Roles of protein kinase Cα isozyme in the regulation of oxidative stress and neuropeptide Y gene expression in phenylpropanolamine‐mediated appetite suppression

Kuo, Dong‐Yih; Yang, Shun‐Fa; Chu, Shu‐Chen; Chen, Chin-Hsiu; Hsieh, Yih‐Shou

doi:10.1111/j.1471-4159.2009.05909.x

Cited by 8 publications

(2 citation statements)

References 54 publications

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“…Numerous findings have revealed that PKC alpha is a mediator in the activation of stress-response kinase. Kuo DY et al demonstrated that PKC alpha knock-down could reverse the increase of SOD gene expression induced by phenylpropanolamine [22]. They revealed that PKC alpha signaling was an upstream mediator that regulates SOD gene expression, and the increase in SOD induced by PKC alpha can reduce oxidative stress.…”

Section: Discussionmentioning

confidence: 99%

Effects of selenoprotein S on oxidative injury in human endothelial cells

Zhao

Men

et al. 2013

J Transl Med

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BackgroundSelenoprotein S (SelS) is an important endoplasmic reticulum and plasma membrane-located selenoprotein implicated in inflammatory responses and insulin resistance. However, the effects of SelS on endothelial cells (ECs) have not been reported. In the present study, the role of SelS in oxidative stress and the underlying mechanism were investigated in human ECs.MethodsA SelS over-expression plasmid (pc-SelS) and a SelS-siRNA plasmid were transfected into human umbilical vein endothelial cells (American Type Culture Collection, USA). The cells were divided into four groups: control, SelS over-expression (transfected with pc-SelS), vector control, and SelS knockdown (transfected with siRNA-SelS). After treating the cells with H2O2, the effects of oxidative stress and the expression of caveolin-1 (Cav-1) and protein kinase Cα (PKCα) were investigated.ResultsFollowing treatment with H2O2, over-expression of SelS significantly increased cell viability and superoxide dismutase (SOD) activity, and decreased malondialdehyde (MDA) production and Cav-1 gene and protein expression. However, no effects on PKCα were observed. In contrast, knockdown of SelS significantly decreased cell viability, SOD activity, and PKCα gene and protein expression, and increased MDA production and Cav-1 gene and protein expression.ConclusionsSelS protects ECs from oxidative stress by inhibiting the expression of Cav-1 and PKCα.

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Section: Discussionmentioning

confidence: 99%

Effects of selenoprotein S on oxidative injury in human endothelial cells

Zhao

Men

et al. 2013

J Transl Med

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“…Previously, we reported that the cPKCα isotype, which depends on Ca 2+ and DAG during activation (Kuo et al. 2009b), was involved in the regulation of NPY‐mediated PPA anorexia.…”

Section: Discussionmentioning

confidence: 99%

The effect of protein kinase C‐delta knockdown on anti‐free radical enzyme and neuropeptide Y gene expression in phenylpropanolamine‐treated rats

Kuo

Yang

Chu

et al. 2010

Journal of Neurochemistry

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J. Neurochem. (2010) 114, 1217–1230. Abstract Hypothalamic neuropeptide Y (NPY) has been reported to involve in regulating behavioral response of phenylpropanolamine (PPA), a sympathomimetic agent. This study explored if protein kinase C (PKC)‐δ signaling participated in this regulation. Moreover, possible roles of anti‐free radical enzyme catalase (CAT) and nitrogen oxide synthase (NOS) were also examined. Rats were treated daily with PPA for 4 days. Changes in food intake and hypothalamic NPY, PKCδ, CAT, and NOS contents were assessed and compared. Results showed that PKCδ and CAT increased during PPA treatment, which were concomitant with decreases in NPY content and food intake, while the change of NOS was expressed differently. Moreover, PKCδ knockdown could modify PPA anorexia as well as NPY and CAT expression, while NOS expression remained unchanged. Furthermore, pre‐treatment with NOS inhibitor could modify both PPA anorexia and NPY content. It is suggested that PKCδ participates in the anorectic response of PPA via the modulation of NPY and CAT, while NOS contribute to this modulation via a different mechanism during PPA treatment. Results provide molecular mechanism of NPY‐mediated PPA anorexia and may aid the therapeutic research of PPA and other anti‐obesity drugs.

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Knocking down the transcript of NF-kappaB modulates the reciprocal regulation of endogenous antioxidants and feeding behavior in phenylpropanolamine-treated rats

et al. 2011

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It has been reported that oxidative stress, antioxidants, and neuropeptide Y (NPY) are involved in regulating the feeding behavior of phenylpropanolamine (PPA), a sympathomimetic drug. This study explored whether transcription factor NF-κB is involved in this effect. Rats were treated daily with PPA for 4 days. Changes in hypothalamic NF-κB, NPY, superoxide dismutase (SOD), and glutathione peroxidase (GPx) levels during PPA treatment were assessed and compared. Results showed that NF-κB, SOD, and GPx increased, with a maximal response on Day 2, while the food intake and NPY decreased with the biggest reduction on Day 2 during PPA treatment. To further determine whether NF-κB was involved, intracerebroventricular infusion of antisense oligonucleotide was performed at 1 h before daily PPA in free-moving rats. Cerebral NF-κB knockdown could modify PPA anorexia and the expressions of NPY, SOD, and GPx. It is suggested that hypothalamic NF-κB participates in the reciprocal regulation of NPY and antioxidants, which mediated the appetite-suppressing effect of PPA. Results may further the understanding of the molecular mechanisms of PPA.

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Roles of protein kinase Cα isozyme in the regulation of oxidative stress and neuropeptide Y gene expression in phenylpropanolamine‐mediated appetite suppression

Cited by 8 publications

References 54 publications

Effects of selenoprotein S on oxidative injury in human endothelial cells

Effects of selenoprotein S on oxidative injury in human endothelial cells

The effect of protein kinase C‐delta knockdown on anti‐free radical enzyme and neuropeptide Y gene expression in phenylpropanolamine‐treated rats

Knocking down the transcript of NF-kappaB modulates the reciprocal regulation of endogenous antioxidants and feeding behavior in phenylpropanolamine-treated rats

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