Shikonin ameliorates D-galactose-induced oxidative stress and cognitive impairment in mice via the MAPK and nuclear factor-κB signaling pathway
•Shikonin ameliorates D-gal induced cognitive impairment.•Shikonin ameliorates D-gal induced oxidative stress, astrocyte activation and neuronal damage in brain of D-gal induced mice.•Shikonin inhibited MAPK and NF-κB signaling pathway in brain of D-gal induced mice. Oxidative stress acts as the maj...
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| Veröffentlicht in: | International immunopharmacology 2020-06, Vol.83, p.106491-106491, Article 106491 |
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| container_title | International immunopharmacology |
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| creator | Zhong, Junjie Wang, Zhifu Xie, Qiang Li, Tianwen Chen, Kezhu Zhu, Tongming Tang, Qisheng Shen, Chao Zhu, Jianhong |
| description | •Shikonin ameliorates D-gal induced cognitive impairment.•Shikonin ameliorates D-gal induced oxidative stress, astrocyte activation and neuronal damage in brain of D-gal induced mice.•Shikonin inhibited MAPK and NF-κB signaling pathway in brain of D-gal induced mice.
Oxidative stress acts as the major causative factor for various age‐associated neurodegenerative diseases, triggering cognitive and memory impairments. In the present study, the underlying neuroprotective mechanism governing how shikonin acts against D-galactose (D-gal)-induced memory impairment, neuroinflammation and neuron damage was examined. The results revealed that chronic administration of D-gal [150 mg/kg intraperitoneally (i.p.)] in mice caused cognitive and memory impairments, as determined by Morris water-maze test. Shikonin treatment, however, alleviated D‐gal-induced memory impairment and reversed the D‐gal-induced neural damage and apoptosis. Furthermore, western blotting and the results of morphological analysis revealed that shikonin treatments markedly reduced D‐gal induced neuroinflammation through inhibition of astrocytosis as determined by glial fibrillary acidic protein (GFAP) detection, and downregulating other inflammatory mediators, including tumor necrosis factor-α (TNF-α), interleukin-1β (IL-1β), and IL-6. Moreover, shikonin treatment led to inhibition of the activation of nuclear factor‐κB (NF‐κB) and the phosphorylation of mitogen-activated protein kinases (MAPKs), preventing neurodegeneration. Hence, taken together, the results of the present study suggested that shikonin attenuated D‐gal-induced memory impairment, neuroinflammation and neurodegeneration, possibly via the NF‐κB/mitogen-activated protein kinase (MAPK) pathway. Our data suggest that shikonin could be a promising, endogenous and compatible antioxidant candidate for age‐associated neurodegenerative diseases, including Alzheimer's disease. |
| doi_str_mv | 10.1016/j.intimp.2020.106491 |
| format | Article |
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Oxidative stress acts as the major causative factor for various age‐associated neurodegenerative diseases, triggering cognitive and memory impairments. In the present study, the underlying neuroprotective mechanism governing how shikonin acts against D-galactose (D-gal)-induced memory impairment, neuroinflammation and neuron damage was examined. The results revealed that chronic administration of D-gal [150 mg/kg intraperitoneally (i.p.)] in mice caused cognitive and memory impairments, as determined by Morris water-maze test. Shikonin treatment, however, alleviated D‐gal-induced memory impairment and reversed the D‐gal-induced neural damage and apoptosis. Furthermore, western blotting and the results of morphological analysis revealed that shikonin treatments markedly reduced D‐gal induced neuroinflammation through inhibition of astrocytosis as determined by glial fibrillary acidic protein (GFAP) detection, and downregulating other inflammatory mediators, including tumor necrosis factor-α (TNF-α), interleukin-1β (IL-1β), and IL-6. Moreover, shikonin treatment led to inhibition of the activation of nuclear factor‐κB (NF‐κB) and the phosphorylation of mitogen-activated protein kinases (MAPKs), preventing neurodegeneration. Hence, taken together, the results of the present study suggested that shikonin attenuated D‐gal-induced memory impairment, neuroinflammation and neurodegeneration, possibly via the NF‐κB/mitogen-activated protein kinase (MAPK) pathway. Our data suggest that shikonin could be a promising, endogenous and compatible antioxidant candidate for age‐associated neurodegenerative diseases, including Alzheimer's disease.</description><identifier>ISSN: 1567-5769</identifier><identifier>EISSN: 1878-1705</identifier><identifier>DOI: 10.1016/j.intimp.2020.106491</identifier><identifier>PMID: 32279045</identifier><language>eng</language><publisher>Netherlands: Elsevier B.V</publisher><subject>Alzheimer's disease ; Animals ; Anti-Inflammatory Agents, Non-Steroidal - therapeutic use ; Antioxidants ; Apoptosis ; Cells, Cultured ; Cognitive ability ; Cognitive Dysfunction ; Cytokines - metabolism ; D-gal ; D-Galactose ; Damage ; Extracellular Signal-Regulated MAP Kinases - metabolism ; Galactose ; Galactose - metabolism ; Glial fibrillary acidic protein ; Gliosis ; Health services ; Humans ; IL-1β ; Impairment ; Inflammation ; Inflammation Mediators - metabolism ; Interleukin 6 ; Kinases ; Male ; MAP kinase ; MAPK/ NF-κB ; Memory ; Mice ; Mice, Inbred C57BL ; Naphthoquinones - therapeutic use ; Neurodegeneration ; Neurodegenerative diseases ; Neurodegenerative Diseases - drug therapy ; Neurogenic Inflammation - drug therapy ; Neuronal-glial interactions ; Neuroprotection ; NF-kappa B - metabolism ; Oxidative Stress ; Phosphorylation ; Protein kinase ; Proteins ; Shikonin ; Signal Transduction ; Tumor necrosis factor-TNF ; Tumor necrosis factor-α ; Water treatment ; Western blotting</subject><ispartof>International immunopharmacology, 2020-06, Vol.83, p.106491-106491, Article 106491</ispartof><rights>2020 Elsevier B.V.</rights><rights>Copyright © 2020 Elsevier B.V. All rights reserved.</rights><rights>Copyright Elsevier BV Jun 2020</rights><lds50>peer_reviewed</lds50><woscitedreferencessubscribed>false</woscitedreferencessubscribed><citedby>FETCH-LOGICAL-c390t-41ff5469b070c4b50889501c42dd97beb94d46c2b17fdb39acc3b68d4cb25d153</citedby><cites>FETCH-LOGICAL-c390t-41ff5469b070c4b50889501c42dd97beb94d46c2b17fdb39acc3b68d4cb25d153</cites></display><links><openurl>$$Topenurl_article</openurl><openurlfulltext>$$Topenurlfull_article</openurlfulltext><thumbnail>$$Tsyndetics_thumb_exl</thumbnail><linktohtml>$$Uhttps://www.sciencedirect.com/science/article/pii/S1567576919330206$$EHTML$$P50$$Gelsevier$$H</linktohtml><link.rule.ids>314,776,780,3537,27903,27904,65309</link.rule.ids><backlink>$$Uhttps://www.ncbi.nlm.nih.gov/pubmed/32279045$$D View this record in MEDLINE/PubMed$$Hfree_for_read</backlink></links><search><creatorcontrib>Zhong, Junjie</creatorcontrib><creatorcontrib>Wang, Zhifu</creatorcontrib><creatorcontrib>Xie, Qiang</creatorcontrib><creatorcontrib>Li, Tianwen</creatorcontrib><creatorcontrib>Chen, Kezhu</creatorcontrib><creatorcontrib>Zhu, Tongming</creatorcontrib><creatorcontrib>Tang, Qisheng</creatorcontrib><creatorcontrib>Shen, Chao</creatorcontrib><creatorcontrib>Zhu, Jianhong</creatorcontrib><title>Shikonin ameliorates D-galactose-induced oxidative stress and cognitive impairment in mice via the MAPK and nuclear factor-κB signaling pathway</title><title>International immunopharmacology</title><addtitle>Int Immunopharmacol</addtitle><description>•Shikonin ameliorates D-gal induced cognitive impairment.•Shikonin ameliorates D-gal induced oxidative stress, astrocyte activation and neuronal damage in brain of D-gal induced mice.•Shikonin inhibited MAPK and NF-κB signaling pathway in brain of D-gal induced mice.
Oxidative stress acts as the major causative factor for various age‐associated neurodegenerative diseases, triggering cognitive and memory impairments. In the present study, the underlying neuroprotective mechanism governing how shikonin acts against D-galactose (D-gal)-induced memory impairment, neuroinflammation and neuron damage was examined. The results revealed that chronic administration of D-gal [150 mg/kg intraperitoneally (i.p.)] in mice caused cognitive and memory impairments, as determined by Morris water-maze test. Shikonin treatment, however, alleviated D‐gal-induced memory impairment and reversed the D‐gal-induced neural damage and apoptosis. Furthermore, western blotting and the results of morphological analysis revealed that shikonin treatments markedly reduced D‐gal induced neuroinflammation through inhibition of astrocytosis as determined by glial fibrillary acidic protein (GFAP) detection, and downregulating other inflammatory mediators, including tumor necrosis factor-α (TNF-α), interleukin-1β (IL-1β), and IL-6. Moreover, shikonin treatment led to inhibition of the activation of nuclear factor‐κB (NF‐κB) and the phosphorylation of mitogen-activated protein kinases (MAPKs), preventing neurodegeneration. Hence, taken together, the results of the present study suggested that shikonin attenuated D‐gal-induced memory impairment, neuroinflammation and neurodegeneration, possibly via the NF‐κB/mitogen-activated protein kinase (MAPK) pathway. Our data suggest that shikonin could be a promising, endogenous and compatible antioxidant candidate for age‐associated neurodegenerative diseases, including Alzheimer's disease.</description><subject>Alzheimer's disease</subject><subject>Animals</subject><subject>Anti-Inflammatory Agents, Non-Steroidal - therapeutic use</subject><subject>Antioxidants</subject><subject>Apoptosis</subject><subject>Cells, Cultured</subject><subject>Cognitive ability</subject><subject>Cognitive Dysfunction</subject><subject>Cytokines - metabolism</subject><subject>D-gal</subject><subject>D-Galactose</subject><subject>Damage</subject><subject>Extracellular Signal-Regulated MAP Kinases - metabolism</subject><subject>Galactose</subject><subject>Galactose - metabolism</subject><subject>Glial fibrillary acidic protein</subject><subject>Gliosis</subject><subject>Health services</subject><subject>Humans</subject><subject>IL-1β</subject><subject>Impairment</subject><subject>Inflammation</subject><subject>Inflammation Mediators - metabolism</subject><subject>Interleukin 6</subject><subject>Kinases</subject><subject>Male</subject><subject>MAP kinase</subject><subject>MAPK/ NF-κB</subject><subject>Memory</subject><subject>Mice</subject><subject>Mice, Inbred C57BL</subject><subject>Naphthoquinones - therapeutic use</subject><subject>Neurodegeneration</subject><subject>Neurodegenerative diseases</subject><subject>Neurodegenerative Diseases - drug therapy</subject><subject>Neurogenic Inflammation - drug therapy</subject><subject>Neuronal-glial interactions</subject><subject>Neuroprotection</subject><subject>NF-kappa B - metabolism</subject><subject>Oxidative Stress</subject><subject>Phosphorylation</subject><subject>Protein kinase</subject><subject>Proteins</subject><subject>Shikonin</subject><subject>Signal Transduction</subject><subject>Tumor necrosis factor-TNF</subject><subject>Tumor necrosis factor-α</subject><subject>Water treatment</subject><subject>Western blotting</subject><issn>1567-5769</issn><issn>1878-1705</issn><fulltext>true</fulltext><rsrctype>article</rsrctype><creationdate>2020</creationdate><recordtype>article</recordtype><sourceid>EIF</sourceid><recordid>eNp9kUuO1DAURSMEoj-wA4QsMWGSwk7sJJ4gNU3zEY1AAsaWY79UvSKxq22noHfBelgEa8LpahgwYGTr6rzrJ5-ieMToilHWPNuu0CWcdquKVkvUcMnuFMesa7uStVTczXfRtKVoG3lUnMS4pTTnnN0vjuqqaiXl4rj48WmDX71DR_QEI_qgE0TyslzrUZvkI5To7GzAEv8drU64BxJTgBiJdpYYv3Z4E-ZNNIYJXCK5bEIDZI-apA2Q92cf393QbjYj6ECGpTqUv36-IBHXTo_o1mSn0-abvn5Q3Bv0GOHh7XlafHl18fn8TXn54fXb87PL0tSSppKzYRC8kT1tqeG9oF0nBWWGV9bKtodecssbU_WsHWxfS21M3Ted5aavhGWiPi2eHnp3wV_NEJOaMBoYR-3Az1FVdScrKjvOMvrkH3Tr55DXzhTndcOFrJdCfqBM8DEGGNQu4KTDtWJULcbUVh2MqcWYOhjLY49vy-d-Avt36I-iDDw_AJB_Y48QVDQILivBACYp6_H_L_wGZParhw</recordid><startdate>202006</startdate><enddate>202006</enddate><creator>Zhong, Junjie</creator><creator>Wang, Zhifu</creator><creator>Xie, Qiang</creator><creator>Li, Tianwen</creator><creator>Chen, Kezhu</creator><creator>Zhu, Tongming</creator><creator>Tang, Qisheng</creator><creator>Shen, Chao</creator><creator>Zhu, Jianhong</creator><general>Elsevier B.V</general><general>Elsevier BV</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>7QO</scope><scope>7T5</scope><scope>7U7</scope><scope>7U9</scope><scope>8FD</scope><scope>C1K</scope><scope>FR3</scope><scope>H94</scope><scope>P64</scope><scope>7X8</scope></search><sort><creationdate>202006</creationdate><title>Shikonin ameliorates D-galactose-induced oxidative stress and cognitive impairment in mice via the MAPK and nuclear factor-κB signaling pathway</title><author>Zhong, Junjie ; 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Oxidative stress acts as the major causative factor for various age‐associated neurodegenerative diseases, triggering cognitive and memory impairments. In the present study, the underlying neuroprotective mechanism governing how shikonin acts against D-galactose (D-gal)-induced memory impairment, neuroinflammation and neuron damage was examined. The results revealed that chronic administration of D-gal [150 mg/kg intraperitoneally (i.p.)] in mice caused cognitive and memory impairments, as determined by Morris water-maze test. Shikonin treatment, however, alleviated D‐gal-induced memory impairment and reversed the D‐gal-induced neural damage and apoptosis. Furthermore, western blotting and the results of morphological analysis revealed that shikonin treatments markedly reduced D‐gal induced neuroinflammation through inhibition of astrocytosis as determined by glial fibrillary acidic protein (GFAP) detection, and downregulating other inflammatory mediators, including tumor necrosis factor-α (TNF-α), interleukin-1β (IL-1β), and IL-6. Moreover, shikonin treatment led to inhibition of the activation of nuclear factor‐κB (NF‐κB) and the phosphorylation of mitogen-activated protein kinases (MAPKs), preventing neurodegeneration. Hence, taken together, the results of the present study suggested that shikonin attenuated D‐gal-induced memory impairment, neuroinflammation and neurodegeneration, possibly via the NF‐κB/mitogen-activated protein kinase (MAPK) pathway. Our data suggest that shikonin could be a promising, endogenous and compatible antioxidant candidate for age‐associated neurodegenerative diseases, including Alzheimer's disease.</abstract><cop>Netherlands</cop><pub>Elsevier B.V</pub><pmid>32279045</pmid><doi>10.1016/j.intimp.2020.106491</doi><tpages>1</tpages></addata></record> |
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| subjects | Alzheimer's disease Animals Anti-Inflammatory Agents, Non-Steroidal - therapeutic use Antioxidants Apoptosis Cells, Cultured Cognitive ability Cognitive Dysfunction Cytokines - metabolism D-gal D-Galactose Damage Extracellular Signal-Regulated MAP Kinases - metabolism Galactose Galactose - metabolism Glial fibrillary acidic protein Gliosis Health services Humans IL-1β Impairment Inflammation Inflammation Mediators - metabolism Interleukin 6 Kinases Male MAP kinase MAPK/ NF-κB Memory Mice Mice, Inbred C57BL Naphthoquinones - therapeutic use Neurodegeneration Neurodegenerative diseases Neurodegenerative Diseases - drug therapy Neurogenic Inflammation - drug therapy Neuronal-glial interactions Neuroprotection NF-kappa B - metabolism Oxidative Stress Phosphorylation Protein kinase Proteins Shikonin Signal Transduction Tumor necrosis factor-TNF Tumor necrosis factor-α Water treatment Western blotting |
| title | Shikonin ameliorates D-galactose-induced oxidative stress and cognitive impairment in mice via the MAPK and nuclear factor-κB signaling pathway |
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