Allicin Purified From Fresh Garlic Cloves Induces Apoptosis in Colon Cancer Cells Via Nrf2

Bat-Chen, Wolf; Golan, Tal; Peri, Irena; Ludmer, Zvi; Schwartz, Betty

doi:10.1080/01635581.2010.509837

Cited by 140 publications

(95 citation statements)

References 24 publications

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“…Furthermore, allicin attenuates oxidative stress responses through the Nrf2 antioxidant signaling pathway as previously suggested in other models [49-53]. However, whether Nrf2 activation mediates the allicin-induced protection from LPS-induced vascular injury is currently unknown.…”

Section: Discussionmentioning

confidence: 69%

Allicin Decreases Lipopolysaccharide-Induced Oxidative Stress and Inflammation in Human Umbilical Vein Endothelial Cells through Suppression of Mitochondrial Dysfunction and Activation of Nrf2

Zhang¹,

Pan²,

Xu³

et al. 2017

Cell Physiol Biochem

101

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Background: Allicin, a major component of garlic, is regarded as a cardioprotective agent and is associated with increased endothelial function. Methods: The effects of allicin on lipopolysaccharide (LPS)-induced vascular oxidative stress and inflammation in cultured human umbilical vein endothelial cells (HUVECs) and the mechanisms underlying these effects were studied. The protective effects were measured using cell viability, a lactate dehydrogenase (LDH) assay and cell apoptosis as indicators, and the anti-oxidative activity was determined by measuring reactive oxygen species (ROS) generation, oxidative products and endogenous antioxidant enzyme activities. HUVEC mitochondrial function was assessed by determining mitochondrial membrane potential (MMP) collapse, cytochrome c production and mitochondrial ATP release. To investigate the potential underlying mechanisms, we also measured the expression of dynamic mitochondrial proteins using western blotting. Furthermore, we evaluated the Nrf2 antioxidant signaling pathway using an enzyme-linked immunosorbent assay (ELISA). Results: Our results demonstrated that allicin enhanced HUVEC proliferation, which was suppressed by LPS exposure, and LDH release. Allicin ameliorated LPS-induced apoptosis, suppressed ROS overproduction, reduced lipid peroxidation and decreased the endogenous antioxidant enzyme activities in HUVECs. These protective effects were associated with the inhibition of mitochondrial dysfunction as indicated by decreases in the MMP collapse, cytochrome c synthesis and mitochondrial ATP release. In addition, allicin attenuated the LPS-induced inflammatory responses, including endothelial cell adhesion and TNF-α and IL-8 production. Furthermore, allicin increased the expression of LXRα in a dose-dependent manner. Allicin-induced attenuation of inflammation was inhibited by LXRα siRNA treatment. Finally, allicin activated NF-E2-related factor 2 (Nrf2), which controls the defense against oxidative stress and inflammation. Conclusions: Taken together, the present data suggest that allicin attenuated the LPS-induced vascular injury process, which may be closely related to the oxidative stress and inflammatory response in HUVECs. Allicin modulated Nrf2 activation and protected the cells against LPS-induced vascular injury. Our findings suggest that allicin attenuated the LPS-induced inflammatory response in blood vessels.

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Section: Discussionmentioning

confidence: 69%

Allicin Decreases Lipopolysaccharide-Induced Oxidative Stress and Inflammation in Human Umbilical Vein Endothelial Cells through Suppression of Mitochondrial Dysfunction and Activation of Nrf2

Zhang¹,

Pan²,

Xu³

et al. 2017

Cell Physiol Biochem

101

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“…It is well-known that Nrf2 mediates an antioxidant response pathway that promotes the primary cellular defense mechanism against oxidative stress induced by xeno biotic exposure and other factors (36,37). The antioxidative effects of allicin are associated with the Nrf2 antioxidant signaling pathway in cardiovascular diseases, neurodegenerative diseases and cancer (15,38,39). To further investigate the antioxidative effects of allicin on ARPE-19 cells exposed to H 2 O 2 , the expression levels of Nrf2 were detected.…”

Section: Discussionmentioning

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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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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“…Previous studies demonstrated that allicin may induce tumor cell apoptosis, inhibit the tumor cell cycle and regulate angiogenesis (14)(15)(16)(17). Numerous mechanisms are involved in the biological activities of allicin, including unfolded protein response, p53-mediated autophagy and p38 mitogen-activated protein kinase/caspase-3 signaling (14)(15)(16)(17)(18). However, to the best of our knowledge, the effects and mechanisms of allicin on lung adenocarcinoma remain undefined.…”

Section: Introductionmentioning

confidence: 99%

Allicin inhibits the invasion of lung adenocarcinoma cells by altering tissue inhibitor of metalloproteinase/matrix metalloproteinase balance via reducing the activity of phosphoinositide 3-kinase/AKT signaling

et al. 2017

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Abstract. Allicin, the main active principle associated with Allium sativum chemistry, has various antitumor activities. However, to the best of our knowledge, there is no available information to address the anti-invasive effect and associated mechanism in lung adenocarcinoma. In the present study, cell viability assay, cell adhesion assay, western blot analysis, Transwell migration and invasion assays and reverse transcription-quantitative polymerase chain reaction were performed. Allicin was identified to inhibit the adhesion, invasion and migration of lung adenocarcinoma cells in a dose-dependent manner, accompanied by decreasing mRNA and protein levels of matrix metalloproteinase (MMP)-2 and MMP-9. Conversely, the mRNA and protein levels of tissue inhibitor of metalloproteinase (TIMP)-1 and TIMP-2 were increased in a dose-dependent manner. Furthermore, it was revealed that allicin treatment significantly suppressed the phosphorylation of AKT (P<0.05), but not the total protein expression of AKT. Combined treatment with LY294002, an inhibitor of phosphoinositide 3-kinase (PI3K)/AKT signaling, and allicin led to the synergistic reduction of MMP-2 and MMP-9 expression, followed by an increase in TIMP-1 and TIMP-2 expression. The invasive capabilities of lung adenocarcinoma cells were also suppressed. However, insulin-like growth factor-1 (an activator of PI3K/AKT signaling) reversed the effects of allicin on cell invasion and expression of MMP-2, MMP-9, TIMP-1 and TIMP-2. The present study concluded that allicin may inhibit invasion of lung adenocarcinoma cells by altering TIMP/MMP balance, via reducing the activity of the PI3K/AKT signaling pathway. This indicated that allicin may be recognized as an anti-invasive agent for lung adenocarcinoma treatment. IntroductionLung cancer is the predominant reason of cancer-associated mortality in developed and developing countries. Lung adenocarcinoma is the most common histological type of lung cancer, and accounts for ~50% of all lung cancers (1). Although the management and treatment of surgery, radiotherapy and chemotherapy have improved, the therapeutic efficacy is poor. One of the major reasons is the lack of adequate treatment against lung adenocarcinoma invasion (2,3). Therefore, the development of novel adjuvant therapeutic strategies specifically targeting the progression of invasion is of critical importance for improving the prognosis of patients with lung adenocarcinoma.Invasion occurs through a complex pathophysiological process involving multiple genetic alterations (4,5). Matrix metalloproteinases (MMPs), particularly MMP-2 and MMP-9, play an important role in the invasion process of numerous malignant tumors by degrading the basement membrane and extracellular matrix (ECM) (6-8). Previous studies have suggested that MMP-2 and MMP-9 are associated with invasion in lung cancer (4,5). In addition, numerous studies have demonstrated that MMPs may be regulated by tissue inhibitor of metalloproteinase (TIMP) (6,9). Disturbing the balance of MMPs and TIMPs ma...

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Allicin Purified From Fresh Garlic Cloves Induces Apoptosis in Colon Cancer Cells Via Nrf2

Cited by 140 publications

References 24 publications

Allicin Decreases Lipopolysaccharide-Induced Oxidative Stress and Inflammation in Human Umbilical Vein Endothelial Cells through Suppression of Mitochondrial Dysfunction and Activation of Nrf2

Allicin Decreases Lipopolysaccharide-Induced Oxidative Stress and Inflammation in Human Umbilical Vein Endothelial Cells through Suppression of Mitochondrial Dysfunction and Activation of Nrf2

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

Allicin inhibits the invasion of lung adenocarcinoma cells by altering tissue inhibitor of metalloproteinase/matrix metalloproteinase balance via reducing the activity of phosphoinositide 3-kinase/AKT signaling

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