Ram Gopal College of Pharmacy

Approved by- AICTE, PCI, MHRD, Govt of India,
Affiliation from Pt. B.D. Sharma University of Health Science, Rohtak, Haryana
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    Articles

    CEREBRAL ISCHEMIC STROKE: SEQUELS OF CASCADE

    ISSN 0975-6299                                         Vol.1/Issue-3/Jul-Sep.2010


    International Journal of Pharma and Bio Sciences

    ====================================================


    1    Ram Gopal College of Pharmacy, Sultanpur, Gurgaon, (Haryana, India)

    2    Panjab University Chandigarh, India

    3    Raj Kumar Goel Institute of Technology, 5 kilometer Milestone, Delhi Meerut Road, Ghaziabad, (Uttar Pradesh, India)

    * Corresponding                                        Author:-   singlashu@gmail.com

    ABSTRACT

    Cerebral Ischemia (stroke) is one of the foremost causes of high morbidity and mortality for both developed and developing countries. Cerebral ischemia impairs the normal neurological functions which are triggered by a complex series of biochemical and molecular mechanism. Understanding of mechanisms of injury and neuroprotection in this disease is important to learn new target sites to treat ischemia. In this article, there is clear understanding of ischemic cascade followed by the mechanism of all damaging factors like energy failure, excitotoxicity, oxidative stress, neuroinflammation, cell death modes: necrosis, apoptosis along with histological changes. Further it also discloses the different epidemiology based on the age, gender and races along with current status of the prevalence in India in comparison with western world. The present authors also describe and relate aponecrosis and necroptosis with cerebral ischemia. The main emphasis is given and described along with diagrammatic view.

    KEY WORDS

    Cerebral Ischemia, Pathophysiology, Epidemiology, Necroptosis, Aponecrosis

    ABBREVIATIONS

     AIF: Apoptosis Inducing Factor; AMPA: α -amino-3-hydroxyl-5-methyl-4-isoxazole-propionate; APAF-1: Apoptotic Proteases-Activating Factor – 1; ATP: Adenosine Try Phosphate; CINC: Cytokine-induced neutrophil chemoattractant; DD: Death Domains; Diablo: Direct IAP-Binding Protein with Low pI; DISC: Death Inducing Signaling Complex; DRs: Death Receptors; FADD: Fas-Associated Death Domain; IAPs: Inhibitors of Apoptotic Proteins; ILs: Interleukins; LTD: long term depression; LTP: Long Term Potentiation; MCAO: Middle Cerebral Artery Occlusion; MCP-1: Monocyte chemoattractant protein–1; MPT: Mitochondrial Permeability Transition ; Nec-1: Necrostatin-1; NF- κ B: Nuclear Factor kappa B; NMDA: N-methyl-D-Aspartic Acid; nNOS: Neuronal Nitric Oxide Synthase; PARP: Poly ADP Ribose polymerase; PMN: Polymorphonuclear; RIP: Receptor interacting proteins; ROS: Reactive Oxygen Species; Smac: Second Mitochondrial-Derived Activator of Caspases; SOD:

     

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