Up-regulation of aldose reductase expression mediated by phosphatidylinositol 3-kinase/Akt and Nrf2 is involved in the protective effect of curcumin against oxidative damage

Kang, Eun Sil; Woo, Im Sun; Kim, Hyo Jung; Eun, So Young; Paek, Kyung Shin; Kim, Hye Jung; Chang, Ki Churl; Lee, Jae Heun; Lee, Hoon Taek; Kim, Jin‐Hoi; Nishinaka, Toru; Yabe‐Nishimura, Chihiro; Seo, Han Geuk

doi:10.1016/j.freeradbiomed.2007.05.006

Cited by 97 publications

(57 citation statements)

References 48 publications

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“…Antioxidants can also exert neuroprotective effects by increasing the activity of pro-survival proteins or by downregulating the expression of pro-apoptotic genes. For example, LA, curcumin, and EGCG can activate the PI-3K pro-survival pathway (Zhang et al, 2001;Muller et al, 2003;Koh et al, 2004;Antonio and Druse, 2006;Kang et al, 2007), and EGCG mediates downregulation of the expression of Bax and Bad (Levites et al, 2002;Mandel et al, 2004), which encode proapoptotic proteins. Moreover, the protein kinase C (PKC) pathway has been implicated with the protective effects of EGCG (Reznichenko et al., 2005).…”

Section: Discussionmentioning

confidence: 99%

“…Some of the non-antioxidant effects, i.e., those of α-lipoic acid (LA), dihydrolipoic acid (DHLA), melatonin, curcumin, and resveratrol, involve the maintenance of cellular levels of endogenous antioxidants and/or antioxidant enzymes (Suh et al, 2004;Shila et al, 2005;Barlow-Walden et al, 1995;Kotler et al, 1998;Zhuang et al, 2003;Juknat et al, 2005;Lin, 2007). In addition, some antioxidants, i.e., LA, curcumin, and EGCG can rapidly activate the PI-3K pro-survival pathway in certain cell types (Zhang et al, 2001;Muller et al, 2003;Koh et al, 2004;Antonio and Druse, 2006;Kang et al, 2007), suggesting that this effect may be directly linked with the action of these antioxidants. Additional pro-survival effects of antioxidants are also likely to be involved; EGCG can down-regulate the expression of several pro-apoptotic genes (Levites et al, 2002;Mandel et al, 2004).…”

Section: Introductionmentioning

confidence: 99%

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Antioxidants prevent ethanol-associated apoptosis in fetal rhombencephalic neurons

Antonio

Druse

2008

Brain Research

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It is well known that ethanol damages the developing nervous system by augmenting apoptosis. Previously, this laboratory reported that ethanol augments apoptosis in fetal rhombencephalic neurons, and that the increased apoptosis is associated with reduced activity of the phosphatidylinositol 3'kinase pathway and downstream expression of pro-survival genes. Other laboratories have shown that another mechanism by which ethanol induces apoptosis in developing neurons is through the generation of reactive oxygen species (ROS) and the associated oxidative stress.The present study used an in vitro model to investigate the potential neuroprotective effects of several antioxidants against ethanol-associated apoptosis in fetal rhombencephalic neurons. The investigated antioxidants included three phenolics: (-)-epigallocatechin-3-gallate (EGCG), a flavanoid polyphenol found in green tea; curcumin, found in tumeric; and resveratrol (3,5,4'-trihydroxystilbene), a component of red wine. Additional antioxidants, including melatonin, a naturally occurring indole, and α-lipoic acid, a naturally occurring dithiol, were also investigated.These studies demonstrated that a 24-hour treatment of fetal rhombencephalic neurons with 75 mM ethanol caused a 3-fold increase in the percentage of apoptotic neurons. However, co-treatment of these cultures with any of the five different antioxidants prevented ethanol-associated apoptosis. Antioxidant treatment did not alter the extent of apoptosis in control neurons, i.e., those cultured in the absence of ethanol. These studies showed that several classes of antioxidants can exert neuroprotection against ethanol-associated apoptosis in fetal rhombencephalic neurons.

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Section: Discussionmentioning

confidence: 99%

Section: Introductionmentioning

confidence: 99%

Antioxidants prevent ethanol-associated apoptosis in fetal rhombencephalic neurons

Antonio

Druse

2008

Brain Research

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“…Substantial evidence indicates that many natural compounds or nutraceuticals can activate Nrf2 [19,85,86] . Notably, resveratrol, curcumin and epigallocatechin-3-gallate are all reported to act as insulin sensitizing agents, reverse hyperglycemia, hyperlipidemia and other symptoms linked to obesity [87][88][89][90] . These natural compounds may initially cause a depolarization of mitochondrial membrane potential and ROS production, then activate the Nrf2 system to exert subsequent protective responses [19,[91][92][93] .…”

Section: Nrf2 System As a Potential Drug Target For Diabetes Treatmentmentioning

confidence: 99%

Role of nuclear factor (erythroid-derived 2)-like 2 in metabolic homeostasis and insulin action: A novel opportunity for diabetes treatment?

Zhong

Li²,

Liu³

et al. 2012

WJD

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Redox balance is fundamentally important for physiological homeostasis. Pathological factors that disturb this dedicated balance may result in oxidative stress, leading to the development or aggravation of a variety of diseases, including diabetes mellitus, cardiovascular diseases, metabolic syndrome as well as inflammation, aging and cancer. Thus, the capacity of endogenous free radical clearance can be of patho-physiological importance; in this regard, the major reactive oxygen species defense machinery, the nuclear factor (erythroid-derived 2)-like 2 (Nrf2) system needs to be precisely modulated in response to pathological alterations. While oxidative stress is among the early events that lead to the development of insulin resistance, the activation of Nrf2 scavenging capacity leads to insulin sensitization. Furthermore, Nrf2 is evidently involved in regulating lipid metabolism. Here we summarize recent findings that link the Nrf2 system to metabolic homeostasis and insulin action and present our view that Nrf2 may serve as a novel drug target for diabetes and its complications.

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“…Furthermore we have demonstrated that APAP upregulate aldose reductase at mRNA and protein levels. Aldose reductase is a detoxify enzyme that is transcriptionally regulated by Nrf2, an increased expression of aldose reductase by curcumin prevent rat aortic VSMC against oxidative stress [16]. Moreover, inhibition of aldose reductase renders J774A.1 macrophage cell line more susceptible to acrolein or hydrogen peroxide-induced cell death [17].…”

Section: Discussionmentioning

confidence: 99%

Overexpression of Aldose Reductase Render Mouse Hepatocytes More Sensitive to Acetaminophen Induced Oxidative Stress and Cell Death

Ahmed

Al-Obosi²,

Osman

et al. 2015

Ind J Clin Biochem

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Acetaminophen (APAP) a commonly used drug for decrease the fever and pain but is capable to induced hepatotoxicity at over dose. This study was carried out to investigate the effect of APAP on the expression of antiapoptotic and antioxidative defense genes, and whether aldose reductase over-expressing plasmid capable to protect against APAP-induced oxidative stress and cell death. APAP treatment induced oxidative stress and hepatotoxicity, and significantly increased aldose reductase mRNA and protein expression in mouse hepatocyte (AML-12).Unexpectedly, AML-12 cells over-expressing aldose reductase augmented APAP-induced reduction in cell viability, reactive oxygen species (ROS) production, glutathione (GSH) depletion and glutathione S-transferase A2 expression. Moreover, over-expression of aldose reductase potentiated APAP induced reduction on proliferating cell nuclear antigen, B cell lymphoma-extra large (bcl-x L ), catalase, glutathione peroxidase-1 (GPx-1) and abolished APAP-induced B-cell lymphoma 2 (bcl-2) inductions. Further, over-expression of aldose reductase significantly abolished AMP activated protein kinase (AMPK) activity in APAP-treated cells and induced p53 expression. This results demonstrate that APAP induced toxicity in AML-12, increased aldose reductase expression, and over-expression of aldose reductase render this cell more susceptible to APAP induced oxidative stress and cell death, this probably due to inhibition AMPK or bcl-2 activity, or may due to competition between aldose reductase and glutathione reductase for NADPH.

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Up-regulation of aldose reductase expression mediated by phosphatidylinositol 3-kinase/Akt and Nrf2 is involved in the protective effect of curcumin against oxidative damage

Cited by 97 publications

References 48 publications

Antioxidants prevent ethanol-associated apoptosis in fetal rhombencephalic neurons

Antioxidants prevent ethanol-associated apoptosis in fetal rhombencephalic neurons

Role of nuclear factor (erythroid-derived 2)-like 2 in metabolic homeostasis and insulin action: A novel opportunity for diabetes treatment?

Overexpression of Aldose Reductase Render Mouse Hepatocytes More Sensitive to Acetaminophen Induced Oxidative Stress and Cell Death

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