) Prevents Bleomycin-Induced Pulmonary Fibrosis in Rats

Yang, Chang; Sun, Peng; Ding, Da zhi; Moriuchi, Hiroshi; Ishitsuka, Yoichi; Irikura, Mitsuru; Irie, Tetsumi

doi:10.1248/bpb.33.1438

Cited by 10 publications

(6 citation statements)

References 24 publications

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“…et al, 2015 ). Pharmacological studies have demonstrated that So-Cheong-Ryoung-Tang possesses protective effects against airway inflammation, nasal allergy, pulmonary fibrosis, and asthma ( Kao et al, 2000 ; Das et al, 2009 ; Yang et al, 2010 ). In a recent study, So-Cheong-Ryoung-Tang effectively suppressed the production of MMP-9 in human bronchial epithelium cell line BEAS-2B stimulated with TNF-α and IL-4.…”

Section: Discussionmentioning

confidence: 99%

So-Cheong-Ryoung-Tang Attenuates Pulmonary Inflammation Induced by Cigarette Smoke in Bronchial Epithelial Cells and Experimental Mice

et al. 2018

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So-Cheong-Ryoung-Tang is a traditionally used herbal formula for the treatment of pulmonary diseases in China, Korea, and Japan. We investigated the protective effects of So-Cheong-Ryong-Tang water extract (SCWE) in cigarette smoke concentrate (CSC) stimulated human airway epithelial cell line NCI-H292 and mice exposed cigarette smoke (CS) and lipopolysaccharide (LPS). In the CSC-stimulated NCI-H292 cells, SCWE inhibited proinflammatory cytokines in a concentration-dependent manner, as evidenced by a reduction in their mRNA levels. Also, SCWE significant reduced inducible nitric oxide synthase (iNOS) expression and nuclear factor kappa B (NF-κB) phosphorylation in CSC-stimulated cells. The mice were exposed to CS for 1 h per day (a total of eight cigarettes per day) for 7 days and received LPS intranasally on day 5. The mice were administered a dose of SCWE (100 and 200 mg/kg) 1 h before CS exposure. In in vivo, SCWE decreased the inflammatory cell count and reduced the expression of the proinflammatory cytokines in the broncho-alveolar lavage fluid (BALF) compared with CS and LPS exposed mice. SCWE attenuated inflammatory cell infiltration in airway induced by CS and LPS exposure, and this decrease was accompanied by a reduction in the expression levels of iNOS and MMP-9 in lung tissue. The extract also inhibited the phosphorylation of inhibitor of kappa B alpha (IκBα) and NF-κB induced by CS and LPS exposure in lung tissue. These results suggest that SCWE may effectively inhibit airway inflammatory responses induced by CS and LPS exposure via the NF-κB pathway. Therefore, SCWE may be a potential treatment for airway inflammatory diseases, such as chronic obstructive pulmonary disease (COPD).

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Section: Discussionmentioning

confidence: 99%

So-Cheong-Ryoung-Tang Attenuates Pulmonary Inflammation Induced by Cigarette Smoke in Bronchial Epithelial Cells and Experimental Mice

et al. 2018

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“…Specifically, the aberrant up-regulation of the ROS-generating enzyme NOX4, coupled with the low-expressed Nrf2, results in a sustained redox imbalance, which promote the activation and differentiation of fibroblasts and make myofibroblast get apoptosis-resistant phenotype ( Amara et al, 2010 ; Hecker et al, 2014 ). Many data have shown the anti-oxidative effects of TCM on PF, for example, Danggui Buxue Tang and TJ-19 (two different TCM compounds) could attenuate BLM-induced PF via increasing SOD activity and decreasing MDA content ( Yang et al, 2010 ; Zhao et al, 2015 ). In this study, we demonstrated that JHF treatment elevated the levels of antioxidant including T-SOD, GSH, CAT, and reduced the levels of oxidant index including MDA, MPO in lung and serum of bleomycin-induced PF rat.…”

Section: Discussionmentioning

confidence: 99%

A Chinese Herbal Formula Ameliorates Pulmonary Fibrosis by Inhibiting Oxidative Stress via Upregulating Nrf2

Bai

Zhao

et al. 2018

Front. Pharmacol.

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This study aimed to explore the protective effects of a Chinese herbal formula, Jinshui Huanxian formula (JHF), on experimental pulmonary fibrosis and its underlying mechanisms. After being treated with single dose of bleomycin (5 mg/kg) intratracheally, rats were orally administered with JHF and pirfenidone from day 1 to 42, then sacrificed at 7, 14, 28, or 42 days post-bleomycin instillation. JHF ameliorated bleomycin-induced pathological changes, collagen deposition in the rat lung and recovered pulmonary function at different days post-bleomycin instillation. In lungs of JHF-treated rats, the levels of total superoxide dismutase, catalase and glutathione were higher, and myeloperoxidase and methane dicarboxylic aldehyde were lower than those in vehicle-treated rats, respectively. Additionally, JHF inhibited the expression of NADPH oxidase 4 (NOX4) and increased the Nuclear Factor Erythroid 2-Related Factor 2 (Nrf2) in lung tissues. In vitro, JHF and ruscogenin, a compound of Ophiopogonis Radix contained in JHF, significantly inhibited transforming growth factor β1 (TGF-β1)-induced differentiation of fibroblasts. Furthermore, JHF markedly decreased the level of reactive oxygen species in TGF-β1-induced fibroblast. In line with this, upregulation of NAD(P)H: quinone oxidoreductase 1 and heme oxygenase 1, and downregulation of NOX4 were found in JHF-treated fibroblast induced by TGF-β1. While on the other hand, Nrf2 siRNA could suppress the JHF-mediated inhibition effect on alpha-smooth muscle actin (α-SMA), and FN1 expression induced by TGF-β1 in fibroblasts. These results indicated that JHF performed remarkably therapeutic and long-term effects on pulmonary fibrosis in rat and suppressed the differentiation of fibroblast into myofibroblast through reducing the oxidative response by upregulating Nrf2 signaling. It might provide a new potential natural drug for the treatment of pulmonary fibrosis.

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“…In the study, TJ-19 was administered orally twice a day at a dose of 1.5 g/kg after intratracheal instillation of a single dose of BLM (5 mg/kg) in rats. TJ-19 treatment could prevent BLM-induced fibrotic changes in the lung histology, attenuate the loss in body weight, and increase in lung index and concentration of Hyp and MDA in the lungs induced by BLM (Yang et al, 2010). Above effects were observed when TJ-19 administration was started 1 week before and simultaneously with the instillation of BLM.…”

Section: In Vivomentioning

confidence: 92%

“…The ethical Kampo formulation Sho-seiryu-to (TJ-19), a traditional medicine used throughout south-east Asia, is a mixture of eight herbal components (Table 3). Yang and partners identified the constituents of TJ-19 including liquiritin and glycyrrhizin (originating from Glycyrrhiza Root), paeoniflorin and albiflorin (Paeony Root), schizandrin (Schisandra Fruit), cinnamic aldehyde and cinnamic acid (Cinnamon Bark) and 6-gingerol (Ginger Rhizome) by three-dimensional HPLC analysis (Yang et al, 2010). In the study, TJ-19 was administered orally twice a day at a dose of 1.5 g/kg after intratracheal instillation of a single dose of BLM (5 mg/kg) in rats.…”

Section: In Vivomentioning

confidence: 99%

Traditional Chinese medicine for pulmonary fibrosis therapy: Progress and future prospects

Kan

2017

Journal of Ethnopharmacology

109

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These research work have shown the therapeutic benefits of TCM in the treatment of PF. However, more continued researches should be undertaken to clarify the unconfirmed chemical composition and regulatory mechanisms, conduct standard clinical trials, and evaluate the possible side effects. The insights provided in present review will be needed for further exploration of botanical drugs in the development of PF therapy.

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The Ethical Kampo Formulation Sho-Seiryu-To (TJ-19) Prevents Bleomycin-Induced Pulmonary Fibrosis in Rats

Cited by 10 publications

References 24 publications

So-Cheong-Ryoung-Tang Attenuates Pulmonary Inflammation Induced by Cigarette Smoke in Bronchial Epithelial Cells and Experimental Mice

So-Cheong-Ryoung-Tang Attenuates Pulmonary Inflammation Induced by Cigarette Smoke in Bronchial Epithelial Cells and Experimental Mice

A Chinese Herbal Formula Ameliorates Pulmonary Fibrosis by Inhibiting Oxidative Stress via Upregulating Nrf2

Traditional Chinese medicine for pulmonary fibrosis therapy: Progress and future prospects

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