Canadian journal of physiology and pharmacology, 2013-07, Vol.91 (7), p.521-527
2013
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- Autor(en) / Beteiligte
- Titel
- Penehyclidine hydrochloride attenuates the cerebral injury in a rat model of cardiopulmonary bypass
- Ist Teil von
- Canadian journal of physiology and pharmacology, 2013-07, Vol.91 (7), p.521-527
- Ort / Verlag
- Canada
- Erscheinungsjahr
- 2013
- Quelle
- MEDLINE
- Beschreibungen/Notizen
- This study investigated the effect of penehyclidine hydrochloride (PHC) on regulatory mediators during the neuroinflammatory response and cerebral cell apoptosis following cardiopulmonary bypass (CPB). Forty-eight rats were randomly divided among 4 groups as follows: sham-operation, vehicle, low-dose PHC (0.6 mg·(kg body mass)(-1)), and high-dose PHC (2.0 mg·(kg body mass)(-1)). CPB was performed in the latter 3 groups. The plasma levels of neuron specific enolase (NSE) and S-100B were tested with ELISA. Real-time PCR and Western blotting were used to evaluate the expression levels of matrix metalloproteinase-9 (MMP-9), IL-10, caspase-3, Bcl-2, and p38 in brain tissue. The ultrastructure of hippocampus tissue was examined under an electron microscope. PHC attenuated the increase of plasma NSE and S-100B following CPB. MMP-9, cleaved caspase-3, and phosphorylated p38 expression were substantially increased in the vehicle group compared with the sham-operation group and gradually diminished with increasing doses of PHC. IL-10 and Bcl-2 expression were markedly lower in the vehicle group than in the sham-operation group and gradually recovered with increasing doses of PHC. PHC attenuated the histopathological changes of cerebral injury following CPB. PHC favorably regulates the inflammatory response and reduces markers of neuronal injury following CPB, potentially by reducing p38 and caspase-3 activation.
- Sprache
- Englisch
- Identifikatoren
- ISSN: 0008-4212eISSN: 1205-7541DOI: 10.1139/cjpp-2012-0329Titel-ID: cdi_pubmed_primary_23827043
- Format
- –
- Schlagworte
- Animals, Apoptosis - drug effects, Brain Injuries - drug therapy, Brain Injuries - etiology, Brain Injuries - genetics, Brain Injuries - metabolism, Cardiopulmonary Bypass - adverse effects, Cardiopulmonary Bypass - methods, Caspase 3 - biosynthesis, Caspase 3 - genetics, Caspase 3 - metabolism, Cerebrum - drug effects, Cerebrum - metabolism, Cerebrum - pathology, Female, Hemodynamics - drug effects, Hippocampus - drug effects, Hippocampus - metabolism, Hippocampus - pathology, Inflammation - drug therapy, Inflammation - genetics, Inflammation - metabolism, Interleukin-10 - biosynthesis, Interleukin-10 - genetics, Interleukin-10 - metabolism, Male, Matrix Metalloproteinase 9 - biosynthesis, Matrix Metalloproteinase 9 - genetics, Matrix Metalloproteinase 9 - metabolism, p38 Mitogen-Activated Protein Kinases - genetics, p38 Mitogen-Activated Protein Kinases - metabolism, Phosphopyruvate Hydratase - blood, Phosphopyruvate Hydratase - metabolism, Phosphorylation - drug effects, Phosphorylation - genetics, Proto-Oncogene Proteins c-bcl-2 - biosynthesis, Proto-Oncogene Proteins c-bcl-2 - genetics, Proto-Oncogene Proteins c-bcl-2 - metabolism, Quinuclidines - pharmacology, Rats, Rats, Sprague-Dawley, RNA, Messenger - biosynthesis, RNA, Messenger - genetics, S100 Calcium Binding Protein beta Subunit - blood, S100 Calcium Binding Protein beta Subunit - metabolism