Hydroxysafflor Yellow A Alleviates Early Inflammatory Response of Bleomycin-Induced Mice Lung Injury

Wu, Yan; Wang, Lin; Jin, Ming; Zang, Baoxia

doi:10.1248/bpb.35.515

Cited by 51 publications

(31 citation statements)

References 26 publications

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“…HSYA is a water‐soluble monomeric constituent of SY and more than 90% in SY of this injection is HSYA. Many researchers have reported that HSYA inhibited LPS‐induced or BLM‐induced pulmonary inflammatory injury in mice . Because the inflammatory response is one of the important pathological mechanisms in pulmonary fibrosis, the anti‐inflammatory properties of HSYA may be beneficial for the treatment of fibrosis.…”

Section: Discussionmentioning

confidence: 99%

Hydroxysafflor yellow A inhibits TGF-β1-induced activation of human fetal lung fibroblastsin vitro

Pan

Zhang

Zang

et al. 2016

Journal of Pharmacy and Pharmacology

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Section: Discussionmentioning

confidence: 99%

Hydroxysafflor yellow A inhibits TGF-β1-induced activation of human fetal lung fibroblastsin vitro

Pan

Zhang

Zang

et al. 2016

Journal of Pharmacy and Pharmacology

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“…17,18 Studies have demonstrated that HSYA exhibits multiple biomedical activities, such as scavenging oxygen-free radicals, 19,20 reducing blood pressure and heart rate, 21 and producing anti-inflammatory activity. 22 Moreover, numerous research studies have also shown that HSYA exhibits neuroprotective effects against cerebral ischemia/reperfusion injuries, which are closely associated with the formation of ROS. 19,23,24 Although the protective effect of HSYA against ischemia is associated with its anti-oxidative activity, little experimental data extend to other disease conditions resulting from oxidative stress, for example, UV-induced photoaging.…”

Section: Introductionmentioning

confidence: 99%

Inhibitory Effect of Hydroxysafflor Yellow A on Mouse Skin Photoaging Induced by Ultraviolet Irradiation

Kong

Shi²,

Feng³

et al. 2013

Rejuvenation Research

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Chronic exposure to ultraviolet (UV) irradiation is believed to be the major cause of skin damage that results in premature aging of the skin, so called photoaging, characterized by increases in skin thickness, formation of wrinkles, and loss of skin elasticity. UV induces damage to skin mainly by oxidative stress and collagen degradation. In this study, we examined the photo-protective effect of hydroxysafflor yellow A (HSYA), a major active chemical component isolated from Carthamus tinctorius L., by topical application on the skin of mice. Exposure of the dorsal depilated skin of mice to UV radiation four times a week for 10 weeks induced epidermal hyperplasia, elastin accumulation, collagen degradation, etc. HSYA at the doses of 50, 100, and 200 lg/mouse was topically applied immediately following each UV exposure. The effects of HSYA were evaluated by a series of tests, including macroscopic and histopathological evaluation of skin, pinch test, and redox homeostasis of skin homogenates. Results showed that the UV-induced skin damage was significantly improved after HSYA treatment, especially at doses of 100 and 200 lg/mouse. This protective effect is possibly related to the antioxidative property of HSYA and mediated by promoting endogenous collagen synthesis. This is the first study providing preclinical evidence for the protective effect of HSYA against photoaging.

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“…Our previous study has shown that HSYA can alleviate lung inflammatory response induced by lipopolysaccharide (LPS) or bleomycin in mice and can attenuate the development of lung fibrosis induced by bleomycin in rats. [11][12][13] Additionally, it has also been reported that the aqueous extract of safflower could ameliorate unilateral ureteral obstruction-induced renal interstitial fibrosis by suppressing autocrine TGF-β1 14) and could protect against liver fibrosis by a decreased expression of TGF-β1. 15) Fibrogenesis is an important hallmark of SAR in lung of COPD.…”

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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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Hydroxysafflor Yellow A Alleviates Early Inflammatory Response of Bleomycin-Induced Mice Lung Injury

Cited by 51 publications

References 26 publications

Hydroxysafflor yellow A inhibits TGF-β1-induced activation of human fetal lung fibroblastsin vitro

Hydroxysafflor yellow A inhibits TGF-β1-induced activation of human fetal lung fibroblastsin vitro

Inhibitory Effect of Hydroxysafflor Yellow A on Mouse Skin Photoaging Induced by Ultraviolet Irradiation

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

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