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Information Seminar Paper

Title

EFFECT OF CALCIUM CHANNEL BLOCKER, NIMODIPINE, ON BRAIN CYTOKINES FOLLOWING TRAUMATIC BRAIN INJURY IN RATS

Pages

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Abstract

 INTRODUCTION: TRAUMATIC BRAIN INJURY (TBI) IS A DEVASTATIVE NEUROLOGICAL DEFICIT INVOLVING PRIMARY AND SECONDARY INJURY CASCADES INCLUDE CONSEQUENCES OF ACTIVATION OF PROINFLAMMATORY CYTOKINES AND CEREBRAL EDEMA. IT HAS SHOWN THAT CALCIUM MEDIATE RELEASE OF MANY FACTORS IN BLOOD AND TISSUE. HOWEVER, ITS EFFECT REMAINS TO BE CLARIFIED REGARDING RELEASE OF CYTOKINES FOLLOWING TBI.METHODS: SEVER TRAUMATIC BRAIN INJURY WAS INDUCED BY MARMARU METHOD THAT IT WAS DONE BY 450G WEIGHT DROPPING ON ANIMAL HEAD IN N-MARI RATS. NIMIDIPINE (40 MG/KG, IV) WERE INJECTED AFTER INDUCTION OF TRAUMA. THE CONCENTRATION OF CYTOKINES IL-1B, IL-6, TNF-Α AND TGF-B WERE MEASURED 8 AND 24 HOURS AFTER TRAUMA IN BRAIN TISSUE.RESULTS: THE RESULTS INDICATED THAT ADMINISTRATION OF NIMODIPINE SIGNIFICANTLY DECREASED TNF-A CONTENT 8 AND 24 HOURS AFTER TRAUMA (P£0.0001, P£0.008, RESPECTIVELY). TGF- Β WAS DECREASED BY NIMODIPINE 8 HOUR AFTER TRAUMA (P£0.01). THERE WAS NO DIFFERENCE IN IL-6 BETWEEN GROUPS. IL-1Β WAS INCREASED BY NIMODIPINE, 8 AND 24 HOURS AFTER TRAUMA (P£0.003, P£0.0001, RESPECTIVELY).CONCLUSION: OUR FINDING INDICATED THAT CALCIUM CHANNEL BLOCKER NIMODIPINE PROBABLY PROTECT THE BRAIN BY CONTROL OF SYNTHESIS AND RELEASE OF TNF-A AND PREVENTION OF CHANGING IN IL-6.

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