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

Chen, Sisi; Tang, Yu-ye; Qian, Ying; Chen, Ruyi; Zhang, Lin; Wo, Like; Chai, Hui

doi:10.1186/1472-6882-14-321

Cited by 45 publications

(42 citation statements)

References 26 publications

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“…Chan et al (13) reported that allicin inhibited intracellular ROS production, rather than scavenging extracellular H 2 O 2 or free radicals in H9C2 cells. Conversely, allicin has been shown to exhibit the ability to indirectly scavenge oxygen free radicals in human umbilical vein endothelial cells (16), which is consistent with the findings of the present study. Therefore, the present study hypothesized that allicin may exert various biological abilities in order to protect against oxidative stress in various cell lines and tissues.…”

Section: Discussionsupporting

confidence: 93%

“…The glutathione (GSH)/glutathione disulfide (GSSG) ratio and malondialdehyde (MDA) concentrations were assessed using the GSH/GSSG Assay kit (Beyotime Institute of Biotechnology, Nantong, China) and the MDA Assay kit (Nanjing Jiancheng Biological Engineering Institute, Nanjing, China), according to the manufacturer's protocols. The superoxide dismutase (SOD) activity was measured using the SOD Assay kit (Nanjing Jiancheng Biological Engineering Institute), according to the manufacturer's protocols (16).…”

Section: Methodsmentioning

confidence: 99%

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Allicin attenuates H2O2-induced cytotoxicity in retinal pigmented epithelial cells by regulating the levels of reactive oxygen species

Zhang

Wei

et al. 2016

Molecular Medicine Reports

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Abstract.Retinal pigmented epithelial cell (RPE) oxidative stress is known to have a vital role in the etiology of age-related macular degeneration (AMD). The present study aimed to investigate whether allicin, a natural product with antioxidant activity, was able to protect RPEs (ARPE-19) from hydrogen peroxide (H 2 O 2 )-induced damage, and to determine the underlying mechanisms. The 3-(4,5-dimethylthiazol-2-yl)-2,5-diphenyl tetrazolium bromide assay was used to determine cellular viability, and reactive oxygen species (ROS) were detected using a ROS Assay kit. The results demonstrated that allicin was able to protect ARPE-19 cells from H 2 O 2 -induced damage in a dose-dependent manner. In addition, allicin attenuated oxidative stress by reducing the levels of intracellular ROS and malondialdehyde (MDA), and enhancing the glutathione/glutathione disulfide (GSSG) ratio. With regards to the underlying mechanism, allicin was able to markedly modulate the expression levels of ROS-associated enzymes, including superoxide dismutase, NADPH oxidase 4 and NAD(P)H dehydrogenase quinone 1, and elevate the activity of nuclear factor erythroid 2-related factor 2 in the H 2 O 2 -stimulated ARPE-19 cells. These results suggested that allicin may exert protective effects against H 2 O 2 -induced cytotoxicity in RPEs via ROS regulation.

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Section: Discussionsupporting

confidence: 93%

Section: Methodsmentioning

confidence: 99%

Allicin attenuates H2O2-induced cytotoxicity in retinal pigmented epithelial cells by regulating the levels of reactive oxygen species

Zhang

Wei

et al. 2016

Molecular Medicine Reports

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“…We found that ectopic expression of SFRP5 downregulated the expression of Bax, a well‐defined proapoptotic protein . Induction of Bax is involved in oxidative stress‐induced apoptosis in human umbilical vein endothelial cells . Most importantly, co‐expression of Bax restored apoptotic response in the presence of SFRP5.…”

Section: Discussionmentioning

confidence: 99%

Secreted frizzled‐related protein 5 protects against oxidative stress‐induced apoptosis in human aortic endothelial cells via downregulation of Bax

Wang

Peng

Jiang

et al. 2017

J Biochem & Molecular Tox

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This study was undertaken to determine the role of secreted frizzled-related protein 5 (SFRP5) in endothelial oxidative injury. Human aortic endothelial cells (HAECs) were exposed to different oxidative stimuli and examined for SFRP5 expression. The effects of SFRP5 overexpression and knockdown on cell viability, apoptosis, and reactive oxygen species production were measured. HAECs treated with angiotensin (Ang) II (1 μM) or oxidized low-density lipoprotein (oxLDL) (150 μg/mL) showed a significant increase in SFRP5 expression. Overexpression of SFRP5 significantly attenuated the viability suppression and apoptosis induction by Ang II and oxLDL, whereas the knockdown of SFRP5 exerted opposite effects. Overexpression of SFRP5 prevented ROS formation and β-catenin activation and reduced Bax expression. Co-expression of Bax significantly reversed the anti-apoptotic effect of SFRP5 overexpression, whereas knockdown of Bax restrained Ang II- and oxLDL-induced apoptosis in HAECs. Taken together, SFRP5 confers protection against oxidative stress-induced apoptosis through inhibition of β-catenin activation and downregulation of Bax.

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“…1B). Based on these results, 500 µΜ was selected as the model dose (6) to induce cell death for subsequent experiments on apoptotic cell death.…”

Section: Mws-19 Inhibits 500 µM H 2 O 2 -Induced Death Of Huvecsmentioning

confidence: 99%

“…Reactive oxygen species (ROS), such as hydrogen peroxide (H 2 O 2 ) and superoxide (O 2-), lead to increases in vascular tone and participate in arterial contraction, and have a direct role in the pathogenesis of hypertension (3,4). The vascular endothelium, a thin layer of cells lining the inner surface of the vascular wall, produces and secretes various substances that preserve the integrity and functioning of the vascular system (5,6). Excessive levels of ROS in endothelial cells leads to impaired endothelial nitric oxide (NO) bioactivity (7,8).…”

Section: Introductionmentioning

confidence: 99%

Isolariciresinol-9'-O-α-L-arabinofuranoside protects against hydrogen peroxide‑induced apoptosis of human umbilical vein endothelial cells via a PI3K/Akt/Bad‑dependent pathway

Liu¹,

Liu

Wang

et al. 2017

Mol Med Report

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Isolariciresinol-9'-O-α-L-arabinofuranoside (MWS‑19) isolated from Pinus massoniana Lamb. Fresh pine needles is the major ingredient of the Songling Xuemaikang capsule therapy used for hypertension. The present study aimed to investigate the effects and underlying mechanisms of MWS‑19 on hydrogen peroxide (H2O2)‑induced apoptosis in human umbilical vein endothelial cells (HUVECs). To investigate the effect of MWS‑19 on apoptosis in HUVECs, an oxidative stress‑induced apoptosis model was established in HUVECs using H2O2, and the present study performed Hoechst 33258 staining and a Cell Counting Kit‑8 (CCK‑8) assay. Furthermore, western blot analysis was also performed to investigate the underlying mechanism of the effects of MWS‑19 on the model. The results demonstrated that MWS‑19 reversed the effects of H2O2 on cell apoptosis at a concentration range of 15.6‑250 µg/ml, with dose‑dependent increases in cell growth. Hoechst staining indicated that 500 µM H2O2 induced HUVEC apoptosis, and MWS‑19 markedly protected HUVECs against apoptosis at 31.3, 62.5 and 125 µg/ml. Furthermore, the protein expression of phosphatidylinositol 3‑kinase (PI3K), phosphorylated‑Akt and Bcl‑2‑associated agonist of cell death (Bad) were increased, and reduced caspase‑3 activation was observed, following treatment with MWS‑19 in H2O2‑treated HUVECs. Additionally, the PI3K inhibitor wortmannin attenuated PI3K/Akt/Bad signaling induced by MWS‑19 treatment and neutralized the effect of MWS‑19 on the growth of HUVECs. In conclusion, the results of the present study indicate that MWS‑19 may protect against H2O2‑induced HUVEC apoptosis via the PI3K/Akt/Bad signaling pathway. MWS‑19 may serve an important role in the prevention of oxidative damage in vascular endothelial cells in hypertension patients.

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

Cited by 45 publications

References 26 publications

Allicin attenuates H2O2-induced cytotoxicity in retinal pigmented epithelial cells by regulating the levels of reactive oxygen species

Allicin attenuates H2O2-induced cytotoxicity in retinal pigmented epithelial cells by regulating the levels of reactive oxygen species

Secreted frizzled‐related protein 5 protects against oxidative stress‐induced apoptosis in human aortic endothelial cells via downregulation of Bax

Isolariciresinol-9'-O-α-L-arabinofuranoside protects against hydrogen peroxide‑induced apoptosis of human umbilical vein endothelial cells via a PI3K/Akt/Bad‑dependent pathway

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