Effects of the duration of hyperlipidemia on cerebral lipids, vessels and neurons in rats
The present study was designed to investigate the effects of hyperlipidemia on the cerebral lipids, vessels and neurons of rats, and to provide experimental evidence for subsequent intervention. One hundred adult SD rats, half of which were male and half of which were female, were randomly divided i...
Gespeichert in:
| Veröffentlicht in: | Lipids in health and disease 2017-01, Vol.16 (1), p.26-26, Article 26 |
|---|---|
| Hauptverfasser: | , , , , , |
| Format: | Artikel |
| Sprache: | eng |
| Schlagworte: | |
| Online-Zugang: | Volltext |
| Tags: |
Tag hinzufügen
Keine Tags, Fügen Sie den ersten Tag hinzu!
|
| container_end_page | 26 |
|---|---|
| container_issue | 1 |
| container_start_page | 26 |
| container_title | Lipids in health and disease |
| container_volume | 16 |
| creator | Yang, Weichun Shi, He Zhang, Jianfen Shen, Ziyi Zhou, Guangyu Hu, Minyu |
| description | The present study was designed to investigate the effects of hyperlipidemia on the cerebral lipids, vessels and neurons of rats, and to provide experimental evidence for subsequent intervention.
One hundred adult SD rats, half of which were male and half of which were female, were randomly divided into five groups on the basis of serum total cholesterol (TC) levels. Four groups were fed a hypercholesterolemic diet (rat chow supplemented with 4% cholesterol, 1% cholic acid and 0.5% thiouracil - this is also called a CCT diet) for periods of 1 week, 2 weeks, 3 weeks and 4 weeks, respectively. A control group was included. The levels of serum lipids, cerebral lipids, free fatty acids (FFA), interleukin-6 (IL-6), interleukin-1 (IL-1), tumor necrosis factor alpha (TNF-α), vascular endothelial growth factor (VEGF), oxidized low density lipoprotein (ox-LDL), A-beta precursor proteins (APP), amyloid beta (Aβ), glial fibrillary acidic protein (GFAP) and tight junction protein Claudin-5 were measured after the experiment. The pathologic changes and apoptosis of the rat brains were evaluated.
Compared with the control group, after 1 week of a CCT diet, the levels of serum total cholesterol (TC), triglycerides (TG), low density lipoprotein cholesterol (LDL-C) and brain triglycerides had increased by 2.40, 1.29 and 1.75 and 0.3 times, respectively. The serum high density lipoprotein cholesterol (HDL-C) had decreased by 0.74 times (P |
| doi_str_mv | 10.1186/s12944-016-0401-6 |
| format | Article |
| fullrecord | <record><control><sourceid>gale_pubme</sourceid><recordid>TN_cdi_pubmedcentral_primary_oai_pubmedcentral_nih_gov_5282812</recordid><sourceformat>XML</sourceformat><sourcesystem>PC</sourcesystem><galeid>A480547960</galeid><sourcerecordid>A480547960</sourcerecordid><originalsourceid>FETCH-LOGICAL-c560t-5add9bb1efe46711a193940f28e24ac50840781964cbc5f8d8e8f099ce02a68c3</originalsourceid><addsrcrecordid>eNptUsFuFSEUJUZja_UD3BgSNy6cemEYBjYmTVOtSRM3muiKMMylj2YePGGmSf9extfW1hgWwOWcw70nh5DXDI4ZU_JDYVwL0QCTDQhgjXxCDpnoZdMx9uPpg_MBeVHKFQCHXsrn5IArJlrJ-SH5eeY9urnQ5Om8QTou2c4hxfW-udlhnsIujLgNltaiw4xDthP9Uy3v6TWWglOhNo404pJTLDREWjXKS_LM26ngq9v9iHz_dPbt9Ly5-Pr5y-nJReM6CXPT2XHUw8DQo5A9Y5bpVgvwXCEX1nWgBPSKaSnc4DqvRoXKg9YOgVupXHtEPu51d8uwxdFhnGuHZpfD1uYbk2wwj19i2JjLdG06rqoPvAq8uxXI6deCZTbbUBxOk42YlmKq061UulWiQt_-A71KS451vBXVge5bkH9Rl3ZCE6JP9V-3ipoToaATvZZQUcf_QdW1uu1SRB9q_RGB7Qkup1Iy-vsZGZg1D2afB1PzYNY8mLWVNw_NuWfcBaD9DehcsAY</addsrcrecordid><sourcetype>Open Access Repository</sourcetype><iscdi>true</iscdi><recordtype>article</recordtype><pqid>1865097306</pqid></control><display><type>article</type><title>Effects of the duration of hyperlipidemia on cerebral lipids, vessels and neurons in rats</title><source>MEDLINE</source><source>DOAJ Directory of Open Access Journals</source><source>SpringerNature Journals</source><source>PubMed Central Open Access</source><source>EZB-FREE-00999 freely available EZB journals</source><source>PubMed Central</source><source>Springer Nature OA/Free Journals</source><source>Free Full-Text Journals in Chemistry</source><creator>Yang, Weichun ; Shi, He ; Zhang, Jianfen ; Shen, Ziyi ; Zhou, Guangyu ; Hu, Minyu</creator><creatorcontrib>Yang, Weichun ; Shi, He ; Zhang, Jianfen ; Shen, Ziyi ; Zhou, Guangyu ; Hu, Minyu</creatorcontrib><description><![CDATA[The present study was designed to investigate the effects of hyperlipidemia on the cerebral lipids, vessels and neurons of rats, and to provide experimental evidence for subsequent intervention.
One hundred adult SD rats, half of which were male and half of which were female, were randomly divided into five groups on the basis of serum total cholesterol (TC) levels. Four groups were fed a hypercholesterolemic diet (rat chow supplemented with 4% cholesterol, 1% cholic acid and 0.5% thiouracil - this is also called a CCT diet) for periods of 1 week, 2 weeks, 3 weeks and 4 weeks, respectively. A control group was included. The levels of serum lipids, cerebral lipids, free fatty acids (FFA), interleukin-6 (IL-6), interleukin-1 (IL-1), tumor necrosis factor alpha (TNF-α), vascular endothelial growth factor (VEGF), oxidized low density lipoprotein (ox-LDL), A-beta precursor proteins (APP), amyloid beta (Aβ), glial fibrillary acidic protein (GFAP) and tight junction protein Claudin-5 were measured after the experiment. The pathologic changes and apoptosis of the rat brains were evaluated.
Compared with the control group, after 1 week of a CCT diet, the levels of serum total cholesterol (TC), triglycerides (TG), low density lipoprotein cholesterol (LDL-C) and brain triglycerides had increased by 2.40, 1.29 and 1.75 and 0.3 times, respectively. The serum high density lipoprotein cholesterol (HDL-C) had decreased by 0.74 times (P < 0.05) and the expression of IL-1, TNF-α and GFAP in the brains had increased (P < 0.05). In the second week, the expression of FFA and APP in the brains, and the amount of apoptotic neurons, had increased (P < 0.05). In the third week, the levels of VEGF, Ox-LDL and Aβ had increased, and the expression of Claudin-5 had decreased in the brains (P < 0.05). In the fourth week, the levels of TC, LDL-C and the amount of apoptotic neurons had increased (P < 0.05). The correlation analysis showed a positive correlation among FFA, TNF-α, VEGF, ox-LDL, Aβ, GFAP and neuronal apoptosis in the rat brains, and they all were negatively correlated with Claudin-5 (P < 0.05).
Hyperlipidemia may activate astrocytes by means of high levels of TG that will have direct toxic effects on the cerebral vessels and neurons by causing the secretion of TNF-α and IL-1 in the brains of rats. In the metabolic procession, brain tissue was shown to generate FFA that aggravated the biosynthesis of ox-LDL. With the extension of the duration of hyperlipidemia, high levels of cerebral TC and LDL-C were shown to aggravate the deposition of Aβ, induce the secretion of VEGF, reduce the expression of tight junction protein Claudin-5 and change the permeability of blood-brain barriers to factors that could damage cerebral vessels and neurons.]]></description><identifier>ISSN: 1476-511X</identifier><identifier>EISSN: 1476-511X</identifier><identifier>DOI: 10.1186/s12944-016-0401-6</identifier><identifier>PMID: 28143622</identifier><language>eng</language><publisher>England: BioMed Central Ltd</publisher><subject>Amyloid beta-Protein Precursor - genetics ; Amyloid beta-Protein Precursor - metabolism ; Animals ; Astrocytes - metabolism ; Astrocytes - pathology ; Blood Vessels - metabolism ; Blood Vessels - pathology ; Brain - metabolism ; C-Reactive Protein - genetics ; C-Reactive Protein - metabolism ; Cholesterol, LDL - metabolism ; Claudin-5 - genetics ; Claudin-5 - metabolism ; Diet, High-Fat - adverse effects ; Fatty Acids, Nonesterified - metabolism ; Female ; Gene Expression Regulation ; Glial Fibrillary Acidic Protein - genetics ; Glial Fibrillary Acidic Protein - metabolism ; Hyperlipidemia ; Hyperlipidemias - etiology ; Hyperlipidemias - genetics ; Hyperlipidemias - metabolism ; Hyperlipidemias - pathology ; Interleukin-6 - genetics ; Interleukin-6 - metabolism ; Lipids ; Lipoproteins, LDL - metabolism ; Male ; Neurons - metabolism ; Neurons - pathology ; Physiological aspects ; Rats ; Rats, Sprague-Dawley ; Risk factors ; Signal Transduction ; Time Factors ; Triglycerides - metabolism ; Tumor Necrosis Factor-alpha - genetics ; Tumor Necrosis Factor-alpha - metabolism ; Vascular Endothelial Growth Factor A - genetics ; Vascular Endothelial Growth Factor A - metabolism</subject><ispartof>Lipids in health and disease, 2017-01, Vol.16 (1), p.26-26, Article 26</ispartof><rights>COPYRIGHT 2017 BioMed Central Ltd.</rights><rights>Copyright BioMed Central 2017</rights><rights>The Author(s). 2017</rights><lds50>peer_reviewed</lds50><oa>free_for_read</oa><woscitedreferencessubscribed>false</woscitedreferencessubscribed><citedby>FETCH-LOGICAL-c560t-5add9bb1efe46711a193940f28e24ac50840781964cbc5f8d8e8f099ce02a68c3</citedby><cites>FETCH-LOGICAL-c560t-5add9bb1efe46711a193940f28e24ac50840781964cbc5f8d8e8f099ce02a68c3</cites></display><links><openurl>$$Topenurl_article</openurl><openurlfulltext>$$Topenurlfull_article</openurlfulltext><thumbnail>$$Tsyndetics_thumb_exl</thumbnail><linktopdf>$$Uhttps://www.ncbi.nlm.nih.gov/pmc/articles/PMC5282812/pdf/$$EPDF$$P50$$Gpubmedcentral$$Hfree_for_read</linktopdf><linktohtml>$$Uhttps://www.ncbi.nlm.nih.gov/pmc/articles/PMC5282812/$$EHTML$$P50$$Gpubmedcentral$$Hfree_for_read</linktohtml><link.rule.ids>230,315,728,781,785,865,886,27929,27930,53796,53798</link.rule.ids><backlink>$$Uhttps://www.ncbi.nlm.nih.gov/pubmed/28143622$$D View this record in MEDLINE/PubMed$$Hfree_for_read</backlink></links><search><creatorcontrib>Yang, Weichun</creatorcontrib><creatorcontrib>Shi, He</creatorcontrib><creatorcontrib>Zhang, Jianfen</creatorcontrib><creatorcontrib>Shen, Ziyi</creatorcontrib><creatorcontrib>Zhou, Guangyu</creatorcontrib><creatorcontrib>Hu, Minyu</creatorcontrib><title>Effects of the duration of hyperlipidemia on cerebral lipids, vessels and neurons in rats</title><title>Lipids in health and disease</title><addtitle>Lipids Health Dis</addtitle><description><![CDATA[The present study was designed to investigate the effects of hyperlipidemia on the cerebral lipids, vessels and neurons of rats, and to provide experimental evidence for subsequent intervention.
One hundred adult SD rats, half of which were male and half of which were female, were randomly divided into five groups on the basis of serum total cholesterol (TC) levels. Four groups were fed a hypercholesterolemic diet (rat chow supplemented with 4% cholesterol, 1% cholic acid and 0.5% thiouracil - this is also called a CCT diet) for periods of 1 week, 2 weeks, 3 weeks and 4 weeks, respectively. A control group was included. The levels of serum lipids, cerebral lipids, free fatty acids (FFA), interleukin-6 (IL-6), interleukin-1 (IL-1), tumor necrosis factor alpha (TNF-α), vascular endothelial growth factor (VEGF), oxidized low density lipoprotein (ox-LDL), A-beta precursor proteins (APP), amyloid beta (Aβ), glial fibrillary acidic protein (GFAP) and tight junction protein Claudin-5 were measured after the experiment. The pathologic changes and apoptosis of the rat brains were evaluated.
Compared with the control group, after 1 week of a CCT diet, the levels of serum total cholesterol (TC), triglycerides (TG), low density lipoprotein cholesterol (LDL-C) and brain triglycerides had increased by 2.40, 1.29 and 1.75 and 0.3 times, respectively. The serum high density lipoprotein cholesterol (HDL-C) had decreased by 0.74 times (P < 0.05) and the expression of IL-1, TNF-α and GFAP in the brains had increased (P < 0.05). In the second week, the expression of FFA and APP in the brains, and the amount of apoptotic neurons, had increased (P < 0.05). In the third week, the levels of VEGF, Ox-LDL and Aβ had increased, and the expression of Claudin-5 had decreased in the brains (P < 0.05). In the fourth week, the levels of TC, LDL-C and the amount of apoptotic neurons had increased (P < 0.05). The correlation analysis showed a positive correlation among FFA, TNF-α, VEGF, ox-LDL, Aβ, GFAP and neuronal apoptosis in the rat brains, and they all were negatively correlated with Claudin-5 (P < 0.05).
Hyperlipidemia may activate astrocytes by means of high levels of TG that will have direct toxic effects on the cerebral vessels and neurons by causing the secretion of TNF-α and IL-1 in the brains of rats. In the metabolic procession, brain tissue was shown to generate FFA that aggravated the biosynthesis of ox-LDL. With the extension of the duration of hyperlipidemia, high levels of cerebral TC and LDL-C were shown to aggravate the deposition of Aβ, induce the secretion of VEGF, reduce the expression of tight junction protein Claudin-5 and change the permeability of blood-brain barriers to factors that could damage cerebral vessels and neurons.]]></description><subject>Amyloid beta-Protein Precursor - genetics</subject><subject>Amyloid beta-Protein Precursor - metabolism</subject><subject>Animals</subject><subject>Astrocytes - metabolism</subject><subject>Astrocytes - pathology</subject><subject>Blood Vessels - metabolism</subject><subject>Blood Vessels - pathology</subject><subject>Brain - metabolism</subject><subject>C-Reactive Protein - genetics</subject><subject>C-Reactive Protein - metabolism</subject><subject>Cholesterol, LDL - metabolism</subject><subject>Claudin-5 - genetics</subject><subject>Claudin-5 - metabolism</subject><subject>Diet, High-Fat - adverse effects</subject><subject>Fatty Acids, Nonesterified - metabolism</subject><subject>Female</subject><subject>Gene Expression Regulation</subject><subject>Glial Fibrillary Acidic Protein - genetics</subject><subject>Glial Fibrillary Acidic Protein - metabolism</subject><subject>Hyperlipidemia</subject><subject>Hyperlipidemias - etiology</subject><subject>Hyperlipidemias - genetics</subject><subject>Hyperlipidemias - metabolism</subject><subject>Hyperlipidemias - pathology</subject><subject>Interleukin-6 - genetics</subject><subject>Interleukin-6 - metabolism</subject><subject>Lipids</subject><subject>Lipoproteins, LDL - metabolism</subject><subject>Male</subject><subject>Neurons - metabolism</subject><subject>Neurons - pathology</subject><subject>Physiological aspects</subject><subject>Rats</subject><subject>Rats, Sprague-Dawley</subject><subject>Risk factors</subject><subject>Signal Transduction</subject><subject>Time Factors</subject><subject>Triglycerides - metabolism</subject><subject>Tumor Necrosis Factor-alpha - genetics</subject><subject>Tumor Necrosis Factor-alpha - metabolism</subject><subject>Vascular Endothelial Growth Factor A - genetics</subject><subject>Vascular Endothelial Growth Factor A - metabolism</subject><issn>1476-511X</issn><issn>1476-511X</issn><fulltext>true</fulltext><rsrctype>article</rsrctype><creationdate>2017</creationdate><recordtype>article</recordtype><sourceid>EIF</sourceid><sourceid>ABUWG</sourceid><sourceid>AFKRA</sourceid><sourceid>AZQEC</sourceid><sourceid>BENPR</sourceid><sourceid>CCPQU</sourceid><sourceid>DWQXO</sourceid><sourceid>GNUQQ</sourceid><recordid>eNptUsFuFSEUJUZja_UD3BgSNy6cemEYBjYmTVOtSRM3muiKMMylj2YePGGmSf9extfW1hgWwOWcw70nh5DXDI4ZU_JDYVwL0QCTDQhgjXxCDpnoZdMx9uPpg_MBeVHKFQCHXsrn5IArJlrJ-SH5eeY9urnQ5Om8QTou2c4hxfW-udlhnsIujLgNltaiw4xDthP9Uy3v6TWWglOhNo404pJTLDREWjXKS_LM26ngq9v9iHz_dPbt9Ly5-Pr5y-nJReM6CXPT2XHUw8DQo5A9Y5bpVgvwXCEX1nWgBPSKaSnc4DqvRoXKg9YOgVupXHtEPu51d8uwxdFhnGuHZpfD1uYbk2wwj19i2JjLdG06rqoPvAq8uxXI6deCZTbbUBxOk42YlmKq061UulWiQt_-A71KS451vBXVge5bkH9Rl3ZCE6JP9V-3ipoToaATvZZQUcf_QdW1uu1SRB9q_RGB7Qkup1Iy-vsZGZg1D2afB1PzYNY8mLWVNw_NuWfcBaD9DehcsAY</recordid><startdate>20170131</startdate><enddate>20170131</enddate><creator>Yang, Weichun</creator><creator>Shi, He</creator><creator>Zhang, Jianfen</creator><creator>Shen, Ziyi</creator><creator>Zhou, Guangyu</creator><creator>Hu, Minyu</creator><general>BioMed Central Ltd</general><general>BioMed Central</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>3V.</scope><scope>7X7</scope><scope>7XB</scope><scope>88E</scope><scope>8FD</scope><scope>8FE</scope><scope>8FH</scope><scope>8FI</scope><scope>8FJ</scope><scope>8FK</scope><scope>ABUWG</scope><scope>AFKRA</scope><scope>AZQEC</scope><scope>BBNVY</scope><scope>BENPR</scope><scope>BHPHI</scope><scope>CCPQU</scope><scope>DWQXO</scope><scope>FR3</scope><scope>FYUFA</scope><scope>GHDGH</scope><scope>GNUQQ</scope><scope>HCIFZ</scope><scope>K9.</scope><scope>LK8</scope><scope>M0S</scope><scope>M1P</scope><scope>M7P</scope><scope>P64</scope><scope>PIMPY</scope><scope>PQEST</scope><scope>PQQKQ</scope><scope>PQUKI</scope><scope>PRINS</scope><scope>RC3</scope><scope>7X8</scope><scope>5PM</scope></search><sort><creationdate>20170131</creationdate><title>Effects of the duration of hyperlipidemia on cerebral lipids, vessels and neurons in rats</title><author>Yang, Weichun ; Shi, He ; Zhang, Jianfen ; Shen, Ziyi ; Zhou, Guangyu ; Hu, Minyu</author></sort><facets><frbrtype>5</frbrtype><frbrgroupid>cdi_FETCH-LOGICAL-c560t-5add9bb1efe46711a193940f28e24ac50840781964cbc5f8d8e8f099ce02a68c3</frbrgroupid><rsrctype>articles</rsrctype><prefilter>articles</prefilter><language>eng</language><creationdate>2017</creationdate><topic>Amyloid beta-Protein Precursor - genetics</topic><topic>Amyloid beta-Protein Precursor - metabolism</topic><topic>Animals</topic><topic>Astrocytes - metabolism</topic><topic>Astrocytes - pathology</topic><topic>Blood Vessels - metabolism</topic><topic>Blood Vessels - pathology</topic><topic>Brain - metabolism</topic><topic>C-Reactive Protein - genetics</topic><topic>C-Reactive Protein - metabolism</topic><topic>Cholesterol, LDL - metabolism</topic><topic>Claudin-5 - genetics</topic><topic>Claudin-5 - metabolism</topic><topic>Diet, High-Fat - adverse effects</topic><topic>Fatty Acids, Nonesterified - metabolism</topic><topic>Female</topic><topic>Gene Expression Regulation</topic><topic>Glial Fibrillary Acidic Protein - genetics</topic><topic>Glial Fibrillary Acidic Protein - metabolism</topic><topic>Hyperlipidemia</topic><topic>Hyperlipidemias - etiology</topic><topic>Hyperlipidemias - genetics</topic><topic>Hyperlipidemias - metabolism</topic><topic>Hyperlipidemias - pathology</topic><topic>Interleukin-6 - genetics</topic><topic>Interleukin-6 - metabolism</topic><topic>Lipids</topic><topic>Lipoproteins, LDL - metabolism</topic><topic>Male</topic><topic>Neurons - metabolism</topic><topic>Neurons - pathology</topic><topic>Physiological aspects</topic><topic>Rats</topic><topic>Rats, Sprague-Dawley</topic><topic>Risk factors</topic><topic>Signal Transduction</topic><topic>Time Factors</topic><topic>Triglycerides - metabolism</topic><topic>Tumor Necrosis Factor-alpha - genetics</topic><topic>Tumor Necrosis Factor-alpha - metabolism</topic><topic>Vascular Endothelial Growth Factor A - genetics</topic><topic>Vascular Endothelial Growth Factor A - metabolism</topic><toplevel>peer_reviewed</toplevel><toplevel>online_resources</toplevel><creatorcontrib>Yang, Weichun</creatorcontrib><creatorcontrib>Shi, He</creatorcontrib><creatorcontrib>Zhang, Jianfen</creatorcontrib><creatorcontrib>Shen, Ziyi</creatorcontrib><creatorcontrib>Zhou, Guangyu</creatorcontrib><creatorcontrib>Hu, Minyu</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>Technology Research Database</collection><collection>ProQuest SciTech Collection</collection><collection>ProQuest Natural Science 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 Essentials</collection><collection>Biological Science Collection</collection><collection>ProQuest Central</collection><collection>Natural Science Collection</collection><collection>ProQuest One Community College</collection><collection>ProQuest Central Korea</collection><collection>Engineering Research Database</collection><collection>Health Research Premium Collection</collection><collection>Health Research Premium Collection (Alumni)</collection><collection>ProQuest Central Student</collection><collection>SciTech Premium Collection</collection><collection>ProQuest Health & Medical Complete (Alumni)</collection><collection>ProQuest Biological Science Collection</collection><collection>Health & Medical Collection (Alumni Edition)</collection><collection>Medical Database</collection><collection>Biological Science Database</collection><collection>Biotechnology and BioEngineering Abstracts</collection><collection>Access via ProQuest (Open Access)</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>Genetics Abstracts</collection><collection>MEDLINE - Academic</collection><collection>PubMed Central (Full Participant titles)</collection><jtitle>Lipids in health and disease</jtitle></facets><delivery><delcategory>Remote Search Resource</delcategory><fulltext>fulltext</fulltext></delivery><addata><au>Yang, Weichun</au><au>Shi, He</au><au>Zhang, Jianfen</au><au>Shen, Ziyi</au><au>Zhou, Guangyu</au><au>Hu, Minyu</au><format>journal</format><genre>article</genre><ristype>JOUR</ristype><atitle>Effects of the duration of hyperlipidemia on cerebral lipids, vessels and neurons in rats</atitle><jtitle>Lipids in health and disease</jtitle><addtitle>Lipids Health Dis</addtitle><date>2017-01-31</date><risdate>2017</risdate><volume>16</volume><issue>1</issue><spage>26</spage><epage>26</epage><pages>26-26</pages><artnum>26</artnum><issn>1476-511X</issn><eissn>1476-511X</eissn><abstract><![CDATA[The present study was designed to investigate the effects of hyperlipidemia on the cerebral lipids, vessels and neurons of rats, and to provide experimental evidence for subsequent intervention.
One hundred adult SD rats, half of which were male and half of which were female, were randomly divided into five groups on the basis of serum total cholesterol (TC) levels. Four groups were fed a hypercholesterolemic diet (rat chow supplemented with 4% cholesterol, 1% cholic acid and 0.5% thiouracil - this is also called a CCT diet) for periods of 1 week, 2 weeks, 3 weeks and 4 weeks, respectively. A control group was included. The levels of serum lipids, cerebral lipids, free fatty acids (FFA), interleukin-6 (IL-6), interleukin-1 (IL-1), tumor necrosis factor alpha (TNF-α), vascular endothelial growth factor (VEGF), oxidized low density lipoprotein (ox-LDL), A-beta precursor proteins (APP), amyloid beta (Aβ), glial fibrillary acidic protein (GFAP) and tight junction protein Claudin-5 were measured after the experiment. The pathologic changes and apoptosis of the rat brains were evaluated.
Compared with the control group, after 1 week of a CCT diet, the levels of serum total cholesterol (TC), triglycerides (TG), low density lipoprotein cholesterol (LDL-C) and brain triglycerides had increased by 2.40, 1.29 and 1.75 and 0.3 times, respectively. The serum high density lipoprotein cholesterol (HDL-C) had decreased by 0.74 times (P < 0.05) and the expression of IL-1, TNF-α and GFAP in the brains had increased (P < 0.05). In the second week, the expression of FFA and APP in the brains, and the amount of apoptotic neurons, had increased (P < 0.05). In the third week, the levels of VEGF, Ox-LDL and Aβ had increased, and the expression of Claudin-5 had decreased in the brains (P < 0.05). In the fourth week, the levels of TC, LDL-C and the amount of apoptotic neurons had increased (P < 0.05). The correlation analysis showed a positive correlation among FFA, TNF-α, VEGF, ox-LDL, Aβ, GFAP and neuronal apoptosis in the rat brains, and they all were negatively correlated with Claudin-5 (P < 0.05).
Hyperlipidemia may activate astrocytes by means of high levels of TG that will have direct toxic effects on the cerebral vessels and neurons by causing the secretion of TNF-α and IL-1 in the brains of rats. In the metabolic procession, brain tissue was shown to generate FFA that aggravated the biosynthesis of ox-LDL. With the extension of the duration of hyperlipidemia, high levels of cerebral TC and LDL-C were shown to aggravate the deposition of Aβ, induce the secretion of VEGF, reduce the expression of tight junction protein Claudin-5 and change the permeability of blood-brain barriers to factors that could damage cerebral vessels and neurons.]]></abstract><cop>England</cop><pub>BioMed Central Ltd</pub><pmid>28143622</pmid><doi>10.1186/s12944-016-0401-6</doi><tpages>1</tpages><oa>free_for_read</oa></addata></record> |
| fulltext | fulltext |
| identifier | ISSN: 1476-511X |
| ispartof | Lipids in health and disease, 2017-01, Vol.16 (1), p.26-26, Article 26 |
| issn | 1476-511X 1476-511X |
| language | eng |
| recordid | cdi_pubmedcentral_primary_oai_pubmedcentral_nih_gov_5282812 |
| source | MEDLINE; DOAJ Directory of Open Access Journals; SpringerNature Journals; PubMed Central Open Access; EZB-FREE-00999 freely available EZB journals; PubMed Central; Springer Nature OA/Free Journals; Free Full-Text Journals in Chemistry |
| subjects | Amyloid beta-Protein Precursor - genetics Amyloid beta-Protein Precursor - metabolism Animals Astrocytes - metabolism Astrocytes - pathology Blood Vessels - metabolism Blood Vessels - pathology Brain - metabolism C-Reactive Protein - genetics C-Reactive Protein - metabolism Cholesterol, LDL - metabolism Claudin-5 - genetics Claudin-5 - metabolism Diet, High-Fat - adverse effects Fatty Acids, Nonesterified - metabolism Female Gene Expression Regulation Glial Fibrillary Acidic Protein - genetics Glial Fibrillary Acidic Protein - metabolism Hyperlipidemia Hyperlipidemias - etiology Hyperlipidemias - genetics Hyperlipidemias - metabolism Hyperlipidemias - pathology Interleukin-6 - genetics Interleukin-6 - metabolism Lipids Lipoproteins, LDL - metabolism Male Neurons - metabolism Neurons - pathology Physiological aspects Rats Rats, Sprague-Dawley Risk factors Signal Transduction Time Factors Triglycerides - metabolism Tumor Necrosis Factor-alpha - genetics Tumor Necrosis Factor-alpha - metabolism Vascular Endothelial Growth Factor A - genetics Vascular Endothelial Growth Factor A - metabolism |
| title | Effects of the duration of hyperlipidemia on cerebral lipids, vessels and neurons in rats |
| url | https://sfx.bib-bvb.de/sfx_tum?ctx_ver=Z39.88-2004&ctx_enc=info:ofi/enc:UTF-8&ctx_tim=2024-12-16T07%3A57%3A50IST&url_ver=Z39.88-2004&url_ctx_fmt=infofi/fmt:kev:mtx:ctx&rfr_id=info:sid/primo.exlibrisgroup.com:primo3-Article-gale_pubme&rft_val_fmt=info:ofi/fmt:kev:mtx:journal&rft.genre=article&rft.atitle=Effects%20of%20the%20duration%20of%20hyperlipidemia%20on%20cerebral%20lipids,%20vessels%20and%20neurons%20in%20rats&rft.jtitle=Lipids%20in%20health%20and%20disease&rft.au=Yang,%20Weichun&rft.date=2017-01-31&rft.volume=16&rft.issue=1&rft.spage=26&rft.epage=26&rft.pages=26-26&rft.artnum=26&rft.issn=1476-511X&rft.eissn=1476-511X&rft_id=info:doi/10.1186/s12944-016-0401-6&rft_dat=%3Cgale_pubme%3EA480547960%3C/gale_pubme%3E%3Curl%3E%3C/url%3E&disable_directlink=true&sfx.directlink=off&sfx.report_link=0&rft_id=info:oai/&rft_pqid=1865097306&rft_id=info:pmid/28143622&rft_galeid=A480547960&rfr_iscdi=true |