Inhibition of Nox-4 activity by plumbagin, a plant-derived bioactive naphthoquinone

Ding, Yaxian; Chen, Zi‐Jiang; Liu, Shiguo; Che, Danian; Vetter, Michael; Chang, Chung-Ho

doi:10.1211/0022357055119

Cited by 122 publications

(96 citation statements)

References 37 publications

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“…Duroquinone as well as tBuBHQ, tBuBQ (the oxidative form of tBuBHQ), and AA-861, stimulated Nox4 activity at a starting concentration of 1 mM, whereas BQ (30 mM), HQ (30 mM) and tMetBQ (100 mM) inhibited this activity in a dose dependent manner. We also confirmed the inhibitory effect of the naphthoquinone, plumbagin, on Nox4 activity as reported [38,39].…”

Section: Quinone Structure May Be Responsible For the Modulation Of Nsupporting

confidence: 88%

Quinone compounds regulate the level of ROS production by the NADPH oxidase Nox4

Nguyen

Lardy

Rousset

et al. 2013

Biochemical Pharmacology

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NADPH oxidase Nox4 is expressed in a wide range of tissues and plays a role in cellular signaling by providing reactive oxygen species (ROS) as intracellular messengers. Nox4 oxidase activity is thought to be constitutive and regulated at the transcriptional level; however, we challenge this point of view and suggest that specific quinone derivatives could modulate this activity. In fact, we demonstrated a significant stimulation of Nox4 activity by 4 quinone derivatives (AA-861, tBuBHQ, tBuBQ, and duroquinone) observed in 3 different cellular models, HEK293E, T-REx™, and chondrocyte cell lines. Our results indicate that the effect is specific toward Nox4 versus Nox2. Furthermore, we showed that NAD(P)H:quinone oxidoreductase (NQO1) may participate in this stimulation. Interestingly, Nox4 activity is also stimulated by reducing agents that possibly act by reducing the disulfide bridge (Cys226, Cys270) located in the extracellular E-loop of Nox4. Such model of Nox4 activity regulation could provide new insight into the understanding of the molecular mechanism of the electron transfer through the enzyme, i.e., its potential redox regulation, and could also define new therapeutic targets in diseases in which quinones and Nox4 are implicated

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Section: Quinone Structure May Be Responsible For the Modulation Of Nsupporting

confidence: 88%

Quinone compounds regulate the level of ROS production by the NADPH oxidase Nox4

Nguyen

Lardy

Rousset

et al. 2013

Biochemical Pharmacology

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“…The preferred substrate for oxidases in macrophages and neutrophils is also NADPH rather than NADH [35]. A similar NADH-and NADPH-dependent activity is found in human skin fibroblasts [85], neonatal rat cardiac myocytes [86] and in human embryonic kidney cells [87], while in rat liver plasma membranes the activity with NADPH is approximately 80% that of NADH [88]. The substrate preference of the superoxide-generating oxidase is thus highly cell type dependent with specificity to NADH oxidase in adult rat cardiac fibroblasts.…”

Section: Ang Ii-induced Ros Generation and Modulation By Apocyninmentioning

confidence: 65%

Modulation of Reactive Oxygen Species and Collagen Synthesis by Angiotensin II in Cardiac Fibroblasts

Lijnen¹

2011

TOHYPERJ

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Angiotensin II increases the NAD(P)H-dependent superoxide anion production and the intracellular generation of reactive oxygen species in cardiac fibroblasts and apocynin, a NAD(P)H oxidase inhibitor, abrogates this rise. The membrane associated NAD(P)H oxidase complex is the predominant source of superoxide anion and reactive oxygen species generation in angiotensin II-stimulated adult cardiac fibroblasts. Inhibition of this NAD(P)H oxidase complex with apocynin completely blocks the angiotensin II-stimulated collagen production, collagen I and III protein and mRNA expression.Superoxide anion production is also increased by the Cu,Zn-superoxide dismutase (SOD) inhibitor diethyldithiocarbamic acid (DETC) and decreased by the superoxide scavenger tempol in control and ANG II-treated fibroblasts. ANG II and DETC stimulate the collagen production and the collagen I and fibronectin content in fibroblasts. The SOD mimetics tempol and EUK-8 as well as polyethyleneglycol-SOD reduce the collagen production.ANG II also decreases the activity and mRNA and protein expression of the mitochondrial antioxidants Mn-SOD and peroxiredoxin-3. Upon phosphorylation of Akt by ANG II, P-Akt is translocated from the cytoplasm to the nucleus and nuclear phosphorylation of FOXO3a by P-Akt leads to relocalisation of FOXO3a from the nucleus to the cytosol, resulting in a decrease in its transcriptional activity and in Mn-SOD expression. These data indicate that ANG II inactivates FOXO3a by activating Akt and this leads to a reduction in the expression of the antioxidant Mn-SOD. A role of SOD and the formed reactive oxygen species in the regulation and organization of collagen in cardiac fibroblasts is suggested.

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“…It is noteworthy that the recently discovered pro-apoptotic Bcl-2 family member Bcl-2 interacting protein (BID) links the intrinsic and extrinsic apoptotic pathways (67). Evidence indicates that dietary agents such as plubagin, a plant-derived naphthoquinone, and diterpenes, found in citrus peel, inhibit nox-4 activity and upregulate BID, respectively, in human kidney, brain tumor, and prostate cancer cells (68,69).…”

Section: Regulation Of Apoptosismentioning

confidence: 99%

Targeting Apoptosis with Dietary Bioactive Agents

Martin

2006

Exp Biol Med (Maywood)

120

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Apoptosls, a form of programmed cell death, Is a pivotal defense against the occurrence of cancer and is essential to metazoans In maintaining tissue homeostasis. Apoptosls exhibits a distinctive phenotype and Involves elimination of potentially deleterious cells. Many diseases have been associated with aberrantly regulated apoptotlc cell death, ultimately leading to Inhibition of apoptosls and propagation of diseases such as cancer. Elucidation of the critical events associated with carcinogenesis provides the opportunity for dietary Intervention to prevent cancer development through Induction of apoptosls, particularly by bloactive agents or functional foods. Diet Is a significant environmental factor In the overall cancer process and can exacerbate or Interfere with carcinogenesis. Apoptosls occurs primarily through two well-recognized pathways In cells, Inciudlng the Intrinsic, or mitochondrial-mediated, effector mechanism and the extrinsic, or death receptor-mediated, effector mechanism. In addition to diet's effects on protein expression and function, evidence Is also accumulating that a large number of dietary food components can exert effects on the human genome, either directly or Indirectly, to modUlate gene expression. In fact, many diet-related genes are Involved In carcinogenesis as well as apoptosls, and thus are ultimately molecular targets for dietary chemopreventlon. There are multiple steps within pathways In which dietary components can alter gene expression and phenotypes of cells and thus Influence cancer outcomes (nutritional transcrlptomlc effect). Thus, apoptosls Is an emerging therapeutic target of bloactlve agents of diet. In this review, the process of apoptosls Is discussed and the potential mechanistic Interaction of bloactlve agents, as

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Inhibition of Nox-4 activity by plumbagin, a plant-derived bioactive naphthoquinone

Cited by 122 publications

References 37 publications

Quinone compounds regulate the level of ROS production by the NADPH oxidase Nox4

Quinone compounds regulate the level of ROS production by the NADPH oxidase Nox4

Modulation of Reactive Oxygen Species and Collagen Synthesis by Angiotensin II in Cardiac Fibroblasts

Targeting Apoptosis with Dietary Bioactive Agents

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