Hydroxysafflor yellow A suppress oleic acid-induced acute lung injury via protein kinase A

Wang, Chaoyun; Huang, Qing; Wang, Chunhua; Zhu, Xiaoxi; YunFeng, Duan; Yuan, Shuai; Bai, Xianyong

doi:10.1016/j.taap.2013.07.021

Cited by 18 publications

(13 citation statements)

References 46 publications

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“…It is reported that lung oxidative stress injury was aggravated in ALI [11–13]. Our results showed that the activity of SOD and GSH-Px was significantly decreased while the content of MDA was significantly increased in ALI, indicating that the traumatic ALI can lead to lung oxidative stress reaction.…”

Section: Discussionsupporting

confidence: 48%

Low Molecular Weight Heparin Nebulization Attenuates Acute Lung Injury

Xie

Huan

Tian

et al. 2017

BioMed Research International

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Background As acute lung injury (ALI) caused high mortality rate, it is important to explore the protection and treatment of ALI. The aim of the current study is to evaluate the effect of low molecular weight heparin (LMWH) nebulization on attenuating acute lung injury and the associated mechanism. Methods The arterial blood gas, total protein content in bronchoalveolar lavage fluid, lung wet/dry weight ratio, malondialdehyde (MDA) content, superoxide dismutase (SOD) and glutathione peroxidase (GSH-Px) activity, and Akt phosphorylation were evaluated after the ALI rabbits were treated with or without LMWH nebulization. Results PaO2 was increased and lung wet/dry weight ratio as well as total protein content in BALF was decreased after LMWH nebulization. After the application of LMWH nebulization therapy, the SOD and GSH-Px activity was rebounded and the increase of MDA content was significantly inhibited. The Akt protein phosphorylation level was decreased after LMWH nebulization therapy. Conclusions LMWH nebulization treatment can relieve the traumatic ALI in rabbits and inhibit oxidative stress possibly by suppressing the Akt phosphorylation.

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Section: Discussionsupporting

confidence: 48%

Low Molecular Weight Heparin Nebulization Attenuates Acute Lung Injury

Xie

Huan

Tian

et al. 2017

BioMed Research International

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“…HSYA could alleviate pulmonary edema, reduce acidosis, increase partial pressure of oxygen (PaO 2 ), and inhibit inflammatory cell infiltration, lung mRNA expressions of TNF- α and ICAM-1, and levels of plasma IL-6 and IL-1 β [ 73 ]. HSYA significantly increased the activities of antioxidant enzymes, inhibited the inflammatory response via the cAMP/PKA pathway activation, and attenuated OA-induced lung injury [ 74 ]. Additionally, HSYA decreased lung permeability, platelet count, and ADP-mediated platelet aggregation as well as cytokine levels in serum and BALF in the aged rats with gasoline engine-induced lung injury.…”

Section: Pharmacologymentioning

confidence: 99%

Hydroxysafflor Yellow A: A Promising Therapeutic Agent for a Broad Spectrum of Diseases

Feng

Peng

2018

Evidence-Based Complementary and Alternative Medicine

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Hydroxysafflor yellow A (HSYA) is one of the major bioactive and water-soluble compounds isolated from Carthami Flos, the flower of safflower (Carthamus tinctorius L.). As a natural pigment with favorable medical use, HSYA has gained extensive attention due to broad and effective pharmacological activities since first isolation in 1993. In clinic, the safflor yellow injection which mainly contains about 80% HSYA was approved by the China State Food and Drug Administration and used to treat cardiac diseases such as angina pectoris. In basic pharmacology, HSYA has been proved to exhibit a broad spectrum of biological effects that include, but not limited to, cardiovascular effect, neuroprotection, liver and lung protection, antitumor activity, metabolism regulation, and endothelium cell protection. Although a great number of studies have been carried out to prove the pharmacological effects and corresponding mechanisms of HYSA, a systemic review of HYSA has not yet been seen. Here, we provide a comprehensive summarization of the pharmacological effects of HYSA. Together with special attention to mechanisms of actions, this review can serve as the basis for further researches and developments of this medicinal compound.

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“…It has been shown to effectively reduce oxidative stress-mediated damage [21,22]. A study by Wang et al demonstrated that HSYA significantly increases antioxidant enzyme activity by activating the cAMP/PKA signaling pathway [23]. SYB (Figure 1(a)) is a yellow amorphous powder with a purity of more than 98% by HPLC, and it is water soluble and has demonstrated protective effects in neuronal injury models induced by oxidative stress [24,25].…”

Section: Introductionmentioning

confidence: 99%

Safflor Yellow B Attenuates Ischemic Brain Injury via Downregulation of Long Noncoding AK046177 and Inhibition of MicroRNA-134 Expression in Rats

Wang

Wan

Wang

et al. 2020

Oxidative Medicine and Cellular Longevity

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Stroke breaks the oxidative balance in the body and causes extra reactive oxygen species (ROS) generation, leading to oxidative stress damage. Long noncoding RNAs (lncRNAs) and microRNAs play pivotal roles in oxidative stress-mediated brain injury. Safflor yellow B (SYB) was able to effectively reduce ischemia-mediated brain damage by increasing antioxidant capacity and inhibiting cell apoptosis. In this study, we investigated the putative involvement of lncRNA AK046177 and microRNA-134 (miR-134) regulation in SYB against ischemia/reperfusion- (I/R-) induced neuronal injury. I/R and oxygen-glucose deprivation/reoxygenation (OGD/R) were established in vivo and in vitro. Cerebral infarct volume, neuronal apoptosis, and protein expression were detected. The effects of SYB on cell activity, cell respiration, nuclear factor erythroid 2-related factor 2 (Nrf2), antioxidant enzymes, and ROS were evaluated. I/R or OGD/R upregulated the expression of AK046177 and miR-134 and subsequently inhibited the activation and expression of CREB, which caused ROS generation and brain/cell injury. SYB attenuated the effects of AK046177, inhibited miR-134 expression, and promoted CREB activation, which in turn promoted Nrf2 expression, and then increased antioxidant capacities, improved cell respiration, and reduced apoptosis. We suggested that the antioxidant effects of SYB were driven by an AK046177/miR-134/CREB-dependent mechanism that inhibited this pathway, and that SYB has potential use in reducing or possibly preventing I/R-induced neuronal injury.

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Hydroxysafflor yellow A suppress oleic acid-induced acute lung injury via protein kinase A

Cited by 18 publications

References 46 publications

Low Molecular Weight Heparin Nebulization Attenuates Acute Lung Injury

Low Molecular Weight Heparin Nebulization Attenuates Acute Lung Injury

Hydroxysafflor Yellow A: A Promising Therapeutic Agent for a Broad Spectrum of Diseases

Safflor Yellow B Attenuates Ischemic Brain Injury via Downregulation of Long Noncoding AK046177 and Inhibition of MicroRNA-134 Expression in Rats

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