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Protective mechanism of Sulindac against animal model of ischemic stroke
Title
Protective mechanism of Sulindac against animal model of ischemic stroke.
Creator
Modi, Jigar P., Graduate College
Date Issued
2012-03-30
PURL
http://purl.flvc.org/fcla/dt/3342413
Format
Document (PDF)
Protective mechanism of Sulindac against animal model of ischemic stroke
Title
Protective mechanism of Sulindac against animal model of ischemic stroke.
Creator
Modi, Jigar P., Charles E. Schmidt College of Medicine, Department of Biological Sciences
Abstract/Description
The Effect of Sulindac was studied on an animal model of ischemic stroke. Sulindac, a non steroid anti inflammatory drug (NSAID) could protect cell death due to hypoxia/reoxygenation. This drug was given 2 days before and 24 hrs after ischemia until animals were sacrificed on 3rd or 11th day. Infarct size was measured for these animals. Sulindac induced Hsp 27 in ischemic penumbra and core on Day 3 & 11 with uncoated nylon suture which shows its cell-survival and anti-apoptotic activity. Also...
Show moreThe Effect of Sulindac was studied on an animal model of ischemic stroke. Sulindac, a non steroid anti inflammatory drug (NSAID) could protect cell death due to hypoxia/reoxygenation. This drug was given 2 days before and 24 hrs after ischemia until animals were sacrificed on 3rd or 11th day. Infarct size was measured for these animals. Sulindac induced Hsp 27 in ischemic penumbra and core on Day 3 & 11 with uncoated nylon suture which shows its cell-survival and anti-apoptotic activity. Also, it increased expression of cell survival markers such as Akt, Bcl2 & Grp 78 in ischemic penumbra and core. With silicon suture it reduced expression of Hsp 27 in ischemic penumbra and core, alleviating cell stress and having pro-survival and anti-stress effects. In conclusion sulindac may have excellent potential as neuro protective agent against oxidative stress in cerebral ischemia.
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Date Issued
2011
PURL
http://purl.flvc.org/FAU/3333056
Subject Headings
Apoptosis, Biochemical markers, Diagnostic use, Oxidation reduction reaction, Cerebral ischemia, Prevention
Format
Document (PDF)
Calpain Cleavage of GAD65 is pathological and impairs gaba neurotransmission
Title
Calpain Cleavage of GAD65 is pathological and impairs gaba neurotransmission.
Creator
Buddhala, Chandana, Suarez, Marjorie, Alexandrescu, Anamaria, Pissaris, Adam, Modi, Jigar P., Wei, Jianning, Prentice, Howard, Wu, Jang-Yen, Graduate College
Date Issued
2011-04-08
PURL
http://purl.flvc.org/fcla/dt/3164511
Subject Headings
Nervous System Diseases, GABA --physiology, Gamma-aminoboterzuur
Format
Document (PDF)
Calpain Cleavage of Brain Glutamic Acid Decarboxylase 65 Is Pathological and Impairs GABA Neurotransmission
Title
Calpain Cleavage of Brain Glutamic Acid Decarboxylase 65 Is Pathological and Impairs GABA Neurotransmission.
Creator
Buddhala, Chandana, Suarez, Marjorie, Modi, Jigar P., Prentice, Howard, Ma, Zhiyuan, Tao, Rui, Wu, Jang-Yen, Smalheiser, Neil R.
Date Issued
2012-03-12
PURL
http://purl.flvc.org/fau/fd/FAUIR000097
Format
Citation
Mechanism of Carbamathione as a therapeutic agent for Stroke.
Title
Mechanism of Carbamathione as a therapeutic agent for Stroke.
Creator
Modi, Jigar P., Wu, Jang-Yen, Florida Atlantic University, Charles E. Schmidt College of Science, Center for Complex Systems and Brain Sciences
Abstract/Description
Stroke is the third leading cause of mortality in the United States, and so far, no clinical interventions have been shown completely effective in stroke treatment. Stroke may result in hypoxia, glutamate release and oxidative stress. One approach for protecting neurons from excitotoxic damage in stroke is to attenuate receptor activity with specific antagonists. Disulfiram requires bio-activation to S-methyl N, N-diethylthiolcarbamate sulfoxide (DETC-MeSO). In vivo, DETC-MeSO is further...
Show moreStroke is the third leading cause of mortality in the United States, and so far, no clinical interventions have been shown completely effective in stroke treatment. Stroke may result in hypoxia, glutamate release and oxidative stress. One approach for protecting neurons from excitotoxic damage in stroke is to attenuate receptor activity with specific antagonists. Disulfiram requires bio-activation to S-methyl N, N-diethylthiolcarbamate sulfoxide (DETC-MeSO). In vivo, DETC-MeSO is further oxidized to the sulfone which is carbamoylated forming Carbamathione, a glutathione adducts. Carbamathione proved to be useful as a pharmacological agent in the treatment of cocaine dependence with the advantage that it lacks ALDH2 inhibitory activity. Carbamathione is a partial NMDA glutamate antagonist. The purpose of this dissertation study is to evaluate the neuroprotective effects of Carbamathione drug on PC-12 cell line and to understand the protective mechanisms underlying in three stroke-related models: excessive glutamate, hypoxia/reoxygenation and bilateral carotid artery occlusion (BCAO). Carbamathione was administered 14 mg/kg subcutaneously for 4 days with the first injection occurring 30 min after occlusion in the mouse BCAO stroke model. Mice were subjected to the locomotor test, and the brain was analyzed for infarct size. Heat shock proteins, key proteins involved in apoptosis and endoplasmic reticulum (ER) stress, were analyzed by immunoblotting. Carbamathione reduced both cell death following hypoxia/reoxygenation and brain infarct size. It improved performance on the locomotor test. The level of pro-apoptotic proteins declined, and anti-apoptotic, P-AKT and HSP27 protein expressions were markedly increased. We found that Carbamathione suppresses the up- regulation of Caspase-12, Caspase-3 and significantly declined ER stress protein markers GRP 78, ATF4, XBP-1, and CHOP. Carbamathione can down- regulate ATF 4 and XBP1 expression, indicating that Carbamathione inhibits the ER stress induced by hypoxia/reoxygenation through suppressing PERK and IRE1 pathways. Carbamathione elicits neuroprotection through the preservation of ER resulting in reduction of apoptosis by increase of anti-apoptotic proteins and decrease of pro-apoptotic proteins. Carbamathione can suppress the activation of both PERK and IRE1 pathways in PC-12 cell cultures and has no inhibitory effect on ATF6 pathway. These findings provide promising and rational strategies for stroke therapy.
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Date Issued
2017
PURL
http://purl.flvc.org/fau/fd/FA00004979, http://purl.flvc.org/fau/fd/FA00004969
Subject Headings
Dissertations, Academic -- Florida Atlantic University, Stroke., Stroke--drug therapy., Carbamathione
Format
Document (PDF)
Mechanisms of Neuronal Protection against Excitotoxicity, Endoplasmic Reticulum Stress, and Mitochondrial Dysfunction in Stroke and Neurodegenerative Diseases
Title
Mechanisms of Neuronal Protection against Excitotoxicity, Endoplasmic Reticulum Stress, and Mitochondrial Dysfunction in Stroke and Neurodegenerative Diseases.
Creator
Prentice, Howard, Modi, Jigar P., Wu, Jang-Yen
Date Issued
2015
PURL
http://purl.flvc.org/fau/fd/FAUIR000111
Format
Citation