Ligustrazine ameliorates lipopolysaccharide‑induced neurocognitive impairment by activating autophagy via the PI3K/AKT/mTOR pathway
Autophagy is a lysosome‑mediated cell content‑dependent degradation pathway that leads to enhanced inflammation in an uncontrolled state. This study examined the role of autophagy in lipopolysaccharide (LPS)‑induced brain inflammation and the effects of the traditional Chinese medicine ligustrazine...
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| Veröffentlicht in: | International journal of molecular medicine 2020-06, Vol.45 (6), p.1711-1720 |
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| creator | Li, Guangming Liu, Sisi Wang, Huili Pan, Rui Tang, Haijie Yan, Xueqin Wang, Yanping Fu, Yongmei Jing, Fujun Dong, Jun |
| description | Autophagy is a lysosome‑mediated cell content‑dependent degradation pathway that leads to enhanced inflammation in an uncontrolled state. This study examined the role of autophagy in lipopolysaccharide (LPS)‑induced brain inflammation and the effects of the traditional Chinese medicine ligustrazine on LPS‑induced neurocognitive impairment in rats. Furthermore, the molecular mechanisms by which ligustrazine influences neurocognitive impairments were explored. The production of the inflammatory mediators interleukin (IL)‑1β and tumor necrosis factor (TNF)‑α was analyzed using ELISAs, and the expression levels of the autophagy marker microtubule‑associated protein light chain 3 (LC3) II/I were analyzed using western blotting. LPS exposure upregulated the expression of IL‑1β and TNF‑α and downregulated the expression of LC3 II/I. Ligustrazine activated autophagy by preventing the expression of phosphoinositide 3‑kinase (PI3K), phosphorylated protein kinase B (p‑AKT), and phosphorylated mammalian target of rapamycin (p‑mTOR). The present results suggest that ligustrazine improved LPS‑induced neurocognitive impairments by activating autophagy and ameliorated neuronal injury by regulating the PI3K/AKT/mTOR signaling pathway. These findings provide an important reference for the prevention and treatment of neuroinflammation. |
| doi_str_mv | 10.3892/ijmm.2020.4548 |
| format | Article |
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This study examined the role of autophagy in lipopolysaccharide (LPS)‑induced brain inflammation and the effects of the traditional Chinese medicine ligustrazine on LPS‑induced neurocognitive impairment in rats. Furthermore, the molecular mechanisms by which ligustrazine influences neurocognitive impairments were explored. The production of the inflammatory mediators interleukin (IL)‑1β and tumor necrosis factor (TNF)‑α was analyzed using ELISAs, and the expression levels of the autophagy marker microtubule‑associated protein light chain 3 (LC3) II/I were analyzed using western blotting. LPS exposure upregulated the expression of IL‑1β and TNF‑α and downregulated the expression of LC3 II/I. Ligustrazine activated autophagy by preventing the expression of phosphoinositide 3‑kinase (PI3K), phosphorylated protein kinase B (p‑AKT), and phosphorylated mammalian target of rapamycin (p‑mTOR). The present results suggest that ligustrazine improved LPS‑induced neurocognitive impairments by activating autophagy and ameliorated neuronal injury by regulating the PI3K/AKT/mTOR signaling pathway. These findings provide an important reference for the prevention and treatment of neuroinflammation.</description><identifier>ISSN: 1107-3756</identifier><identifier>EISSN: 1791-244X</identifier><identifier>DOI: 10.3892/ijmm.2020.4548</identifier><identifier>PMID: 32236586</identifier><language>eng</language><publisher>Greece: Spandidos Publications</publisher><subject>Aging ; Alzheimer's disease ; Analysis ; Animal memory ; Animals ; Apoptosis - drug effects ; Asian medicine ; Autophagy ; Autophagy - drug effects ; Disabilities ; Down-Regulation - drug effects ; Experiments ; Female ; Inflammation ; Inflammation - drug therapy ; Inflammation - metabolism ; Interleukin-1beta - metabolism ; Interleukins ; Lipopolysaccharides - pharmacology ; Male ; Mitogens ; Necrosis ; Neurocognitive Disorders - chemically induced ; Neurocognitive Disorders - drug therapy ; Neurocognitive Disorders - metabolism ; Neurons ; Older people ; Phosphatidylinositol 3-Kinases - metabolism ; Protein kinases ; Proto-Oncogene Proteins c-akt - metabolism ; Pyrazines - pharmacology ; Rats ; Rats, Sprague-Dawley ; Signal Transduction - drug effects ; TOR Serine-Threonine Kinases - metabolism ; Traditional Chinese medicine ; Tumor necrosis factor ; Tumor necrosis factor-TNF ; Tumors</subject><ispartof>International journal of molecular medicine, 2020-06, Vol.45 (6), p.1711-1720</ispartof><rights>COPYRIGHT 2020 Spandidos Publications</rights><rights>Copyright Spandidos Publications UK Ltd. 2020</rights><rights>Copyright: © Li et al. 2020</rights><oa>free_for_read</oa><woscitedreferencessubscribed>false</woscitedreferencessubscribed><citedby>FETCH-LOGICAL-c485t-1d0ca08b88ac2a35fd3c6da062efb0d335175e75af98cb594534ac5ba156a9663</citedby><cites>FETCH-LOGICAL-c485t-1d0ca08b88ac2a35fd3c6da062efb0d335175e75af98cb594534ac5ba156a9663</cites></display><links><openurl>$$Topenurl_article</openurl><openurlfulltext>$$Topenurlfull_article</openurlfulltext><thumbnail>$$Tsyndetics_thumb_exl</thumbnail><link.rule.ids>230,314,780,784,885,27924,27925</link.rule.ids><backlink>$$Uhttps://www.ncbi.nlm.nih.gov/pubmed/32236586$$D View this record in MEDLINE/PubMed$$Hfree_for_read</backlink></links><search><creatorcontrib>Li, Guangming</creatorcontrib><creatorcontrib>Liu, Sisi</creatorcontrib><creatorcontrib>Wang, Huili</creatorcontrib><creatorcontrib>Pan, Rui</creatorcontrib><creatorcontrib>Tang, Haijie</creatorcontrib><creatorcontrib>Yan, Xueqin</creatorcontrib><creatorcontrib>Wang, Yanping</creatorcontrib><creatorcontrib>Fu, Yongmei</creatorcontrib><creatorcontrib>Jing, Fujun</creatorcontrib><creatorcontrib>Dong, Jun</creatorcontrib><title>Ligustrazine ameliorates lipopolysaccharide‑induced neurocognitive impairment by activating autophagy via the PI3K/AKT/mTOR pathway</title><title>International journal of molecular medicine</title><addtitle>Int J Mol Med</addtitle><description>Autophagy is a lysosome‑mediated cell content‑dependent degradation pathway that leads to enhanced inflammation in an uncontrolled state. This study examined the role of autophagy in lipopolysaccharide (LPS)‑induced brain inflammation and the effects of the traditional Chinese medicine ligustrazine on LPS‑induced neurocognitive impairment in rats. Furthermore, the molecular mechanisms by which ligustrazine influences neurocognitive impairments were explored. The production of the inflammatory mediators interleukin (IL)‑1β and tumor necrosis factor (TNF)‑α was analyzed using ELISAs, and the expression levels of the autophagy marker microtubule‑associated protein light chain 3 (LC3) II/I were analyzed using western blotting. LPS exposure upregulated the expression of IL‑1β and TNF‑α and downregulated the expression of LC3 II/I. Ligustrazine activated autophagy by preventing the expression of phosphoinositide 3‑kinase (PI3K), phosphorylated protein kinase B (p‑AKT), and phosphorylated mammalian target of rapamycin (p‑mTOR). The present results suggest that ligustrazine improved LPS‑induced neurocognitive impairments by activating autophagy and ameliorated neuronal injury by regulating the PI3K/AKT/mTOR signaling pathway. These findings provide an important reference for the prevention and treatment of neuroinflammation.</description><subject>Aging</subject><subject>Alzheimer's disease</subject><subject>Analysis</subject><subject>Animal memory</subject><subject>Animals</subject><subject>Apoptosis - drug effects</subject><subject>Asian medicine</subject><subject>Autophagy</subject><subject>Autophagy - drug effects</subject><subject>Disabilities</subject><subject>Down-Regulation - drug effects</subject><subject>Experiments</subject><subject>Female</subject><subject>Inflammation</subject><subject>Inflammation - drug therapy</subject><subject>Inflammation - metabolism</subject><subject>Interleukin-1beta - metabolism</subject><subject>Interleukins</subject><subject>Lipopolysaccharides - pharmacology</subject><subject>Male</subject><subject>Mitogens</subject><subject>Necrosis</subject><subject>Neurocognitive Disorders - chemically induced</subject><subject>Neurocognitive Disorders - drug therapy</subject><subject>Neurocognitive Disorders - metabolism</subject><subject>Neurons</subject><subject>Older people</subject><subject>Phosphatidylinositol 3-Kinases - metabolism</subject><subject>Protein kinases</subject><subject>Proto-Oncogene Proteins c-akt - metabolism</subject><subject>Pyrazines - pharmacology</subject><subject>Rats</subject><subject>Rats, Sprague-Dawley</subject><subject>Signal Transduction - drug effects</subject><subject>TOR Serine-Threonine Kinases - metabolism</subject><subject>Traditional Chinese medicine</subject><subject>Tumor necrosis factor</subject><subject>Tumor necrosis factor-TNF</subject><subject>Tumors</subject><issn>1107-3756</issn><issn>1791-244X</issn><fulltext>true</fulltext><rsrctype>article</rsrctype><creationdate>2020</creationdate><recordtype>article</recordtype><sourceid>EIF</sourceid><sourceid>ABUWG</sourceid><sourceid>AFKRA</sourceid><sourceid>BENPR</sourceid><sourceid>CCPQU</sourceid><recordid>eNptUk2L1EAQDaK46-rVozR4zkx_p3MRhsWPZQdWZARvTaXTSXpIp2OnMzKevPgD_Iv-EjO4rgpLHaqoevV4Rb0se07wiqmSrt3e-xXFFK-44OpBdk6KkuSU808Pl5rgImeFkGfZk2naY0wFL9Xj7IxRyqRQ8jz7vnXtPKUIX91gEXjbuxAh2Qn1bgxj6I8TGNNBdLX9-e2HG-rZ2BoNdo7BhHZwyR0scn4EF70dEqqOCMzShOSGFsGcwthBe0QHByh1Fr2_YtfrzfVu7Xc3H9AIqfsCx6fZowb6yT67zRfZxzevd5fv8u3N26vLzTY3XImUkxobwKpSCgwFJpqaGVkDltQ2Fa4ZE6QQthDQlMpUouSCcTCiAiIklFKyi-zVb95xrrytzSI4Qq_H6DzEow7g9P-TwXW6DQddEFlKwRaCl7cEMXye7ZT0PsxxWDRrykpOuFAF_4tqobfaDU1YyIx3k9EbSRmjvFDFglrdg1qitt6ZMNjGLf37FkwM0xRtcyecYH1ygz65QZ_coE9uWBZe_HvuHfzP-9kvYSe09g</recordid><startdate>20200601</startdate><enddate>20200601</enddate><creator>Li, Guangming</creator><creator>Liu, Sisi</creator><creator>Wang, Huili</creator><creator>Pan, Rui</creator><creator>Tang, Haijie</creator><creator>Yan, Xueqin</creator><creator>Wang, Yanping</creator><creator>Fu, Yongmei</creator><creator>Jing, Fujun</creator><creator>Dong, Jun</creator><general>Spandidos Publications</general><general>Spandidos Publications UK Ltd</general><general>D.A. 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drug effects</topic><topic>Asian medicine</topic><topic>Autophagy</topic><topic>Autophagy - drug effects</topic><topic>Disabilities</topic><topic>Down-Regulation - drug effects</topic><topic>Experiments</topic><topic>Female</topic><topic>Inflammation</topic><topic>Inflammation - drug therapy</topic><topic>Inflammation - metabolism</topic><topic>Interleukin-1beta - metabolism</topic><topic>Interleukins</topic><topic>Lipopolysaccharides - pharmacology</topic><topic>Male</topic><topic>Mitogens</topic><topic>Necrosis</topic><topic>Neurocognitive Disorders - chemically induced</topic><topic>Neurocognitive Disorders - drug therapy</topic><topic>Neurocognitive Disorders - metabolism</topic><topic>Neurons</topic><topic>Older people</topic><topic>Phosphatidylinositol 3-Kinases - metabolism</topic><topic>Protein kinases</topic><topic>Proto-Oncogene Proteins c-akt - metabolism</topic><topic>Pyrazines - pharmacology</topic><topic>Rats</topic><topic>Rats, Sprague-Dawley</topic><topic>Signal Transduction - drug effects</topic><topic>TOR Serine-Threonine Kinases - metabolism</topic><topic>Traditional Chinese medicine</topic><topic>Tumor necrosis factor</topic><topic>Tumor necrosis factor-TNF</topic><topic>Tumors</topic><toplevel>online_resources</toplevel><creatorcontrib>Li, Guangming</creatorcontrib><creatorcontrib>Liu, Sisi</creatorcontrib><creatorcontrib>Wang, Huili</creatorcontrib><creatorcontrib>Pan, Rui</creatorcontrib><creatorcontrib>Tang, Haijie</creatorcontrib><creatorcontrib>Yan, Xueqin</creatorcontrib><creatorcontrib>Wang, Yanping</creatorcontrib><creatorcontrib>Fu, Yongmei</creatorcontrib><creatorcontrib>Jing, Fujun</creatorcontrib><creatorcontrib>Dong, Jun</creatorcontrib><collection>Medline</collection><collection>MEDLINE</collection><collection>MEDLINE (Ovid)</collection><collection>MEDLINE</collection><collection>MEDLINE</collection><collection>PubMed</collection><collection>CrossRef</collection><collection>ProQuest Central (Corporate)</collection><collection>Health & Medical Collection</collection><collection>ProQuest Central (purchase pre-March 2016)</collection><collection>Medical Database (Alumni Edition)</collection><collection>ProQuest Pharma Collection</collection><collection>Hospital Premium Collection</collection><collection>Hospital Premium Collection (Alumni Edition)</collection><collection>ProQuest Central (Alumni) (purchase pre-March 2016)</collection><collection>ProQuest Central (Alumni Edition)</collection><collection>ProQuest Central UK/Ireland</collection><collection>ProQuest Central</collection><collection>ProQuest One Community College</collection><collection>Health Research Premium Collection</collection><collection>Health Research Premium Collection (Alumni)</collection><collection>ProQuest Health & Medical Complete (Alumni)</collection><collection>Health & Medical Collection (Alumni Edition)</collection><collection>Medical Database</collection><collection>ProQuest One Academic Eastern Edition (DO NOT USE)</collection><collection>ProQuest One Academic</collection><collection>ProQuest One Academic UKI Edition</collection><collection>ProQuest Central China</collection><collection>PubMed Central (Full Participant titles)</collection><jtitle>International journal of molecular medicine</jtitle></facets><delivery><delcategory>Remote Search Resource</delcategory><fulltext>fulltext</fulltext></delivery><addata><au>Li, Guangming</au><au>Liu, Sisi</au><au>Wang, Huili</au><au>Pan, Rui</au><au>Tang, Haijie</au><au>Yan, Xueqin</au><au>Wang, Yanping</au><au>Fu, Yongmei</au><au>Jing, Fujun</au><au>Dong, Jun</au><format>journal</format><genre>article</genre><ristype>JOUR</ristype><atitle>Ligustrazine ameliorates lipopolysaccharide‑induced neurocognitive impairment by activating autophagy via the PI3K/AKT/mTOR pathway</atitle><jtitle>International journal of molecular medicine</jtitle><addtitle>Int J Mol Med</addtitle><date>2020-06-01</date><risdate>2020</risdate><volume>45</volume><issue>6</issue><spage>1711</spage><epage>1720</epage><pages>1711-1720</pages><issn>1107-3756</issn><eissn>1791-244X</eissn><abstract>Autophagy is a lysosome‑mediated cell content‑dependent degradation pathway that leads to enhanced inflammation in an uncontrolled state. This study examined the role of autophagy in lipopolysaccharide (LPS)‑induced brain inflammation and the effects of the traditional Chinese medicine ligustrazine on LPS‑induced neurocognitive impairment in rats. Furthermore, the molecular mechanisms by which ligustrazine influences neurocognitive impairments were explored. The production of the inflammatory mediators interleukin (IL)‑1β and tumor necrosis factor (TNF)‑α was analyzed using ELISAs, and the expression levels of the autophagy marker microtubule‑associated protein light chain 3 (LC3) II/I were analyzed using western blotting. LPS exposure upregulated the expression of IL‑1β and TNF‑α and downregulated the expression of LC3 II/I. Ligustrazine activated autophagy by preventing the expression of phosphoinositide 3‑kinase (PI3K), phosphorylated protein kinase B (p‑AKT), and phosphorylated mammalian target of rapamycin (p‑mTOR). The present results suggest that ligustrazine improved LPS‑induced neurocognitive impairments by activating autophagy and ameliorated neuronal injury by regulating the PI3K/AKT/mTOR signaling pathway. These findings provide an important reference for the prevention and treatment of neuroinflammation.</abstract><cop>Greece</cop><pub>Spandidos Publications</pub><pmid>32236586</pmid><doi>10.3892/ijmm.2020.4548</doi><tpages>10</tpages><oa>free_for_read</oa></addata></record> |
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| source | Spandidos Publications Journals; MEDLINE; EZB-FREE-00999 freely available EZB journals; Alma/SFX Local Collection |
| subjects | Aging Alzheimer's disease Analysis Animal memory Animals Apoptosis - drug effects Asian medicine Autophagy Autophagy - drug effects Disabilities Down-Regulation - drug effects Experiments Female Inflammation Inflammation - drug therapy Inflammation - metabolism Interleukin-1beta - metabolism Interleukins Lipopolysaccharides - pharmacology Male Mitogens Necrosis Neurocognitive Disorders - chemically induced Neurocognitive Disorders - drug therapy Neurocognitive Disorders - metabolism Neurons Older people Phosphatidylinositol 3-Kinases - metabolism Protein kinases Proto-Oncogene Proteins c-akt - metabolism Pyrazines - pharmacology Rats Rats, Sprague-Dawley Signal Transduction - drug effects TOR Serine-Threonine Kinases - metabolism Traditional Chinese medicine Tumor necrosis factor Tumor necrosis factor-TNF Tumors |
| title | Ligustrazine ameliorates lipopolysaccharide‑induced neurocognitive impairment by activating autophagy via the PI3K/AKT/mTOR pathway |
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