Gene/Protein Disease Symptom Drug Enzyme Compound
Pivot Concepts:   Target Concepts:
Query: EC:3.4.22.62 (caspase-9)
 7,507 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

Post-traumatic stress disorder (PTSD) is a stress-related mental disorder caused by experience of a traumatic event, and presents with characteristic symptoms including intrusive memories, hyperarousal, and avoidance. Recently, structural neuroimaging studies showed that hippocampal volumes were relatively low in PTSD patients. However, the mechanisms that cause such atrophy are not well understood. The aim of this study was to reveal the possible mechanisms involved in apoptosis induced by single-prolonged stress (SPS) in hippocampus of PTSD rats. SPS is one of the animal models proposed for PTSD. Rats exposure to SPS showed enhanced inhibition of the hypothalamo-pituitary-adrenal (HPA) axis, which has been reliably reproduced in patients with PTSD. Wistar rats were killed at 1, 4, 7, 14 and 28 days after exposure to SPS. Expression of caspase-9, caspase-3, cytochrome c, Bcl-2 and Bax was detected by immunohistochemistry, immunofluorescence, Western blotting and electron microscopy. Apoptotic cells were assessed by TUNEL method. Our results showed apoptotic cells were significantly increased in hippocampus of SPS rats, accompanied by release of cytochrome c from the mitochondria into the cytosol, increase of caspase-9 and caspase-3 expression and decrease of the Bcl-2/Bax ratio. The results indicate that SPS-induced apoptosis in hippocampus of PTSD rats, and the mitochondrial pathway was involved in the process of SPS-induced apoptosis.
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PMID:Single-prolonged stress induced mitochondrial-dependent apoptosis in hippocampus in the rat model of post-traumatic stress disorder. 2062 56

The purpose of this study was to provide a novel insight into the mechanism of how amygdala might participate in PTSD by investigating the changes of cytochrome c oxidase (COX), caspase-9, and caspase-3 in the amygdala of single-prolonged stress (SPS) rats. A total of 80 healthy, male Wistar rats were selected for this study. The models of post-traumatic stress disorder (PTSD) were created by SPS, which is an established animal model for PTSD. The change of COX was detected by light microscope and transmission electron microscopy (TEM). The expression of caspase-9 and caspase-3 in the basolateral amygdala was examined by immunofluorescence and reverse transcription-polymerase chain reaction (RT-PCR). SPS exposure resulted in a significant change of COX in the SPS model groups compared with the normal control group. Evaluation by enzymohistochemistry indicated translocation of COX from mitochondria to cytoplasm. The expression of both caspase-9 and caspase-3 significantly increased 1 day after SPS stimulation, then gradually increased and peaked at SPS 7d. This findings suggest changes of COX, caspase-9, and caspase-3 in the amygdala of SPS rats, which may play important roles in the pathogenesis of PTSD.
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PMID:Single-prolonged stress induces apoptosis by activating cytochrome C/caspase-9 pathway in a rat model of post-traumatic stress disorder. 2080 13

Mitochondria play a significant role in the pathophysiology of post-traumatic stress disorder (PTSD). Risperidone and paroxetine were evaluated for their effect on mitochondrial dysfunction and mitochondria-dependent apoptosis in discrete brain regions in modified stress re-stress (SRS) animal model of PTSD. Male rats were subjected to stress protocol of 2 h restraint and 20 min forced swim followed by halothane anesthesia on day 2 (D-2). Thereafter, rats were exposed to re-stress (forced swim) on D-8 and at 6-day intervals on D-14, D-20, D-26, and D-32. The rats were treated with risperidone (0.01, 0.1, and 1.0 mg/kg p.o.) and paroxetine (10.0 mg/kg p.o.) from D-8 to D-32. Risperidone at median dose and paroxetine ameliorated modified SRS-induced depressive-like symptom (increase in immobility period) in forced swim, anxiety-like behavior (decrease in percentage of open arm entries and time spent) in elevated plus maze and cognitive deficits (loss in spatial recognition memory) in Y-maze tests on D-32. Risperidone, but not paroxetine, attenuated modified SRS-induced decreases in plasma corticosterone levels. Risperidone ameliorated increase in the activity of mitochondrial respiratory complex (I, II, IV, and V), decreases in the levels of mitochondrial membrane potential, cytochrome-C and caspase-9 in the hippocampus, hypothalamus, pre-frontal cortex, and amygdala. However, both drugs attenuated modified SRS-induced increase in the number of apoptotic cells and caspase-3 levels in all the brain regions indicating anti-apoptotic activity of these drugs. Hence, these results suggest that anti-apoptotic activity could be a common mechanism for anti-PTSD-like effect irrespective of the pathways of apoptosis in the modified SRS model.
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PMID:Risperidone Attenuates Modified Stress-Re-stress Paradigm-Induced Mitochondrial Dysfunction and Apoptosis in Rats Exhibiting Post-traumatic Stress Disorder-Like Symptoms. 2575 29