Rottlerin induces heme oxygenase-1 (HO-1) up-regulation through reactive oxygen species (ROS) dependent and PKC δ-independent pathway in human colon cancer HT29 cells

Park, Eun Jung; Lim, Jun Hee; Nam, Sung Il; Park, Jong Wook; Kwon, Taeg Kyu

doi:10.1016/j.biochi.2009.10.001

Cited by 43 publications

(25 citation statements)

References 30 publications

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“…Induction of the HO-1 gene protects cells against the cytotoxicity of oxidative stress based on antioxidant properties. Up-regulation of HO-1 is associated with activation of the p38, MAP, kinase, and JNK pathways (37,38).…”

Section: Resultsmentioning

confidence: 99%

Effect of anthocyanins from rabbit-eye blueberry (Vaccinium virgatum) on cognitive function in mice under trimethyltin-induced neurotoxicity

Jin

Jeong

et al. 2015

Food Sci Biotechnol

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Extracts of rabbit-eye blueberries (Vaccinium virgatum) were investigated for in vitro neuroprotective and in vivo learning and memory effects in mice under trimethyltin (TMT)-induced neurotoxicity. Blueberry anthocyanins showed high in vitro antioxidant activities in ABTS and 2',7'-dichlorofluorescein diacetate (DCF-DA) assays. In a cell viability assay using MTT, anthocyanins showed protective effects, and lactate dehydrogenase release into the medium was effectively inhibited. Druginduced cognitive deficits, examined in vivo using Y-maze and passive avoidance testing, were ameliorated by the anthocyanin fraction. HPLC analysis showed that delphinidin was the predominant anthocyanin. After behavioral testing, acetylcholinesterase (AChE) activities and lipid peroxidation in the mouse brain were investigated for biochemical changes. Administration of blueberry anthocyanins reduced the level of TMT-induced memory injury via inhibition of the AChE activity and lipid peroxidation.

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Section: Resultsmentioning

confidence: 99%

Effect of anthocyanins from rabbit-eye blueberry (Vaccinium virgatum) on cognitive function in mice under trimethyltin-induced neurotoxicity

Jin

Jeong

et al. 2015

Food Sci Biotechnol

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“…It has been reported that rottlerin is a specific inhibitor of PKC δ (Gschwendt et al, 1994), However, some recent studies showed that rottlerin might not act directly on PKC δ, but instead elicit cellular changes that mimic those caused by the direct inhibition of PKC δ (Gschwendt et al, 1994;Soltoff, 2007;Song et al, 2008;Lim et al, 2009;Park et al, 2010). Therefore, we tested the possibility that rottlerin could enhance IL-1β-induced COX-2 expression in human breast cancer cells.…”

Section: Discussionmentioning

confidence: 99%

“…A representative result is shown; two additional experiments yielded similar results. Song et al, 2008;Lim et al, 2009;Park et al, 2010).…”

Section: Introductionmentioning

confidence: 99%

Rottlerin enhances IL-1β-induced COX-2 expression through sustained p38 MAPK activation in MDA-MB-231 human breast cancer cells

Park

Kwon

2011

Exp Mol Med

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Cyclooxygenase-2 (COX-2) is an important enzyme in inflammation. In this study, we investigated the underlying molecular mechanism of the synergistic effect of rottlerin on interleukin1β (IL-1β)-induced COX-2 expression in MDA-MB-231 human breast cancer cell line. Treatment with rottlerin enhanced IL-1β-induced COX-2 expression at both the protein and mRNA levels. Combined treatment with rottlerin and IL-1β significantly induced COX-2 expression, at least in part, through the enhancement of COX-2 mRNA stability. In addition, rottlerin and IL-1β treatment drove sustained activation of p38 Mitogen-activated protein kinase (MAPK), which is involved in induced COX-2 expression. Also, a pharmacological inhibitor of p38 MAPK (SB 203580) and transient transfection with inactive p38 MAPK inhibited rottlerin and IL-1β-induced COX-2 upregulation. However, suppression of protein kinase C δ (PKC δ) expression by siRNA or overexpression of dominant-negative PKC δ (DN-PKC-δ) did not abrogate the rottlerin plus IL-1β-induced COX-2 expression. Furthermore, rottlerin also enhanced tumor necrosis factor-α (TNF-α), phorbol myristate acetate (PMA), and lipopolysaccharide (LPS)-induced COX-2 expression. Taken together, our results suggest that rottlerin causes IL-1β-induced COX-2 upregulation through sustained p38 MAPK activation in MDA-MB-231 human breast cancer cells.

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“…Because reactive oxygen species (ROS) are important signaling molecules associated with HO-1 expression [31,32], we examined whether Bay could induce intracellular ROS production using a H2DCFDA-based flow cytometer detection method. Bay (5 μM) significantly increased intracellular ROS levels, and pretreatment with antioxidants, such as 10 mM N-acetylcystein (NAC) and 10 mM glutathione (GSH), completely blocked Bay-induced ROS production 30 min after Bay treatment (Fig.…”

Section: Generation Of Reactive Oxygen Species Is Involved In Bay-indmentioning

confidence: 99%

An IκBα phosphorylation inhibitor induces heme oxygenase-1(HO-1) expression through the activation of reactive oxygen species (ROS)–Nrf2–ARE signaling and ROS–PI3K/Akt signaling in an NF-κB-independent mechanism

Min

Lee

Joe

et al. 2011

Cellular Signalling

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Rottlerin induces heme oxygenase-1 (HO-1) up-regulation through reactive oxygen species (ROS) dependent and PKC δ-independent pathway in human colon cancer HT29 cells

Cited by 43 publications

References 30 publications

Effect of anthocyanins from rabbit-eye blueberry (Vaccinium virgatum) on cognitive function in mice under trimethyltin-induced neurotoxicity

Effect of anthocyanins from rabbit-eye blueberry (Vaccinium virgatum) on cognitive function in mice under trimethyltin-induced neurotoxicity

Rottlerin enhances IL-1β-induced COX-2 expression through sustained p38 MAPK activation in MDA-MB-231 human breast cancer cells

An IκBα phosphorylation inhibitor induces heme oxygenase-1(HO-1) expression through the activation of reactive oxygen species (ROS)–Nrf2–ARE signaling and ROS–PI3K/Akt signaling in an NF-κB-independent mechanism

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