Curculigoside attenuates human umbilical vein endothelial cell injury induced by H2O2

Wang, Yun Kai; Hong, Ya; Mao, Wei; Wu, Ye; Huang, Zhao Quan; Chen, Rui Zhen; Chen, Hao Zhu

doi:10.1016/j.jep.2010.08.008

Cited by 55 publications

(42 citation statements)

References 46 publications

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“…The activities of GPX, SOD, CAT, T-AOC, and the concentration of MDA were measured using commercial colourimetric assay kit (Nanjing Jiancheng Bioengineering Institute, Nanjing, China) according to the manufacturer's instructions (Wang et al 2010). The assay of TRXR activity was based on a method in which the reduction of dithio-bis-nitrobenzoic acid (DTNB) was monitored at 412 nm (Hill et al 1997).…”

Section: Preparation Of Reagentsmentioning

confidence: 99%

Effects of retinoic acid on the synthesis of selenoprotein and the antioxidative indices of bovine mammary epithelial cells in vitro

Jin¹,

Yan²,

Shi³

et al. 2016

CZECH J ANIM SCI

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The present study was conducted to examine the effects of retinoic acid (RA) on the synthesis of selenoprotein and the antioxidative indices of bovine mammary epithelial cells (BMEC) in vitro and to explore the antioxidative mechanisms of RA in the BMEC. The subconfluenced BMEC were divided into six treatments with six replicates per treatment and cultured in a Dulbecco's Modified Eagle's Medium/F12 media (10% fetal bovine serum, 5 µg/ml ovine prolactin, 10 ng/ml epidermal growth factor, 1 g/ml hydrocortisone, 0.5% insulin-transferrin-selenium) containing different levels of RA (0 (control), 0.05, 0.1, 0.2, 1 or 2 mg/ml) for 24 h. Addition of RA promoted the proliferation of BMEC, increased the activities of catalase, superoxide dismutase, total antioxidant capacity, glutathione peroxidase (GPX), thioredoxin reductase (TRXR), and the content of selenoprotein P (SELP) in a dose-dependent manner (P < 0.05). The optimal RA dose was 1 μg/ml. However, positive effect of RA tended to be suppressed when RA was increased to 2 μg/ml. The expressions of mRNA and protein of GPX in BMEC were up-regulated by RA in a quadratic dose-response relationship (P < 0.01), and the addition of 1 μg/ml RA showed the best effect. The mRNA expressions of TRXR1 and SELP as well as the protein expression of TRXR1 were higher at 1-2 μg/ml RA. These results suggested that RA promoted antioxidant function of BMEC by regulating the synthesis of selenoprotein including GPX, TRXR, and SELP in vitro. Keywords: vitamin A; antioxidant function; dairy cowsList of abbreviations: BMEC = bovine mammary epithelial cells, NO = nitric oxide, VA = vitamin A, GPX = glutathione peroxidase, TRXR = thioredoxin reductase, ROS = reactive oxygen species, MDA = malondialdehyde, SELP = selenoprotein P, RA = retinoic acid, ID = iodothyronine deiodinases, BW = body weight, DMEM = Dulbecco's Modified Eagle's Medium, DMSO = dimethyl sulfoxide, MTT = methyl thiazolyl tetrazolium, DTNB = dithio-bis-nitrobenzoic acid, GAPDH = glyceraldehyde phosphate dehydrogenase, SOD = superoxide dismutase, CAT = catalase, T-AOC = total antioxidant capacity, iNOS = inducible nitric oxide synthase, MAPK = mitogen-activated protein kinase, RT = reverse transcriptase, RT-PCR = real-time polymerase chain reaction, PBS = phosphate buffered solution

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Section: Preparation Of Reagentsmentioning

confidence: 99%

Effects of retinoic acid on the synthesis of selenoprotein and the antioxidative indices of bovine mammary epithelial cells in vitro

Jin¹,

Yan²,

Shi³

et al. 2016

CZECH J ANIM SCI

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“…However the production process of ox-LDL is complicated, and it is stable for only 1 month at 4°C. Conversely, H 2 O 2 is economical, simple and practical, so it is commonly used in injury models to replicate the effects of ox-LDL [6, 7]. …”

Section: Introductionmentioning

confidence: 99%

Allicin prevents H2O2-induced apoptosis of HUVECs by inhibiting an oxidative stress pathway

Chen

Tang²,

Qian

et al. 2014

BMC Complement Altern Med

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BackgroundAllicin, a primary ingredient of garlic, has been proposed to possess cardioprotective properties, which are commonly mediated by improved endothelial function.MethodsTo investigate the effect and mechanism of allicin on the apoptosis of human umbilical vein endothelial cells (HUVECs), we used Propidium iodide (PI) staining and Annexin V/ PI staining assays to establish a model of oxidative stress apoptosis induced by H2O2. MTT, RT-PCR and western-blot assays were used to detect the effects and mechanism of allicin on the model.ResultsPI staining, Annexin V/ PI staining assays and morphological assessment suggest that the cell death induced by 0.5 mM H2O2 is primarily apoptotic. Conversely, allicin reverses the effect of H2O2 on cell death, suggesting a role in protecting HUVECs from apoptosis. We demonstrated that H2O2 activates PARP cleavage, reduces pro-Caspase-3 levels and activates Bax expression; however, allicin inhibits each of these apoptotic signaling indicators. Allicin also reduces the levels of malondialdehyde and increases the levels of superoxide dismutase, nitric oxide release and endothelial nitric oxide synthase mRNA, but has no significant effect on inducible nitric oxide synthase mRNA levels.ConclusionThese results demonstrate that allicin has powerful effects in protecting HUVECs from apoptosis and suggest that protection occurs via a mechanism involving the protection from H2O2-mediated oxidative stress.

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“…Injury of endothelial cells is the first stage of AS, and oxidative stress is regarded as a critical pathogenic factor in endothelial cell injury (5). Oxidative stress is mainly caused by the excessive accumulation of reactive oxygen species (ROS), which include hydrogen peroxide (H 2 O 2 ), superoxide anions (O 2-·) and hydroxyl radicals (·OH).…”

Section: Introductionmentioning

confidence: 99%

Protective effect of rhein against oxidative stress-related endothelial cell injury

et al. 2012

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Abstract. Endothelial cell injury caused by reactive oxygen species (ROS) plays a critical role in the pathogenesis of atherosclerosis. Therefore, phytochemicals or antioxidants that inhibit the production of ROS have clinical value for the treatment of atherosclerosis. Rhein is one of the most important active components of rhubarb (Rheum officinale), a famous traditional Chinese remedy that possesses potent antioxidant properties through undefined mechanism(s). The aim of the present study was to determine whether rhein inhibits hydrogen peroxide (H 2 O 2 )-induced injury in human umbilical vein endothelial cells (HUVECs). The oxidative injury model was established with H 2 O 2 . HUVECs were treated with different concentrations of rhein in the presence/absence of H 2 O 2 . The protective effects of rhein against the injury caused by H 2 O 2 were evaluated. HUVECs incubated with 200 µmol/l H 2 O 2 had significantly decreased cell viability, which was accompanied by cell apoptosis and upregulated Bid and caspase-3, -8 and -9 mRNA expression. Meanwhile, H 2 O 2 treatment induced a marked increase in malondialdehyde (MDA) and lactate dehydrogenase (LDH) content and decreased the nitric oxide (NO) content and nitrogen oxide synthase (NOS), superoxide dismutase (SOD) and glutathione peroxidase (GSH-PX) activity. However, pre-treatment with different rhein concentrations (2, 4, 8 and 16 µmol/l) significantly increased the viability of H 2 O 2 -injured HUVECs, decreased the MDA and LDH content, increased the NO content and NOS, SOD and GSH-PX activity in a dose-dependent manner and resulted in significant recovery from H 2 O 2 -induced cell apoptosis. In addition, the results of the qRT-PCR indicated that pre-treatment with rhein downregulates the expression of Bid and caspase-3, -8 and -9 mRNA, which plays a key role in H 2 O 2 -induced cell apoptosis. The present study shows that rhein protects endothelial cells against oxidative injury induced by H 2 O 2 , suggesting that rhein is a potential compound for the prevention and treatment of atherosclerosis. IntroductionCardiovascular disease (CVD) is the primary cause of morbidity and mortality worldwide (1). Atherosclerosis (AS), a chronic inflammatory disease that results in the deposition of oxidized lipoproteins that form fatty plaques, accounts for nearly 75% of all deaths from CVD (2,3). Vascular inflammation, especially at the endothelium cell level, has been shown to play a pivotal role in the initiation, progression and clinical complications of AS (4).Endothelial cells regulate cardiovascular health and control the elasticity of vessels. Injury of endothelial cells is the first stage of AS, and oxidative stress is regarded as a critical pathogenic factor in endothelial cell injury (5). Oxidative stress is mainly caused by the excessive accumulation of reactive oxygen species (ROS), which include hydrogen peroxide (H 2 O 2 ), superoxide anions (O 2-·) and hydroxyl radicals (·OH).ROS are continuously produced in cells as products of cellular oxidation-reductio...

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Curculigoside attenuates human umbilical vein endothelial cell injury induced by H2O2

Cited by 55 publications

References 46 publications

Effects of retinoic acid on the synthesis of selenoprotein and the antioxidative indices of bovine mammary epithelial cells in vitro

Effects of retinoic acid on the synthesis of selenoprotein and the antioxidative indices of bovine mammary epithelial cells in vitro

Allicin prevents H2O2-induced apoptosis of HUVECs by inhibiting an oxidative stress pathway

Protective effect of rhein against oxidative stress-related endothelial cell injury

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