Simvastatin Attenuates Stroke-induced Splenic Atrophy and Lung Susceptibility to Spontaneous Bacterial Infection in Mice
Statins are widely used in the primary and secondary prevention of ischemic stroke, but their effects on stroke-induced immunodepression and poststroke infections are elusive. We investigated the effects of simvastatin treatment on stroke-induced splenic atrophy and lung susceptibility to bacterial...
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Published in | Stroke (1970) Vol. 44; no. 4; pp. 1135 - 1143 |
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Main Authors | , , , , , |
Format | Journal Article |
Language | English |
Published |
Hagerstown, MD
Lippincott Williams & Wilkins
01.04.2013
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Abstract | Statins are widely used in the primary and secondary prevention of ischemic stroke, but their effects on stroke-induced immunodepression and poststroke infections are elusive. We investigated the effects of simvastatin treatment on stroke-induced splenic atrophy and lung susceptibility to bacterial infection in acute experimental stroke in mice.
Ischemic stroke was induced by transient middle cerebral artery occlusion, followed by reperfusion. In some experiments, splenectomies were performed 2 weeks before middle cerebral artery occlusion. Animals were randomly assigned to sham and middle cerebral artery occlusion groups treated subcutaneously with vehicle or simvastatin (20 mg/kg per day). Brain infarction, neurological function, brain interferon-γ expression, splenic atrophy and apoptosis, and lung infection were examined.
Simvastatin reduced stroke-induced spleen atrophy and splenic apoptosis via increased mitochrondrial antiapoptotic Bcl-2 expression and decreased proapoptotic Bax translocation from cytosol into mitochondria. Splenectomy reduced brain interferon-γ (3 days) and infarct size (5 days) after stroke, and these effects were reversed by adoptive transfer of splenocytes. Simvastatin inhibited brain interferon-γ (3 days) and reduced infarct volume and neurological deficits (5 days) after stroke, and these protective effects were observed not only in naive stroke mice but also in splenectomied stroke mice adoptively transferred with splenocytes. Simvastatin also decreased the stroke-associated lung susceptibility to spontaneous bacterial infection.
Results provide the first direct experimental evidence that simvastatin ameliorates stroke-induced peripheral immunodepression by attenuating spleen atrophy and lung bacterial infection. These findings contribute to a better understanding of the beneficial effects of statins in the treatment of stroke. |
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AbstractList | BACKGROUND AND PURPOSEStatins are widely used in the primary and secondary prevention of ischemic stroke, but their effects on stroke-induced immunodepression and poststroke infections are elusive. We investigated the effects of simvastatin treatment on stroke-induced splenic atrophy and lung susceptibility to bacterial infection in acute experimental stroke in mice. METHODSIschemic stroke was induced by transient middle cerebral artery occlusion, followed by reperfusion. In some experiments, splenectomies were performed 2 weeks before middle cerebral artery occlusion. Animals were randomly assigned to sham and middle cerebral artery occlusion groups treated subcutaneously with vehicle or simvastatin (20 mg/kg per day). Brain infarction, neurological function, brain interferon-γ expression, splenic atrophy and apoptosis, and lung infection were examined. RESULTSSimvastatin reduced stroke-induced spleen atrophy and splenic apoptosis via increased mitochrondrial antiapoptotic Bcl-2 expression and decreased proapoptotic Bax translocation from cytosol into mitochondria. Splenectomy reduced brain interferon-γ (3 days) and infarct size (5 days) after stroke, and these effects were reversed by adoptive transfer of splenocytes. Simvastatin inhibited brain interferon-γ (3 days) and reduced infarct volume and neurological deficits (5 days) after stroke, and these protective effects were observed not only in naive stroke mice but also in splenectomied stroke mice adoptively transferred with splenocytes. Simvastatin also decreased the stroke-associated lung susceptibility to spontaneous bacterial infection. CONCLUSIONSResults provide the first direct experimental evidence that simvastatin ameliorates stroke-induced peripheral immunodepression by attenuating spleen atrophy and lung bacterial infection. These findings contribute to a better understanding of the beneficial effects of statins in the treatment of stroke. Statins are widely used in the primary and secondary prevention of ischemic stroke, but their effects on stroke-induced immunodepression and poststroke infections are elusive. We investigated the effects of simvastatin treatment on stroke-induced splenic atrophy and lung susceptibility to bacterial infection in acute experimental stroke in mice. Ischemic stroke was induced by transient middle cerebral artery occlusion, followed by reperfusion. In some experiments, splenectomies were performed 2 weeks before middle cerebral artery occlusion. Animals were randomly assigned to sham and middle cerebral artery occlusion groups treated subcutaneously with vehicle or simvastatin (20 mg/kg per day). Brain infarction, neurological function, brain interferon-γ expression, splenic atrophy and apoptosis, and lung infection were examined. Simvastatin reduced stroke-induced spleen atrophy and splenic apoptosis via increased mitochrondrial antiapoptotic Bcl-2 expression and decreased proapoptotic Bax translocation from cytosol into mitochondria. Splenectomy reduced brain interferon-γ (3 days) and infarct size (5 days) after stroke, and these effects were reversed by adoptive transfer of splenocytes. Simvastatin inhibited brain interferon-γ (3 days) and reduced infarct volume and neurological deficits (5 days) after stroke, and these protective effects were observed not only in naive stroke mice but also in splenectomied stroke mice adoptively transferred with splenocytes. Simvastatin also decreased the stroke-associated lung susceptibility to spontaneous bacterial infection. Results provide the first direct experimental evidence that simvastatin ameliorates stroke-induced peripheral immunodepression by attenuating spleen atrophy and lung bacterial infection. These findings contribute to a better understanding of the beneficial effects of statins in the treatment of stroke. Background and Purpose— Statins are widely used in the primary and secondary prevention of ischemic stroke, but their effects on stroke-induced immunodepression and poststroke infections are elusive. We investigated the effects of simvastatin treatment on stroke-induced splenic atrophy and lung susceptibility to bacterial infection in acute experimental stroke in mice. Methods— Ischemic stroke was induced by transient middle cerebral artery occlusion, followed by reperfusion. In some experiments, splenectomies were performed 2 weeks before middle cerebral artery occlusion. Animals were randomly assigned to sham and middle cerebral artery occlusion groups treated subcutaneously with vehicle or simvastatin (20 mg/kg per day). Brain infarction, neurological function, brain interferon-γ expression, splenic atrophy and apoptosis, and lung infection were examined. Results— Simvastatin reduced stroke-induced spleen atrophy and splenic apoptosis via increased mitochrondrial antiapoptotic Bcl-2 expression and decreased proapoptotic Bax translocation from cytosol into mitochondria. Splenectomy reduced brain interferon-γ (3 days) and infarct size (5 days) after stroke, and these effects were reversed by adoptive transfer of splenocytes. Simvastatin inhibited brain interferon-γ (3 days) and reduced infarct volume and neurological deficits (5 days) after stroke, and these protective effects were observed not only in naive stroke mice but also in splenectomied stroke mice adoptively transferred with splenocytes. Simvastatin also decreased the stroke-associated lung susceptibility to spontaneous bacterial infection. Conclusions— Results provide the first direct experimental evidence that simvastatin ameliorates stroke-induced peripheral immunodepression by attenuating spleen atrophy and lung bacterial infection. These findings contribute to a better understanding of the beneficial effects of statins in the treatment of stroke. |
Author | XIAOLEI ZHU NEIL GRANGER, D GUOHONG LI RONG JIN NANDA, Anil LIN LIU |
Author_xml | – sequence: 1 surname: RONG JIN fullname: RONG JIN organization: Vascular Biology and Stroke Research Laboratory, Department of Neurosurgery, Louisiana State University Health Science Center Shreveport, Shreveport. LA, United States – sequence: 2 surname: XIAOLEI ZHU fullname: XIAOLEI ZHU organization: Vascular Biology and Stroke Research Laboratory, Department of Neurosurgery, Louisiana State University Health Science Center Shreveport, Shreveport. LA, United States – sequence: 3 surname: LIN LIU fullname: LIN LIU organization: Vascular Biology and Stroke Research Laboratory, Department of Neurosurgery, Louisiana State University Health Science Center Shreveport, Shreveport. LA, United States – sequence: 4 givenname: Anil surname: NANDA fullname: NANDA, Anil organization: Vascular Biology and Stroke Research Laboratory, Department of Neurosurgery, Louisiana State University Health Science Center Shreveport, Shreveport. LA, United States – sequence: 5 givenname: D surname: NEIL GRANGER fullname: NEIL GRANGER, D organization: Department of Physiology, Louisiana State University Health Science Center Shreveport, Shreveport. LA, United States – sequence: 6 surname: GUOHONG LI fullname: GUOHONG LI organization: Vascular Biology and Stroke Research Laboratory, Department of Neurosurgery, Louisiana State University Health Science Center Shreveport, Shreveport. LA, United States |
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Keywords | Cardiovascular disease Hypocholesterolemic agent Vascular disease HMG-CoA reductase inhibitor Cerebrovascular disease Stroke Nervous system diseases Immune response Enzyme spleen Simvastatin Rodentia Enzyme inhibitor Statin derivative bacterial infection Cerebral disorder Infection Vertebrata Mammalia Mouse statin Animal Central nervous system disease Bacteriosis Brain ischemia Hydroxymethylglutaryl-CoA reductase Oxidoreductases Antilipemic agent |
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Snippet | Statins are widely used in the primary and secondary prevention of ischemic stroke, but their effects on stroke-induced immunodepression and poststroke... Background and Purpose— Statins are widely used in the primary and secondary prevention of ischemic stroke, but their effects on stroke-induced... BACKGROUND AND PURPOSEStatins are widely used in the primary and secondary prevention of ischemic stroke, but their effects on stroke-induced immunodepression... |
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SubjectTerms | Animals Anticholesteremic Agents - pharmacology Apoptosis Atrophy - therapy Bacterial Infections - drug therapy Bacterial Infections - metabolism bcl-2-Associated X Protein - metabolism Biological and medical sciences Brain Infarction Disease Models, Animal Headache. Facial pains. Syncopes. Epilepsia. Intracranial hypertension. Brain oedema. Cerebral palsy Humans Infarction, Middle Cerebral Artery Infection Interferon-gamma - metabolism Lung - drug effects Lung - microbiology Lung - pathology Medical sciences Mice Mice, Inbred C57BL Nervous system (semeiology, syndromes) Neurology Proto-Oncogene Proteins c-bcl-2 - metabolism Simvastatin - pharmacology Spleen - cytology Spleen - drug effects Spleen - pathology Splenectomy Stroke - complications Stroke - drug therapy Stroke - physiopathology Vascular diseases and vascular malformations of the nervous system |
Title | Simvastatin Attenuates Stroke-induced Splenic Atrophy and Lung Susceptibility to Spontaneous Bacterial Infection in Mice |
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