Source:http://linkedlifedata.com/resource/pubmed/id/19135993
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Predicate | Object |
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rdf:type | |
lifeskim:mentions | |
pubmed:issue |
1-3
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pubmed:dateCreated |
2009-2-6
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pubmed:abstractText |
S 35171 is one of a family of compounds that have been designed to protect mitochondrial function. We tested the hypothesis that S 35171 exerts protective effects in spontaneously hypertensive stroke-prone rats (SHRSPs), an animal model developing spontaneous brain damage preceded by proteinuria and systemic inflammation revealed by the urinary accumulation of acute-phase proteins (APPs) originating in the liver. Male SHRSPs fed a permissive diet received vehicle or S 35171 (10 mg/kg/day) started simultaneously with a high-sodium diet (group A) or after the establishment of proteinuria (group B). The drug delayed urinary APPs accumulation and the appearance of magnetic resonance imaging (MRI)-monitored brain lesions (after 62+/-3 days in group A, and 51+/-2 days in controls, P<0.01). The delay was more pronounced in group B as 30% of the animals survived the entire 90-day experimental period without brain abnormality. Proteomic analysis showed no significant alteration in the expression pattern of brain mitochondrial proteins, but the liver mitochondrial levels of carbamoylphosphate synthase I (CPS-I), an enzyme involved in urea metabolism) and the antioxidant peroxiredoxin-3 spot were affected by hypertension and S 35171. Stress reduces CPS-I and induces the peroxiredoxin-3 spot, whereas S 35171 brought about normal CPS-I expression and a 12-fold higher level of the peroxiredoxin-3 spot. As both enzymes are involved in maintaining mitochondrial functions, their increased expression after S 35171 treatment may be responsible for delaying the pathological condition that leads to the development of brain damage in SHRSPs.
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pubmed:language |
eng
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pubmed:journal | |
pubmed:citationSubset |
IM
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pubmed:chemical | |
pubmed:status |
MEDLINE
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pubmed:month |
Feb
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pubmed:issn |
1879-0712
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pubmed:author | |
pubmed:issnType |
Electronic
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pubmed:day |
14
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pubmed:volume |
604
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pubmed:owner |
NLM
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pubmed:authorsComplete |
Y
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pubmed:pagination |
117-24
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pubmed:meshHeading |
pubmed-meshheading:19135993-Acute-Phase Proteins,
pubmed-meshheading:19135993-Animals,
pubmed-meshheading:19135993-Antihypertensive Agents,
pubmed-meshheading:19135993-Blood Pressure,
pubmed-meshheading:19135993-Blotting, Western,
pubmed-meshheading:19135993-Electrophoresis, Gel, Two-Dimensional,
pubmed-meshheading:19135993-Hypertension,
pubmed-meshheading:19135993-Liver,
pubmed-meshheading:19135993-Magnetic Resonance Imaging,
pubmed-meshheading:19135993-Male,
pubmed-meshheading:19135993-Mitochondria,
pubmed-meshheading:19135993-Proteinuria,
pubmed-meshheading:19135993-Rats,
pubmed-meshheading:19135993-Rats, Inbred SHR,
pubmed-meshheading:19135993-Sodium, Dietary,
pubmed-meshheading:19135993-Stroke,
pubmed-meshheading:19135993-Trimetazidine
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pubmed:year |
2009
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pubmed:articleTitle |
S 35171 exerts protective effects in spontaneously hypertensive stroke-prone rats by preserving mitochondrial function.
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pubmed:affiliation |
Department of Pharmacological Sciences, University of Milan, Italy.
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pubmed:publicationType |
Journal Article,
Research Support, Non-U.S. Gov't
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