Botanical formulation, TADIOS, alleviates lipopolysaccharide (LPS)-Induced acute lung injury in mice via modulation of the Nrf2-HO-1 signaling pathway

Lee, Wonwoo; Lee, Chang Hyung; Lee, Jung‐Kyu; Jeong, Yoonseon; Park, Jong Hyung; Nam, In Jeong; Lee, Doo Suk; Lee, Hyun Myung; Lee, Jae-Hyun; Yun, Na-Ra; Song, Jisun; Choi, Se‐Young; Kim, Sun‐Young

doi:10.1016/j.jep.2021.113795

Cited by 23 publications

(21 citation statements)

References 64 publications

(42 reference statements)

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“…Daidzein (100 μM,), a diphenolic isoflavone 15 min after LPS stimulation, obviously inhibited the expressions of myeloid differentiation factor 88 (MyD88), toll-like receptor 4 (TLR4), and the activation of NF-κB in the A549 alveolar epithelial cells stimulated by 10 μg/ml LPS ( 56 ). In the RAW264.7 cells, treatment with a mixture of Taraxacum officinale (a herbal formulation) (0.5, 1, and 2 mg/mL), repressed the LPS (100 ng/mL)-induced inflammatory responses ( 57 ). Also, the expression of pro-inflammatory cytokines activated the Nrf2-HO-1 axis and oxidative stress was inhibited in the treated LPS-stimulated cells ( 57 ).…”

Section: Resultsmentioning

confidence: 99%

“…In the RAW264.7 cells, treatment with a mixture of Taraxacum officinale (a herbal formulation) (0.5, 1, and 2 mg/mL), repressed the LPS (100 ng/mL)-induced inflammatory responses ( 57 ). Also, the expression of pro-inflammatory cytokines activated the Nrf2-HO-1 axis and oxidative stress was inhibited in the treated LPS-stimulated cells ( 57 ).…”

Section: Resultsmentioning

confidence: 99%

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Experimental and Clinical Studies on the Effects of Natural Products on Noxious Agents-Induced Lung Disorders, a Review

et al. 2022

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The harmful effects of various noxious agents (NA) are well-known and there are reports regarding the induction of various lung disorders due to exposure to these agents both in animal and human studies. In addition, various studies have shown the effects of natural products (NP) on NA-induced lung disorders. The effects of various NP, including medicinal plants and their derivatives, on lung injury induced by NA, were reviewed in this study. The improving effects of various NP including medicinal plants, such as Aloe vera, Anemarrhena asphodeloides, Avena sativa, Crocus sativus, Curcuma longa, Dioscorea batatas, Glycyrrhiza glabra, Gentiana veitchiorum, Gentiopicroside, Houttuynia cordata, Hibiscus sabdariffa, Hochu-ekki-to, Hippophae rhamnoides, Juglans regia, Melanocarpa fruit juice, Mikania glomerata, Mikania laevigata, Moringa oleifera, Myrtus communis L., Lamiaceae, Myrtle, Mosla scabra leaves, Nectandra leucantha, Nigella sativa, Origanum vulgare L, Pulicaria petiolaris, Paulownia tomentosa, Pomegranate seed oil, Raphanus sativus L. var niger, Rosa canina, Schizonepeta tenuifolia, Thymus vulgaris, Taraxacum mongolicum, Tribulus Terrestris, Telfairia occidentalis, Taraxacum officinale, TADIOS, Xuebijing, Viola yedoensis, Zataria multiflora, Zingiber officinale, Yin-Chiao-San, and their derivatives, on lung injury induced by NA were shown by their effects on lung inflammatory cells and mediators, oxidative stress markers, immune responses, and pathological changes in the experimental studies. Some clinical studies also showed the therapeutic effects of NP on respiratory symptoms, pulmonary function tests (PFT), and inflammatory markers. Therefore, the results of this study showed the possible therapeutic effects of various NP on NA-induced lung disorders by the amelioration of various features of lung injury. However, further clinical studies are needed to support the therapeutic effects of NP on NA-induced lung disorders for clinical practice purposes.

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Section: Resultsmentioning

confidence: 99%

Section: Resultsmentioning

confidence: 99%

Experimental and Clinical Studies on the Effects of Natural Products on Noxious Agents-Induced Lung Disorders, a Review

et al. 2022

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“…This Nrf2-induced anti-oxidative stress enzyme scavenges excessive ROS and inhibit inordinate inflammatory responses [ 26 ]. The research results of Lee et al suggested that Botanical formulation, TADIOS, could alleviate LPS-induced acute lung injury in mice via activation of the Nrf2-HO-1 signaling pathway [ 39 ]. By modulating Nrf2-mediated HO-1 signaling pathway, Baicalin suppressed oxidative stress and inflammation, thereby relieving LPS-induced acute lung injury in a mice model [ 40 ].…”

Section: Discussionmentioning

confidence: 99%

Ramelteon protects against human pulmonary microvascular endothelial cell injury induced by lipopolysaccharide (LPS) via activating nuclear factor erythroid 2-related factor 2 (Nrf2)/heme oxygenase-1 (HO-1) pathway

Yang

Zhang

et al. 2022

Bioengineered

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Acute lung injury (ALI) is classified as a moderate or mild acute respiratory distress syndrome and is a prominent cause of morbidity and mortality among the critically ill population. Ramelteon is a melatonin receptor agonist with anti-inflammatory and antioxidant effects. The current study investigated the role of ramelteon in lipopolysaccharide (LPS)-induced human pulmonary microvascular endothelial cells (HPMECs) and its potential regulatory mechanisms. A CCK-8 assay was used to examine the effect of ramelteon on the viability of LPS-induced HPMECs, HPMECs treated with ML385 [a Nrf2 inhibitor] and HPMECs treated with SnPP [a HO-1 inhibitor]. The Nrf2/HO-1 signaling pathway was additionally assessed by performing Western blotting. The levels of oxidative stress and inflammatory cytokines in HPMECs were detected using kits and reverse transcription-quantitative PCR. Cell apoptosis was evaluated via TUNEL staining. Furthermore, cell permeability was assessed using a FITC-dextran fluorescent probe, ZO-1 and occludin expression was determined via Western blotting. The results demonstrated that ramelteon elevated HPMEC viability after LPS stimulation. Additionally, ramelteon markedly reduced LPS-induced oxidative stress, inflammation and apoptosis. Moreover, cell permeability was notably decreased in ramelteon-treated groups and was accompanied by upregulated ZO-1 and occludin expression. Ramelteon treatment also activated the Nrf2/HO-1 signaling pathway in LPS-induced HPMECs. Furthermore, the addition of ML385 or SnPP reversed the protective effects of ramelteon on LPS-induced oxidative stress, inflammation, apoptosis and cell dysfunction in HPMECs. Collectively, the results suggested that ramelteon alleviated LPS-induced HPMEC damage by activating the Nrf2/HO-1 signaling pathway, making it an effective treatment for ALI.

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“…This suggests that oridonin not only has an antioxidant effect by increasing expression of Nrf2 via MAPK and Akt pathway but also has an anti-inflammatory effect by inhibiting NF-κB pathways independently of Nrf2 [47]. Several plant extracts, such as isorhapontigenin and TADIOS, have also been reported to activate Nrf2 in ARDS models [48,49]. In addition, small molecular compounds, such as cordycepin and syringin, caused Nrf2 activation in ARDS animal models [50][51][52].…”

Section: Ards/alimentioning

confidence: 99%

An Update on the Role of Nrf2 in Respiratory Disease: Molecular Mechanisms and Therapeutic Approaches

Lee

Jang

Park

et al. 2021

IJMS

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Nuclear factor erythroid 2-related factor (Nrf2) is a transcriptional activator of the cell protection gene that binds to the antioxidant response element (ARE). Therefore, Nrf2 protects cells and tissues from oxidative stress. Normally, Kelch-like ECH-associated protein 1 (Keap1) inhibits the activation of Nrf2 by binding to Nrf2 and contributes to Nrf2 break down by ubiquitin proteasomes. In moderate oxidative stress, Keap1 is inhibited, allowing Nrf2 to be translocated to the nucleus, which acts as an antioxidant. However, under unusually severe oxidative stress, the Keap1-Nrf2 mechanism becomes disrupted and results in cell and tissue damage. Oxide-containing atmospheric environment generally contributes to the development of respiratory diseases, possibly leading to the failure of the Keap1-Nrf2 pathway. Until now, several studies have identified changes in Keap1-Nrf2 signaling in models of respiratory diseases, such as acute respiratory distress syndrome (ARDS)/acute lung injury (ALI), chronic obstructive pulmonary disease (COPD), idiopathic pulmonary fibrosis (IPF), and asthma. These studies have confirmed that several Nrf2 activators can alleviate symptoms of respiratory diseases. Thus, this review describes how the expression of Keap1-Nrf2 functions in different respiratory diseases and explains the protective effects of reversing this expression.

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Botanical formulation, TADIOS, alleviates lipopolysaccharide (LPS)-Induced acute lung injury in mice via modulation of the Nrf2-HO-1 signaling pathway

Cited by 23 publications

References 64 publications

Experimental and Clinical Studies on the Effects of Natural Products on Noxious Agents-Induced Lung Disorders, a Review

Experimental and Clinical Studies on the Effects of Natural Products on Noxious Agents-Induced Lung Disorders, a Review

Ramelteon protects against human pulmonary microvascular endothelial cell injury induced by lipopolysaccharide (LPS) via activating nuclear factor erythroid 2-related factor 2 (Nrf2)/heme oxygenase-1 (HO-1) pathway

An Update on the Role of Nrf2 in Respiratory Disease: Molecular Mechanisms and Therapeutic Approaches

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