Reversal of Beta-Amyloid-Induced Neurotoxicity in PC12 Cells by Curcumin, the Important Role of ROS-Mediated Signaling and ERK Pathway

Progressive accumulation of beta-amyloid (Aβ) will form the senile plaques and cause oxidative damage and neuronal cell death, which was accepted as the major pathological mechanism to the Alzheimer’s disease (AD). Hence, inhibition of Aβ-induced oxidative damage and neuronal cell apoptosis by agent...

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Veröffentlicht in:Cellular and molecular neurobiology 2017-03, Vol.37 (2), p.211-222
Hauptverfasser: Fan, Cun-dong, Li, Yuan, Fu, Xiao-ting, Wu, Qing-jian, Hou, Ya-jun, Yang, Ming-feng, Sun, Jing-yi, Fu, Xiao-yan, Zheng, Zun-cheng, Sun, Bao-liang
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container_title Cellular and molecular neurobiology
container_volume 37
creator Fan, Cun-dong
Li, Yuan
Fu, Xiao-ting
Wu, Qing-jian
Hou, Ya-jun
Yang, Ming-feng
Sun, Jing-yi
Fu, Xiao-yan
Zheng, Zun-cheng
Sun, Bao-liang
description Progressive accumulation of beta-amyloid (Aβ) will form the senile plaques and cause oxidative damage and neuronal cell death, which was accepted as the major pathological mechanism to the Alzheimer’s disease (AD). Hence, inhibition of Aβ-induced oxidative damage and neuronal cell apoptosis by agents with potential antioxidant properties represents one of the most effective strategies in combating human AD. Curcumin (Cur) a natural extraction from curcuma longa has potential of pharmacological efficacy, including the benefit to antagonize Aβ-induced neurotoxicity. However, the molecular mechanism remains elusive. The present study evaluated the protective effect of Cur against Aβ-induced cytotoxicity and apoptosis in PC12 cells and investigated the underlying mechanism. The results showed that Cur markedly reduced Aβ-induced cytotoxicity by inhibition of mitochondria-mediated apoptosis through regulation of Bcl-2 family. The PARP cleavage, caspases activation, and ROS-mediated DNA damage induced by Aβ were all significantly blocked by Cur. Moreover, regulation of p38 MAPK and AKT pathways both contributed to this protective potency. Our findings suggested that Cur could effectively suppress Aβ-induced cytotoxicity and apoptosis by inhibition of ROS-mediated oxidative damage and regulation of ERK pathway, which validated its therapeutic potential in chemoprevention and chemotherapy of Aβ-induced neurotoxicity.
doi_str_mv 10.1007/s10571-016-0362-3
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inhibitors</subject><subject>Reactive Oxygen Species - metabolism</subject><subject>Senile plaques</subject><subject>Signal Transduction - drug effects</subject><subject>Signal Transduction - physiology</subject><subject>β-Amyloid</subject><issn>0272-4340</issn><issn>1573-6830</issn><issn>1573-6830</issn><fulltext>true</fulltext><rsrctype>article</rsrctype><creationdate>2017</creationdate><recordtype>article</recordtype><sourceid>EIF</sourceid><recordid>eNp1kcFuFCEYgImxsWv1AbwYEi8epPLDDDNzrJOqG1vbbPU8YeHfLc3MsAKjzgv43LLZ2hgTuXDg-z8gHyEvgJ8C59XbCLysgHFQjEslmHxEFlBWkqla8sdkwUUlWCELfkyexnjHOW84L5-QY6GaCkpRLMivFX7HEHVP_Ya-w6TZ2TD33lm2HO1k0NLPOAWf_E9nXJqpG-l1C4K22PeRrmfaTsFMgxvf0HSLdDnsfEh6THTle9w7V1c37BKt0ym7btx21L0bt1SPlp6vPtFrnW5_6PkZOdroPuLz-_2EfH1__qX9yC6uPizbswtmClknZmADUBYIDYpGVkaty9LUheCAeQm9RlCikBx1YwthjK0tKA1Qy9qWyjTyhLw-eHfBf5swpm5w0eS_6BH9FDuohVJKQKMy-uof9M5PIT9_T9W8qqSQVabgQJngYwy46XbBDTrMHfBuH6k7ROpypG4fqZN55uW9eVoPaB8m_lTJgDgAMR-NWwx_Xf1f629-qJsM</recordid><startdate>20170301</startdate><enddate>20170301</enddate><creator>Fan, Cun-dong</creator><creator>Li, Yuan</creator><creator>Fu, Xiao-ting</creator><creator>Wu, Qing-jian</creator><creator>Hou, Ya-jun</creator><creator>Yang, Ming-feng</creator><creator>Sun, Jing-yi</creator><creator>Fu, Xiao-yan</creator><creator>Zheng, Zun-cheng</creator><creator>Sun, Bao-liang</creator><general>Springer US</general><general>Springer Nature B.V</general><scope>CGR</scope><scope>CUY</scope><scope>CVF</scope><scope>ECM</scope><scope>EIF</scope><scope>NPM</scope><scope>AAYXX</scope><scope>CITATION</scope><scope>7X8</scope></search><sort><creationdate>20170301</creationdate><title>Reversal of Beta-Amyloid-Induced Neurotoxicity in PC12 Cells by Curcumin, the Important Role of ROS-Mediated Signaling and ERK Pathway</title><author>Fan, Cun-dong ; Li, Yuan ; Fu, Xiao-ting ; Wu, Qing-jian ; Hou, Ya-jun ; Yang, Ming-feng ; Sun, Jing-yi ; Fu, Xiao-yan ; Zheng, Zun-cheng ; Sun, Bao-liang</author></sort><facets><frbrtype>5</frbrtype><frbrgroupid>cdi_FETCH-LOGICAL-c438t-c1f1154e19e2937c6b55c84201eeee2abe162430ea9d42ccd8d16a11838d56c93</frbrgroupid><rsrctype>articles</rsrctype><prefilter>articles</prefilter><language>eng</language><creationdate>2017</creationdate><topic>AKT protein</topic><topic>Alzheimer's disease</topic><topic>Amyloid beta-Peptides - toxicity</topic><topic>Animals</topic><topic>Anti-Inflammatory Agents, Non-Steroidal - pharmacology</topic><topic>Apoptosis</topic><topic>Apoptosis - drug effects</topic><topic>Apoptosis - physiology</topic><topic>Bcl protein</topic><topic>Bcl-2 protein</topic><topic>Biomedical and Life Sciences</topic><topic>Biomedicine</topic><topic>Cell Biology</topic><topic>Cell death</topic><topic>Cell Survival - drug effects</topic><topic>Cell Survival - physiology</topic><topic>Chemotherapy</topic><topic>Curcumin</topic><topic>Curcumin - pharmacology</topic><topic>Cytotoxicity</topic><topic>DNA damage</topic><topic>Dose-Response Relationship, Drug</topic><topic>Extracellular signal-regulated kinase</topic><topic>MAP kinase</topic><topic>MAP Kinase Signaling System - drug effects</topic><topic>MAP Kinase Signaling System - physiology</topic><topic>Metabolic pathways</topic><topic>Mitochondria</topic><topic>Neurobiology</topic><topic>Neurodegenerative diseases</topic><topic>Neurosciences</topic><topic>Neurotoxicity</topic><topic>Original Research</topic><topic>PC12 Cells</topic><topic>Peptide Fragments - toxicity</topic><topic>Pheochromocytoma cells</topic><topic>Poly(ADP-ribose) polymerase</topic><topic>Rats</topic><topic>Reactive Oxygen Species - antagonists &amp; inhibitors</topic><topic>Reactive Oxygen Species - metabolism</topic><topic>Senile plaques</topic><topic>Signal Transduction - drug effects</topic><topic>Signal Transduction - physiology</topic><topic>β-Amyloid</topic><toplevel>peer_reviewed</toplevel><toplevel>online_resources</toplevel><creatorcontrib>Fan, Cun-dong</creatorcontrib><creatorcontrib>Li, Yuan</creatorcontrib><creatorcontrib>Fu, Xiao-ting</creatorcontrib><creatorcontrib>Wu, Qing-jian</creatorcontrib><creatorcontrib>Hou, Ya-jun</creatorcontrib><creatorcontrib>Yang, Ming-feng</creatorcontrib><creatorcontrib>Sun, Jing-yi</creatorcontrib><creatorcontrib>Fu, Xiao-yan</creatorcontrib><creatorcontrib>Zheng, Zun-cheng</creatorcontrib><creatorcontrib>Sun, Bao-liang</creatorcontrib><collection>Medline</collection><collection>MEDLINE</collection><collection>MEDLINE (Ovid)</collection><collection>MEDLINE</collection><collection>MEDLINE</collection><collection>PubMed</collection><collection>CrossRef</collection><collection>MEDLINE - Academic</collection><jtitle>Cellular and molecular neurobiology</jtitle></facets><delivery><delcategory>Remote Search Resource</delcategory><fulltext>fulltext</fulltext></delivery><addata><au>Fan, Cun-dong</au><au>Li, Yuan</au><au>Fu, Xiao-ting</au><au>Wu, Qing-jian</au><au>Hou, Ya-jun</au><au>Yang, Ming-feng</au><au>Sun, Jing-yi</au><au>Fu, Xiao-yan</au><au>Zheng, Zun-cheng</au><au>Sun, Bao-liang</au><format>journal</format><genre>article</genre><ristype>JOUR</ristype><atitle>Reversal of Beta-Amyloid-Induced Neurotoxicity in PC12 Cells by Curcumin, the Important Role of ROS-Mediated Signaling and ERK Pathway</atitle><jtitle>Cellular and molecular neurobiology</jtitle><stitle>Cell Mol Neurobiol</stitle><addtitle>Cell Mol Neurobiol</addtitle><date>2017-03-01</date><risdate>2017</risdate><volume>37</volume><issue>2</issue><spage>211</spage><epage>222</epage><pages>211-222</pages><issn>0272-4340</issn><issn>1573-6830</issn><eissn>1573-6830</eissn><abstract>Progressive accumulation of beta-amyloid (Aβ) will form the senile plaques and cause oxidative damage and neuronal cell death, which was accepted as the major pathological mechanism to the Alzheimer’s disease (AD). Hence, inhibition of Aβ-induced oxidative damage and neuronal cell apoptosis by agents with potential antioxidant properties represents one of the most effective strategies in combating human AD. Curcumin (Cur) a natural extraction from curcuma longa has potential of pharmacological efficacy, including the benefit to antagonize Aβ-induced neurotoxicity. However, the molecular mechanism remains elusive. The present study evaluated the protective effect of Cur against Aβ-induced cytotoxicity and apoptosis in PC12 cells and investigated the underlying mechanism. The results showed that Cur markedly reduced Aβ-induced cytotoxicity by inhibition of mitochondria-mediated apoptosis through regulation of Bcl-2 family. The PARP cleavage, caspases activation, and ROS-mediated DNA damage induced by Aβ were all significantly blocked by Cur. Moreover, regulation of p38 MAPK and AKT pathways both contributed to this protective potency. 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subjects AKT protein
Alzheimer's disease
Amyloid beta-Peptides - toxicity
Animals
Anti-Inflammatory Agents, Non-Steroidal - pharmacology
Apoptosis
Apoptosis - drug effects
Apoptosis - physiology
Bcl protein
Bcl-2 protein
Biomedical and Life Sciences
Biomedicine
Cell Biology
Cell death
Cell Survival - drug effects
Cell Survival - physiology
Chemotherapy
Curcumin
Curcumin - pharmacology
Cytotoxicity
DNA damage
Dose-Response Relationship, Drug
Extracellular signal-regulated kinase
MAP kinase
MAP Kinase Signaling System - drug effects
MAP Kinase Signaling System - physiology
Metabolic pathways
Mitochondria
Neurobiology
Neurodegenerative diseases
Neurosciences
Neurotoxicity
Original Research
PC12 Cells
Peptide Fragments - toxicity
Pheochromocytoma cells
Poly(ADP-ribose) polymerase
Rats
Reactive Oxygen Species - antagonists & inhibitors
Reactive Oxygen Species - metabolism
Senile plaques
Signal Transduction - drug effects
Signal Transduction - physiology
β-Amyloid
title Reversal of Beta-Amyloid-Induced Neurotoxicity in PC12 Cells by Curcumin, the Important Role of ROS-Mediated Signaling and ERK Pathway
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