Inhibitory Effects of Hydroxysafflor Yellow A on the Formation of Advanced Glycation End Products &lt;i&gt;in Vitro&lt;/i&gt;

Ni, Zhenzhen; Zhuge, Zhengbing; Li, Wenlu; Xu, Huimin; Zhang, Zhongmiao; Dai, Haibin

doi:10.1248/bpb.b12-00249

Cited by 14 publications

(8 citation statements)

References 30 publications

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“…To gain further insight into the mechanism, the temporal changes in AGEs protein levels following MGO treatment were addressed. Our results demonstrated that AGEs accumulation significantly increased after 24 h MGO treatment which was consistent with our previous reports [12], [14]. Intriguingly, edaravone could decrease AGEs accumulation, which was known to impair cellular function by increasing cellular oxidative stress on binding to their specific cell surface receptors, such as RAGE and galectin-3 [22], [29].…”

Section: Discussionsupporting

confidence: 92%

“…BSA- MGO assay was adopted from previous report with some modification [14], which was used for investigation of inhibitors on the middle stage of the glycation of protein [15]. BSA (50 mg/ml) was incubated with MGO (100 mmol/l) under sterile, dark conditions in 0.1 mmol/l phosphate buffer (pH 7.4) at 37°C for 24 h in the presence or absence of various concentrations of the compounds.…”

Section: Methodsmentioning

confidence: 99%

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Edaravone Protected Human Brain Microvascular Endothelial Cells from Methylglyoxal-Induced Injury by Inhibiting AGEs/RAGE/Oxidative Stress

et al. 2013

PLoS ONE

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Subjects with diabetes experience an increased risk of cerebrovascular disease and stroke compared with nondiabetic age-matched individuals. Increased formation of reactive physiological dicarbonyl compound methylglyoxal (MGO) seems to be implicated in the development of diabetic vascular complication due to its protein glycation and oxidative stress effect. Edaravone, a novel radical scavenger, has been reported to display the advantageous effects on ischemic stroke both in animals and clinical trials; however, little is known about whether edaravone has protective effects on diabetic cerebrovascular injury. Using cultured human brain microvascular endothelial cells (HBMEC), protective effects of edaravone on MGO and MGO enhancing oxygen-glucose deprivation (OGD) induced injury were investigated. Cell injury was measured by 3-(4,5-Dimethylthiazol-2-yl)-2,5-diphenyltetrazolium bromide (MTT) formation, cell account, lactate dehydrogenase (LDH) release and Rhodamine 123 staining. Advanced glycation end-products (AGEs) formation and receptor for advanced glycation end-products (RAGE) expression were measured by western blotting. Cellular oxidative stress was measured by reactive oxygen species (ROS) release. Treatment of MGO for 24 h significantly induced HBMEC injury, which was inhibited by pretreatment of edaravone from 10–100 µmol/l. What’s more, treatment of MGO enhanced AGEs accumulation, RAGE expression and ROS release in the cultured HBMEC, which were inhibited by 100 µmol/l edaravone. Finally, treatment of MGO for 24 h and then followed by 3 h OGD insult significantly enhanced cell injury when compared with OGD insult only, which was also protected by 100 µmol/l edaravone. Thus, edaravone protected HBMEC from MGO and MGO enhancing OGD-induced injury by inhibiting AGEs/RAGE/oxidative stress.

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Section: Discussionsupporting

confidence: 92%

Section: Methodsmentioning

confidence: 99%

Edaravone Protected Human Brain Microvascular Endothelial Cells from Methylglyoxal-Induced Injury by Inhibiting AGEs/RAGE/Oxidative Stress

et al. 2013

PLoS ONE

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“…AGEs accumulation is one of the major pathways involved in the development of diabetic complications. Recently, hydroxysafflor yellow A and salvianolic acid A have been proved to inhibit the formation and accumulation of AGEs 42 43 . In the cultured mesangial cells, salvianolic acid B inhibits high glucose-induced mesangial cell proliferation and fibronectin secretion 44 45 .…”

Section: Discussionmentioning

confidence: 99%

Administration of Danhong Injection to diabetic db/db mice inhibits the development of diabetic retinopathy and nephropathy

Pan

Chen

et al. 2015

Sci Rep

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Danhong Injection (DHI), a Chinese medicine for treatment of patients with coronary heart disease, inhibits primary abdominal aortic aneurysms in apoE deficient (apoE−/−) mice. Formation of microaneurysms plays an important role in the development of diabetic retinopathy and nephropathy. It remains unknown if DHI can reduce these diabetic complications. In this study, diabetic db/db mice in two groups were injected with saline and DHI, respectively, for 14 weeks. Blood and tissue samples were collected to determine serum glucose, lipids and tissue structure. DHI reduced diabetes-induced body weight gain, serum cholesterol and glucose levels. In retinas, DHI blocked the shrink of whole retina and retinal sub-layers by inhibiting expression of caspase 3, matrix metalloproteinase 2 (MMP-2) and MMP-9, accumulation of carbohydrate macromolecules and formation of acellular capillaries. DHI improved renal functions by inhibiting mesangial matrix expansion, expression of vascular endothelial growth factor A, fibronectin and advanced glycation end products in kidneys. Mechanistically, DHI induced expression of glucokinase, AMPKα/phosphorylated AMPKα, insulin receptor substrate 1, fibroblast growth factor 21 and peroxisome proliferator-activated γ. Expression of genes responsible for energy expenditure was also activated by DHI. Therefore, DHI inhibits diabetic retinopathy and nephropathy by ameliorating glucose metabolism and demonstrates a potential application in clinics.

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“…Ni et al . [ 96 ] demonstrated that MGO-induced bovine serum albumin (BSA) glycation could be inhibited by HYSA. Besides, HSYA showed significantly inhibitory effect on glucose- (GLU-) induced development of AGEs formation and N -acetyl-glycyl-lysine methyl Ester (G.K.) peptide-mediated ribose glycation.…”

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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Inhibitory Effects of Hydroxysafflor Yellow A on the Formation of Advanced Glycation End Products <i>in Vitro</i>

Cited by 14 publications

References 30 publications

Edaravone Protected Human Brain Microvascular Endothelial Cells from Methylglyoxal-Induced Injury by Inhibiting AGEs/RAGE/Oxidative Stress

Edaravone Protected Human Brain Microvascular Endothelial Cells from Methylglyoxal-Induced Injury by Inhibiting AGEs/RAGE/Oxidative Stress

Administration of Danhong Injection to diabetic db/db mice inhibits the development of diabetic retinopathy and nephropathy

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

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