Hydroxysafflor yellow A ameliorates lipopolysaccharide-induced acute lung injury in mice via modulating toll-like receptor 4 signaling pathways

Liu, Yali; Liu, Yajuan; Liu, Yang; Li, Xuesong; Liu, Shuan-Hu; Yingjie, Pan; Zhang, Jian; Liu, Qiang; Hao, Ying-Yan

doi:10.1016/j.intimp.2014.10.018

Cited by 54 publications

(34 citation statements)

References 37 publications

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“…HSYA is the major active chemical component of yellow color pigments extracted from safflower; it was demonstrated to have potent antioxidative and neuroprotective effects in vitro and in vivo [29, 43]. Recent studies revealed that in rats, HSYA can alleviate lipopolysaccharide-induced lung injury [19] and ischemia-reperfusion-induced brain injury by inhibiting inflammatory responses [25]. Studies also reported that HSYA protects human umbilical vein endothelial cells against hypoxic injury by inhibiting cell apoptosis [44, 45].…”

Section: Discussionmentioning

confidence: 99%

“…Studies showed that HSYA plays a protective role in animal models of pulmonary inflammatory injury [19, 20], cardiac failure [21, 22], and liver fibrosis [23, 24]. HSYA features extreme neuroprotection in animal models of acute and chronic central nervous system (CNS) injuries, including spinal cord ischemia, ischemia-reperfusion injury [17, 25, 26], and Parkinson’s disease [27].…”

Section: Introductionmentioning

confidence: 99%

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HSYA alleviates secondary neuronal death through attenuating oxidative stress, inflammatory response, and neural apoptosis in SD rat spinal cord compression injury

Pei¹,

Fan²,

Nan³

et al. 2017

J Neuroinflammation

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BackgroundHydroxysafflor yellow A (HSYA) is a major active component of yellow pigment extracted from safflowers; this compound possesses potent neuroprotective effects both in vitro and in vivo. However, underlying mechanism of HSYA is not fully elucidated. The present study investigated the protective effects of HSYA in rat spinal cord compression injury model and related mechanisms involved.MethodsSprague–Dawley rats were divided as Sham, Control, and HSYA groups (n = 30 per group). Spinal cord injury (SCI) model was induced by application of vascular clips (force of 50 g, 1 min) to the dura at T9–T10 level of vertebra. Injured animals were administered with either HSYA (8 mg/kg at 1 and 6 h after injury, then 14 mg/kg, for a total of 7 days at 24-h time intervals) or equal volume of saline by intraperitoneal injection.ResultsFrom this experiment, we discovered that SCI in rats resulted in severe trauma, which is characterized by tissue damage, lipid peroxidation, neutrophil infiltration, inflammation mediator release, and neuronal apoptosis. However, HSYA treatment significantly reduced the following: (1) degree of tissue injury (histological score) and edema; (2) neutrophil infiltration (myeloperoxidase activity); (3) oxidative stress (superoxide dismutase, malondialdehyde, and nitric oxide); (4) pro-inflammatory cytokine expression (tumor necrosis factor-α, interleukin-6, inducible nitric oxide synthase, cyclooxygenase-2); (5) nuclear factor-κB activation; (6) apoptosis (terminal deoxynucleotidyl transferase dUTP nick end labeling staining and cysteine-aspartic protease-3 activity). Moreover, in a separate set of experiments, we clearly demonstrated that HSYA treatment significantly ameliorated recovery of limb function (as evaluated by Basso, Beattie, and Bresnahan behavioral recovery scores).ConclusionsTreatment with HSYA restrains development of oxidative stress, inflammation response, and apoptotic events associated with SCI of rats, demonstrating that HSYA is a potential neuroprotectant for human SCI therapy.

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Section: Discussionmentioning

confidence: 99%

Section: Introductionmentioning

confidence: 99%

HSYA alleviates secondary neuronal death through attenuating oxidative stress, inflammatory response, and neural apoptosis in SD rat spinal cord compression injury

Pei¹,

Fan²,

Nan³

et al. 2017

J Neuroinflammation

View full text Add to dashboard Cite

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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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“…LPS is known to induce the production of several inflammatory and chemotactic cytokines [27]. TNF-α and IL-6 are characterized cytokines involved in the inflammatory process of ALI [28,29]. These cytokines, as well as other pro-inflammatory compounds, participate in the initiation, amplification and perpetuation of the inflammatory response in ALI.…”

Section: Discussionmentioning

confidence: 99%

Platycodin D attenuates acute lung injury by suppressing apoptosis and inflammation in vivo and in vitro

Tao

Wang

et al. 2015

International Immunopharmacology

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Hydroxysafflor yellow A ameliorates lipopolysaccharide-induced acute lung injury in mice via modulating toll-like receptor 4 signaling pathways

Cited by 54 publications

References 37 publications

HSYA alleviates secondary neuronal death through attenuating oxidative stress, inflammatory response, and neural apoptosis in SD rat spinal cord compression injury

HSYA alleviates secondary neuronal death through attenuating oxidative stress, inflammatory response, and neural apoptosis in SD rat spinal cord compression injury

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

Platycodin D attenuates acute lung injury by suppressing apoptosis and inflammation in vivo and in vitro

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