Effects of Sodium Houttuyfonate on Pulmonary Inflammation in COPD Model Rats

Wu, Zhiyong; Tan, Bo; Zhang, Haiying; Guo, Yinuo; Tu, Yan-Jie; Qiu, Furong; Yang, Aidong

doi:10.1007/s10753-017-0650-1

Cited by 28 publications

(17 citation statements)

References 23 publications

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“…H. cordata is a classical Chinese herb used in traditional Chinese medicine for inflammatory diseases, such as pneumonia. Recently, SH, which was a pure compound extracted from H. cordata , has been found exerting anti-inflammatory and anti-fibrotic effects on animal and cell models of various diseases ( Gao et al, 2010 ; Du et al, 2012 ; Kang and Koppula, 2014a , 2015 ; Xu et al, 2015 ; Zhu et al, 2015 ; Wu et al, 2017 ). On LPS-induced bovine endometrial epithelial cell inflammation, SH treatment significantly decreased the expression of pro-inflammatory cytokines and alleviated the inflammatory process.…”

Section: Discussionmentioning

confidence: 99%

“…Sodium Houttuyfonate (SH), which was a pure compound extracted from a Chinese herb Houttuynia cordata , has shown potent anti-inflammatory and anti-fibrotic activities on various animal and cell models of diseases, like lipopolysaccharide (LPS)-induced acute lung injury (ALI), LPS-induced bovine endometrial epithelial cell inflammation, smoking-induced chronic obstructive pulmonary disease (COPD), ventricular remodeling induced by abdominal aortic banding and so on ( Gao et al, 2010 ; Du et al, 2012 ; Kang and Koppula, 2014a , 2015 ; Xu et al, 2015 ; Zhu et al, 2015 ; Wu et al, 2017 ). Based on these findings, we doubted whether SH with an inherent anti-inflammatory and anti-fibrotic potency, could ameliorate post-infarct cardiac remodeling and heart failure.…”

Section: Introductionmentioning

confidence: 99%

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Sodium Houttuyfonate Alleviates Post-infarct Remodeling in Rats via AMP-Activated Protein Kinase Pathway

Cheng

Lin

et al. 2018

Front. Pharmacol.

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With the chronic ischemia persisting after acute myocardial infarction, the accompanying low-degree inflammation and subsequent fibrosis result in progression of cardiac remodeling and heart failure. Recently, Sodium Houttuyfonate (SH), a pure compound extracted from Houttuynia cordata, has been confirmed exerting anti-inflammatory and anti-fibrotic effects under diseased situations. Here, we aimed to investigate whether SH could reverse the cardiac remodeling post-myocardial infarction by alleviating cardiac inflammation and fibrosis. Left anterior descending coronary artery of adult male Sprague-Dawley rats was ligated to elicit myocardial infarction. Low and high dose of SH was administered by oral gavage for four consecutive weeks post-myocardial infarction. Long-term SH treatment decreased heart rate, heart weight/ body weight (HW/BW), and left ventricle weight/body weight (LVW/BW), reduced cardiac expression of brain natriuretic peptide (BNP), improved left ventricular heart function, and ameliorated the histopathological changes caused by myocardial infarction. Western blotting revealed the expression of tumor necrosis factor-α (TNF-α), interleukin-6 (IL-6), transforming growth factor-β (TGF-β), collagen I, and collagen III of the infarcted ventricle were reduced by SH treatment. Meanwhile, we found that SH treatment post-myocardial infarction activated AMP-activated protein kinase (AMPK) and suppressed nuclear factor-κB p65 (NF-κB p65). Furthermore, on H9C2 cells induced hypoxic injury with cobalt chloride (CoCl2), the reduction of inflammatory cytokines (IL-6, TNF-α, and TGF-β), activation of AMPK, and suppression of NF-κB p65 were also observed by SH treatment. However, transfection of H9C2 with AMPKα siRNA blunted the suppression of NF-κB p65 and inflammatory cytokines (IL-6, TNF-α, and TGF-β) by SH post-hypoxia. Taken together, these findings suggested that long-term administration of SH post-myocardial infarction reduced cardiac inflammatory and fibrotic responses, and reversed cardiac remodeling process. The underlying mechanism may be activating AMPK and suppressing NF-κB pathway.

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Section: Discussionmentioning

confidence: 99%

Section: Introductionmentioning

confidence: 99%

Sodium Houttuyfonate Alleviates Post-infarct Remodeling in Rats via AMP-Activated Protein Kinase Pathway

Cheng

Lin

et al. 2018

Front. Pharmacol.

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“…Sodium houttuyfonate (SH) ( Fig. 1) is one of the main compounds in the volatile oil of Houttuynia cordata Thunb., which has been used as an anti-pyretic and detoxicated herbal medicine for the therapy of infections for an extensive period of time (15,16). The effects of SH on diabetic nephropathy and glomerulonephritis have been reported in experimental animals (17,18).…”

Section: Introductionmentioning

confidence: 99%

Sodium houttuyfonate inhibits LPS‑induced mastitis in mice via the NF‑κB signalling pathway

et al. 2019

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Sodium houttuyfonate (SH) has been indicated to play an important anti-inflammatory role. Previous studies have confirmed that SH can inhibit the NF-κB pathway in lipopolysaccharide (LPS)-induced mastitis in bovine mammary epithelial cells. However, the effects of SH on LPS-induced mastitis in animals should be verified to further evaluate its actual value. In the present study, the anti-inflammatory effects of SH were investigated in mouse models and a mouse mammary epithelial cell line. Hematoxylin and eosin staining (H&E) showed that SH therapy significantly alleviated the pathological changes in mammary glands. Myeloperoxidase (MPO) activity analysis demonstrated that SH substantially decreased MPO activity in vivo. RT-qPCR results showed that SH reduced the expression of interleukin (IL)-1, IL-6 and tumor necrosis factor α both in vivo and in vitro. In addition, western blot results indicated that SH suppressed the phosphorylation of nuclear factor kappa-light-chain-enhancer of activated B-cells (NF-κB) p65 protein and reduced the degradation of inhibitor of kappa light polypeptide gene enhancer in B-cells alpha protein in vivo and in vitro. These results demonstrated that SH ameliorates LPS-induced mastitis by inhibiting the NF-κB pathway.

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“…Several studies highlight the role of TLR4/NF-κB signaling in the in ammatory lung diseases, such as asthma and COPD [28,29]. We found that exposure to CSE signi cantly induced the activation of TLR4/NF-κB signaling pathway in 16HBE cells.…”

Section: Discussionmentioning

confidence: 60%

Sappanone A inhibits oxidative stress, inflammation and apoptosis in cigarette smoke-induced human bronchial epithelial cells through regulating Nrf2/HO-1 and TLR4/NF-κB signaling pathways

Zhang¹,

Wang²,

Liu³

et al. 2020

Preprint

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Chronic obstructive pulmonary disease (COPD) is a common respiratory disease associated with inflammation and oxidative stress. Sappanone A (SA) is a homoisoflavanone that has been proven to have anti-inflammatory and anti-oxidant effects. However, the role of SA in COPD remains unclear. Thus, the present study was aimed to evaluate the beneficial effect of SA on COPD in vitro. The human bronchial epithelial cells were exposed to 5% cigarette smoke extracts (CSE) to induce an in vitro model of COPD. Our results showed that SA treatment significantly attenuated the CSE-caused induction of ROS and reduction of SOD and GPx activities in 16HBE cells. In addition, SA inhibited the production of inflammatory cytokines IL-6, IFN-γ, and TNF-α in CSE-stimulated 16HBE cells. Moreover, the CSE-stimulated cell apoptosis of 16HBE cells were abrogated by SA. Furthermore, we observed that SA treatment greatly promoted the activation of Nrf2/HO-1 signaling pathway, as well as inhibited the activation of TLR4/NF-κB signaling pathway in CSE-stimulated 16HBE cells. Subsequent rescue assay revealed that the protective effects of SA on CSE-stimulated 16HBE cells were reversed by Nrf2 knockdown or TLR4 overexpression. Taken together, these findings demonstrated that SA inhibits oxidative stress, inflammation and apoptosis in CSE-induced human bronchial epithelial cells through regulating Nrf2/HO-1 and TLR4/NF-κB signaling pathways.

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Effects of Sodium Houttuyfonate on Pulmonary Inflammation in COPD Model Rats

Cited by 28 publications

References 23 publications

Sodium Houttuyfonate Alleviates Post-infarct Remodeling in Rats via AMP-Activated Protein Kinase Pathway

Sodium Houttuyfonate Alleviates Post-infarct Remodeling in Rats via AMP-Activated Protein Kinase Pathway

Sodium houttuyfonate inhibits LPS‑induced mastitis in mice via the NF‑κB signalling pathway

Sappanone A inhibits oxidative stress, inflammation and apoptosis in cigarette smoke-induced human bronchial epithelial cells through regulating Nrf2/HO-1 and TLR4/NF-κB signaling pathways

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