Effects of a High-Fat Diet on Neuroinflammation and Apoptosis in Acute Stage After Moderate Traumatic Brain Injury in Rats.
Animals
Antigens, Nuclear
/ metabolism
Apoptosis
Astrocytes
/ metabolism
Brain Injuries, Traumatic
/ metabolism
CD11b Antigen
/ metabolism
Caspase 3
/ metabolism
Cerebral Cortex
/ metabolism
Diet, High-Fat
Glial Fibrillary Acidic Protein
/ metabolism
In Situ Nick-End Labeling
Inflammation
/ metabolism
Male
Microglia
/ metabolism
Nerve Tissue Proteins
/ metabolism
Neurons
/ metabolism
Rats
Tumor Necrosis Factor-alpha
/ metabolism
Apoptosis
Cholesterol
High-fat diet
Traumatic brain injury
Triglycerides
Tumor necrosis factor-alpha
Journal
Neurocritical care
ISSN: 1556-0961
Titre abrégé: Neurocrit Care
Pays: United States
ID NLM: 101156086
Informations de publication
Date de publication:
08 2020
08 2020
Historique:
pubmed:
13
12
2019
medline:
17
8
2021
entrez:
13
12
2019
Statut:
ppublish
Résumé
A high-fat diet (HFD) is correlated with a higher risk of metabolic syndrome. The effect of HFD on neuroinflammation and apoptosis in acute stage after traumatic brain injury (TBI) in rats is not well known. Five-week-old male Sprague-Dawley (SD) rats were fed a HFD or normal diet (ND) for 8 weeks. Anesthetized male SD rats were divided into two subgroups: sham-operated and TBI. Motor function was measured using an inclined plane. The numbers of apoptotic neurons (markers Neu-N, TUNEL, caspase-3), activated astrocytes (marker GFAP) and microglia (marker OX42), and TNF-α expression in microglia and astrocytes in the ischemic cortex were investigated using an immunofluorescence assay. All of the parameters were measured on the 3rd day after TBI. Rats fed a HFD for 8 weeks had higher body weight, serum cholesterol, and triglycerides. TBI-induced motor deficits, neuronal decrease, neuronal apoptosis, astrocyte and microglia activation, and TNF-α expression in microglia and astrocytes in the ischemia cortex were significantly increased in ND and HFD rats compared to sham rats. However, these parameters were not significantly different between the ND and HFD TBI groups, except motor deficit. HFD has no significant effects on neuronal apoptosis or neuroinflammation in acute stage compared with ND for 8 weeks after moderate TBI in experimental rats.
Sections du résumé
BACKGROUND
A high-fat diet (HFD) is correlated with a higher risk of metabolic syndrome. The effect of HFD on neuroinflammation and apoptosis in acute stage after traumatic brain injury (TBI) in rats is not well known.
MATERIALS AND METHODS
Five-week-old male Sprague-Dawley (SD) rats were fed a HFD or normal diet (ND) for 8 weeks. Anesthetized male SD rats were divided into two subgroups: sham-operated and TBI. Motor function was measured using an inclined plane. The numbers of apoptotic neurons (markers Neu-N, TUNEL, caspase-3), activated astrocytes (marker GFAP) and microglia (marker OX42), and TNF-α expression in microglia and astrocytes in the ischemic cortex were investigated using an immunofluorescence assay. All of the parameters were measured on the 3rd day after TBI.
RESULTS
Rats fed a HFD for 8 weeks had higher body weight, serum cholesterol, and triglycerides. TBI-induced motor deficits, neuronal decrease, neuronal apoptosis, astrocyte and microglia activation, and TNF-α expression in microglia and astrocytes in the ischemia cortex were significantly increased in ND and HFD rats compared to sham rats. However, these parameters were not significantly different between the ND and HFD TBI groups, except motor deficit.
CONCLUSIONS
HFD has no significant effects on neuronal apoptosis or neuroinflammation in acute stage compared with ND for 8 weeks after moderate TBI in experimental rats.
Identifiants
pubmed: 31828728
doi: 10.1007/s12028-019-00891-5
pii: 10.1007/s12028-019-00891-5
doi:
Substances chimiques
Antigens, Nuclear
0
CD11b Antigen
0
GFAP protein, rat
0
Glial Fibrillary Acidic Protein
0
Nerve Tissue Proteins
0
Rbfox3 protein, rat
0
Tumor Necrosis Factor-alpha
0
Casp3 protein, rat
EC 3.4.22.-
Caspase 3
EC 3.4.22.-
Types de publication
Journal Article
Langues
eng
Sous-ensembles de citation
IM
Pagination
230-240Références
Laaksonen DE, Niskanen L, Lakka HM, Lakka TA, Uusitupa M. Epidemiology and treatment of the metabolic syndrome. Ann Med. 2004;36:332–46.
doi: 10.1080/07853890410031849
O’Neill S, O’Driscoll L. Metabolic syndrome: a closer look at the growing epidemic and its associated pathologies. Obes Rev. 2015;16:1–12.
doi: 10.1111/obr.12229
Wu A, Molteni R, Ying Z, Gomez-Pinilla F. A saturated-diet aggravates the outcome of traumatic brain injury on hippocampal plasticity and cognitive function by reducing brain-derived neurotrophic factor. Neuroscience. 2003;119:365–75.
doi: 10.1016/S0306-4522(03)00154-4
Salama AAA, Ibrahim BMM. Neurotherapeutic effects of allopurinol against brain injury in hyperlipidemic rats. Afr J Pharm Pharmacol. 2015;9:567–75.
doi: 10.5897/AJPP2014.4247
Xue QS, Sparks DL, Streit WJ. Microglial activation in the hippocampus of hypercholesterolemic rabbits occurs independent of increased amyloid production. J Neuroinflamm. 2007;4:20.
doi: 10.1186/1742-2094-4-20
Gomez-Pinilla F. Brain foods: the effects of nutrients on brain function. Nat Rev Neurosci. 2008;9:568–78.
doi: 10.1038/nrn2421
Pistell P, Morrison CD, Gupta S, Knight A, Keller JN, Ingram D. Cognitive impairment following high fat diet consumption is associated with brain inflamation. J Neuroimmunol. 2010;219:25–32.
doi: 10.1016/j.jneuroim.2009.11.010
Hoane MR, Swan AA, Herk SE. The effects of a high-fat sucrose diet on functional outcome following cortical contusion injury in rat. Behav Brain Res. 2011;223:119–24.
doi: 10.1016/j.bbr.2011.04.028
Mychasiuk R, Hehar H, Ma I, Esser MJ. Dietary intake alters behavioral recovery and gene expression profiles in the brain of juvenile rats that have experienced a concussion. Front BehavNeurosci. 2015;9:17.
Kang DH, Heo RW, Yi CO, Kim H, Choin CH, Roh GS. High fat diet-induced obesity exacerbates kainic acid-induced hippocampal cell death. BMC Neurosci. 2015;16:72.
doi: 10.1186/s12868-015-0202-2
Spagnuolo MS, Mollica MP, Maresca B, Cavaliere G, Cefaliello C, Trinchese G, et al. High fat diet and inflammation—modulation of haptoglobin level in rat. Front Cell Neurosci. 2015;9:479.
doi: 10.3389/fncel.2015.00479
Lim SW, Wang CC, Wang YH, Chio CC, Niu KC, Kuo JR. Microglial activation induced by traumatic brain injury is suppressed by postinjury treatment with hyperbaric oxygen therapy. J Surg Res. 2013;184:1076–84.
doi: 10.1016/j.jss.2013.04.070
Block ML, Hong JS. Microglia and inflammation mediated neuro-degeneration: multiple triggers with a common mechanism. Prog Neurobiol. 2005;76:77.
doi: 10.1016/j.pneurobio.2005.06.004
Zhang D, Hu X, Qian L, O’Callaghan JP, Hong JS. Astrogliosis in CNS pathologies: is there a role for microglia? Mol Neurobiol. 2010;41:232.
doi: 10.1007/s12035-010-8098-4
Chuang TJ, Lin KC, Chio CC, Wang CC, Chang CP, Kuo JR. Effects of secretome obtained from normoxia-preconditioned human mesenchymal stem cells in traumatic brain injury rats. J Trauma Acute Care Surg. 2012;73:1161–7.
doi: 10.1097/TA.0b013e318265d128
Mullen RJ, Buck CR, Smith AM. Neu-N, a neuronal specific nuclear protein in vertebrates. Development. 1992;116:201–11.
pubmed: 1483388
Kuo JR, Lo CJ, Chang CP, Lin KC, Lin MT, Chio CC. Agmatinepromotedangiogenesis, neurogenesis, and inhibition of gliosis-reduced traumatic brain injury in rats. J Trauma Acute Care Surg. 2011;71:87.
doi: 10.1097/TA.0b013e31820932e2
Koshinaga M, Katayama Y, Fukushima M. Rapid and widespread microglial activation induced by traumatic brain injury in rat brain slices. J Neurotrauma. 2000;17:185–92.
doi: 10.1089/neu.2000.17.185
Buettner R, Parhofer KG, Woenckhaus M, Wrede CE, Kunz-Schughart LA, Scholmerich J, et al. Defining high fat diet rat models: metabolic and molecular effects of different fat types. J Mol Endocrinol. 2006;36:485–501.
doi: 10.1677/jme.1.01909
Dietschy JM, Turley SD. Cholesterol metabolism in the brain. Curr Opin Lipidol. 2001;12:105–12.
doi: 10.1097/00041433-200104000-00003
Zhang J, Liu Q. Cholesterol metabolism and homeostasis in the brain. Protein Cell. 2015;6:25–64.
Kay AD, Day SP, Kerr M, Nicoll JA, Packard CJ, Caslake MJ. Remodeling of cerebrospinal fluid lipoprotein particles after human traumatic brain injury. J Neurotrauma. 2003;20:717–23.
doi: 10.1089/089771503767869953
Farr S, Taher J, Adeli K. Central nervous system regulation of intestinal lipid and lipoprotein metabolism. Curr Opin Lipidol. 2016;27:1–7.
doi: 10.1097/MOL.0000000000000254
Herz J, Hagen SI, Bergmüller E, Sabellek P, Göthert JR, Buer J, et al. Exacerbation of ischemic brain injury in hypercholesterolemic mice is associated with pronounced changes in peripheral and cerebral immune responses. Neurobiol Dis. 2014;62:456–68.
doi: 10.1016/j.nbd.2013.10.022
Thirumangalakudi L, Prakasam A, Zhang R, Bimonte-Nelson H, Sambamurti K, Kindy MS, et al. High cholesterol-induced neuroinflammation and amyloid precursor protein processing correlate with loss of working memory in mice. J Neurochem. 2008;106:475–85.
doi: 10.1111/j.1471-4159.2008.05415.x
Hallam TM, Floyd CL, Folkerts MM, Lee LL, Gong QZ, Lyeth BG, et al. Comparison of behavioral deficits and acute neuronal degeneration in rat lateral fluid percussion and weight-drop brain injury models. J Neurotrauma. 2004;21:521–39.
doi: 10.1089/089771504774129865
Wang CC, Wee HY, Hu CY, Chio CC, Kuo JR. The effects of memantine on glutamic receptor associated nitrosative stress in a traumatic brain injury rat model. World Neurosurg. 2018;112:e719–31.
doi: 10.1016/j.wneu.2018.01.140
Jia J, Yan M, Lu Z, Sun M, He J, Xia C. Regulated expression of pancreatic triglyceride lipase after rat traumatic brain injury. Mol Cell Biochem. 2010;335:127–36.
doi: 10.1007/s11010-009-0249-4
Rosenson RS, Lowe GD. Effects of lipids and lipoproteins on thrombosis and rheology. Atherosclerosis. 1998;140:271–80.
doi: 10.1016/S0021-9150(98)00144-0
Arvanitidis AP, Corbett D, Colbourne F. A high fat diet does not exacerbate CA1 injury and cognitive deficits following global ischemia in rats. Brain Res. 2009;1252:192–200.
doi: 10.1016/j.brainres.2008.11.058
Mychasiuk R, Hehar H, van Waes L, Esser MJ. Diet, age, and prior injury status differentially alter behavioral outcomes following concussion in rats. Neurobiol Dis. 2015;73:1–11.
doi: 10.1016/j.nbd.2014.09.003
Palmisano BT, Zhu L, Eckel RH, Stafford JM. Sex differences in lipid and lipoprotein metabolism. Mol Metab. 2018;15:45–55.
doi: 10.1016/j.molmet.2018.05.008