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Paper Information

Title: 

CHRONIC INFLAMMATORY PAIN CAN INDUCE APOPTOSIS IN HIPPOCAMPUS NEURONS

Type: SPEECH
Author(s): JALAVAND E.,JAVAN MOHAMMAD,HAERI ROUHANI ALI,AHMADIAN A.A.H.
 
 
 
Name of Seminar: IRANIAN CONGRESS OF PHYSIOLOGY AND PHARMACOLOGY
Type of Seminar:  CONGRESS
Sponsor:  PHYSIOLOGY AND PHARMACOLOGY SOCIETY, MASHHAD UNIVERSITY OF MEDICAL SCIENCE
Date:  2007Volume 18
 
 
Abstract: 

Introduction: Cells die in response to a variety of stimuli and during apoptosis they do so in a controlled, regulated fashion. The role of glucocorticoids in the regulation of apoptosis remains incongruous .The aim of this study was to investigate the effect of chronic inflammatory pain on programmed cell death that it can change plasma corticosterone level.
Material and methods: 5% formalin was administered subcutaneously in the wistar rat hind paws for 4 days. In other group, rats adrenalectomized before injection of formalin. On 5th day corticosterone concentration in blood serum was determined using radio immunoassay kit and hippocampus of each rat was froze in -70oc and homogenized to determine caspase-3 as apoptosis indicator .Protein were extracted from hippocampus tissue. Their contents was determined and then used for western blot immunodetection.
Results: Blood plasma corticosterone level was raised with induction of pain. Western blot analyses showed that chronic inflammatory pain can activate caspase-3 enzyme significantly but it was not seen in adrenalectomized rats that they had injection of %5 formalin.
Conclusion: Since the hippocampus which has a high concentration of glucocorticoids (GCs) receptors is a principal target of increasing levels of GCs, we suggest that, there is a relation between increased blood plasma corticosterone and induction of apoptosis in hippocampus neurons.

 
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