Hydroxysafflor yellow a inhibits lipopolysaccharide-induced inflammatory signal transduction in human alveolar epithelial A549 cells

Song, Lijuan; Zhu, Yu; Jin, Ming; Zang, Baoxia

doi:10.1016/j.fitote.2012.11.004

Cited by 44 publications

(30 citation statements)

References 31 publications

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“…32) We have found that HSYA effectively inhibited LPSinduced inflammatory signal transduction in A549 cells by suppressing the expression of TLR-4, TNFα, IL-1β and IL-6 and by inhibiting the phosphorylation of p38 MAPK. 33) In this study, we found that p38 MAPK was activated in the lung of the COPD groups, which was also found by Marwick.…”

Section: Disscusionsupporting

confidence: 84%

Hydroxysafflor Yellow A Attenuates Small Airway Remodeling in a Rat Model of Chronic Obstructive Pulmonary Disease

Wang

Xue

Dong

et al. 2014

Biological & Pharmaceutical Bulletin

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Our previous studies found that hydroxysafflor yellow A (HSYA), an active ingredient in Carthamus tinctorius L., has anti-inflammatory and anti-fibrosis properties. In this study, we investigated the effect of HSYA on small airway remodeling (SAR) in a chronic obstructive pulmonary disease (COPD) rat model induced by cigarette smoke and lipopolysaccharide (LPS). SAR is a common lesion in COPD characterized by thickening of the airway wall, mainly by subepithelial fibrosis. In this study the thickness of the small airway was determined by total wall area/basement membrane perimeter (WAt/Pbm). Collagen deposition of the small airway was assessed by Masson's trichrome staining. HSYA significantly attenuated the thickening and collagen deposition of the small airway and inhibited transforming growth factor β1 (TGF-β1) mRNA and protein expression in COPD rat. In addition, HSYA inhibited the phosphorylation of p38 mitogen-activated protein kinases (MAPK) in the lung tissue of rat. HSYA can attenuate experimentally induced airway remodeling and this attenuation may be attributed to suppression of TGF-β1 expression.Key words hydroxysafflor yellow A; airway remodeling; transforming growth factor-β1; p38 mitogen-activated protein kinase (MAPK); chronic obstructive pulmonary disease (COPD)Chronic obstructive pulmonary disease (COPD), characterized by airflow limitation that is progressive and persistent, is a leading cause of death worldwide.1) Cigarette smoking and bacterial infection have been widely recognized as the main causes of COPD.2,3) The main pathological changes of the lung from COPD are emphysema and small airway remodeling (SAR).4) SAR, characterized by subepithelial fibrosis, goblet cell metaplasia and excessive mucus production, is now accepted as an important cause of airflow obstruction in COPD.5) No ideal medication has been able to effectively reverse the airway remodeling. Therefore the development of novel medications for the prevention of airway remodeling in COPD is urgently needed.More recently, the role of transforming growth factor β1 (TGF-β1) in the pathogenesis of SAR in COPD has attracted more interests, particularly since genetic studies have demonstrated gene polymorphisms of the TGF-β superfamily is associated with COPD. TGF-β1 is ubiquitously expressed and is secreted by many lung cell types including airway epithelial cells, vascular endothelial cells, smooth muscle cells, fibroblasts and inflammatory cells. 6)TGF-β1 can increase deposition of extracellular matrix in the airways and can stimulate lung fibroblast differentiating into myofibroblast.7) It has been reported that intratracheal instillation of TGF-β1 in mice leads to airway remodeling with peribronchiolar collagen deposition and basal membrane thickening. 8) Thus, it seems reasonable to hypothesize that targeting the TGF-β1 expression may provide a novel therapeutic method for attenuating SAR in COPD.Safflower is the dry flower of Carthamus tinctorius L. and naturally distributed around the world.9) It has been used extensively...

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Section: Disscusionsupporting

confidence: 84%

Hydroxysafflor Yellow A Attenuates Small Airway Remodeling in a Rat Model of Chronic Obstructive Pulmonary Disease

Wang

Xue

Dong

et al. 2014

Biological & Pharmaceutical Bulletin

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“…p38 MAPK is involved in the regulation of proinflammatory cytokines such as TGF-b1 and TNF-a, and exhibits an inverse relationship with hepatocyte proliferation (Awad et al, 2000;Goldstein et al, 2010). Previous studies have demonstrated that the protective effect of HSYA against LPS-induced acute lung injury was associated with the significant inhibition of p38 MAPK phosphorylation in vitro and in vivo (Song et al, 2013;Sun et al, 2010). He et al (2008) revealed that the non-receptor tyrosine phosphatase Shp2 promotes adipogenesis through the Shp2-p38MAPK-p300-PPARg signaling pathway, by inhibiting the phosphorylation of p38 MAPK and enhancing PPAR-g expression.…”

Section: Discussionmentioning

confidence: 99%

Hydroxysafflor yellow A suppresses liver fibrosis induced by carbon tetrachloride with high-fat diet by regulating PPAR-γ/p38 MAPK signaling

Liu

Wang

Liu

et al. 2014

Pharmaceutical Biology

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Context: One approach to protect against liver fibrosis is the use of herb-derived natural compounds, such as hydroxysafflor yellow A (HSYA). The antifibrosis effect of HYSA against liver fibrosis has been investigated; however, its mechanisms have not yet been entirely revealed. Objectives: To study the protective effects of HSYA on liver fibrosis induced by carbon tetrachloride (CCl 4 ) and a high-fat diet (HFD), and to determine the mechanism of action of HSYA. Materials and methods: CCl 4 and HFD were used to mimic liver fibrosis in rats, and serum biochemical indicators were determined. The antifibrosis effects of HSYA were evaluated and its mechanisms were investigated by histopathological analysis, immunohistochemical staining, enzyme-linked immunosorbent assays, real-time-PCR, and western blotting. Results: HSYA reduced CCl 4 -and HFD-mediated liver fibrosis and ameliorated serum biochemical indicator, downregulated the expression of tissue inhibitor of metalloproteinase-1 (TIMP-1) (0.31 ± 0.03 protein, 0.59 ± 0.02 mRNA) and transformin growth factor-b1 (TGF-b1) (0.81 ± 0.02 protein, 0.58 ± 0.04 mRNA), and upregulated the expression of peroxisome proliferator-activated receptor-g (PPAR-g) (1.57 ± 0.13 protein, 2.48 ± 0.19 mRNA) and matrix metallopeptidases-2 (MMP-2) (2.31 ± 0.16 protein, 2.79 ± 0.22 mRNA) (p50.01, versus model group). These effects were significantly attenuated by PPAR-g antagonist GW9662 via blocking the phosphorylation of p38 MAPK. Discussion and conclusion: These data demonstrate a novel role for HSYA in inhibiting CCl 4 -and HFD-mediated liver fibrosis, and reveal that PPAR-g and p38 MAPK signaling play pivotal roles in the prevention of liver fibrosis induced by CCl 4 and HFD.

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“…18 Human epithelial cell strain A549 has been stimulated by LPS to activate the TLR4/ Myd88/NF-κB inflammatory pathway, while HYSA also reduces TLR4 expression on mRNA and protein levels. 19 In many CNS disorders, microglia are the cells principally responsible for the development of a neuroinflammatory microenvironment. Inhibition of the microglial inflammatory pathway is therefore of primary importance for improving the neuroinflammatory microenvironment, reducing neuronal injury, and promoting tissue regeneration and repair in the CNS.…”

Section: Safflower Yellow Regulates Microglial Polarization and Inhibmentioning

confidence: 99%

Safflower Yellow regulates microglial polarization and inhibits inflammatory response in LPS-stimulated Bv2 cells

Yang

Zhang

et al. 2015

Int J Immunopathol Pharmacol

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Activated microglia, especially polarized M1 cells, produce pro-inflammatory cytokines and free radicals, thereby contributing directly to neuroinflammation and various brain disorders. Given that excessive or chronic neuroinflammation within the central nervous system (CNS) exacerbates neuronal damage, molecules that modulate neuroinflammation are candidates as neuroprotective agents. In this study, we provide evidence that Safflor yellow (SY), the main active component in the traditional Chinese medicine safflower, modulates inflammatory responses by acting directly on BV2 microglia. LPS stimulated BV2 cells to upregulate expression of TLR4-Myd88 and MAPK-NF-κB signaling pathways and to release IL-1β, IL-6, TNF-α, and COX-2. However, SY treatment inhibited expression of TLR4-Myd88 and p-38/p-JNK-NF-κB, downregulated expression of iNOS, CD16/32, and IL-12, and upregulated CD206 and IL-10. In conclusion, our results demonstrate that SY exerts an anti-inflammatory effect on BV2 microglia, possibly through TLR-4/p-38/p-JNK/ NF-κB signaling pathways and the conversion of microglia from inflammatory M1 to an anti-inflammatory M2 phenotype.

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Hydroxysafflor yellow a inhibits lipopolysaccharide-induced inflammatory signal transduction in human alveolar epithelial A549 cells

Cited by 44 publications

References 31 publications

Hydroxysafflor Yellow A Attenuates Small Airway Remodeling in a Rat Model of Chronic Obstructive Pulmonary Disease

Hydroxysafflor Yellow A Attenuates Small Airway Remodeling in a Rat Model of Chronic Obstructive Pulmonary Disease

Hydroxysafflor yellow A suppresses liver fibrosis induced by carbon tetrachloride with high-fat diet by regulating PPAR-γ/p38 MAPK signaling

Safflower Yellow regulates microglial polarization and inhibits inflammatory response in LPS-stimulated Bv2 cells

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