Cellular and Molecular Pathways of Ischemic Neuronal Death

Abstract

Three routes have been identified triggering neuronal death under physiological and pathological conditions. Excess activation of ionotropic glutamate receptors cause influx and accumulation of Ca 2+ and Na + that result in rapid swelling and subsequent neuronal death within a few hours. The second route is caused by oxidative stress due to accumulation of reactive oxygen and nitrogen species. Apoptosis or programmed cell death that often occurs during developmental process has been coined as additional route to pathological neuronal death in the mature nervous system. Evidence is being accumulated that excitotoxicity, oxidative stress, and apoptosis propagate through distinctive and mutually exclusive signal transduction pathway and contribute to neuronal loss following hypoxic-ischemic brain injury. Thus, the therapeutic intervention of hypoxic-ischemic neuronal injury should be aimed to prevent excitotoxicity, oxidative stress, and apoptosis in a concerted way.

Proteomic Analysis of Mouse Hypothalamus under Simulated Microgravity

“…Oxidative stress induced NF κB in mouse brain has been reported in terrestrial model of microgravity [10]. The oxidative stress altered several signal transduction pathways and therefore was considered as one of the major factors that can modulate cellular signaling [12]. We previously demonstrated generation of oxidative stress in different regions of mouse brain and the responses were discrete among different regions [10].…”

Protective effects of edaravone against cobalt chloride-induced apoptosis in PC12 cells

“…Hypoxic/ischemic condition has long been recognized as an important mediator or modulator of apoptosis in neuronal cells because this condition is accompanied by the production of reactive oxygen species (ROS) which can attack nucleic acids, proteins and membrane phospholipids [2,3] . The distinct mechanisms that execute apoptosis through various apoptotic stimuli, are ultimately classified into the mitochondria-dependent pathway (intrinsic pathway) and the death receptor-dependent pathway (extrinsic pathway) [4] .…”

Kombinasi Artemisinin dan Ekstrak Moringa oleifera Menurunkan Ekspresi NF-κB namun Tidak Menurunkan Ekspresi iNOS pada Otak Mencit Diinfeksi Malaria

“…Produksi NO secara berlebihan akan membahayakan neuron, karena akan menyebabkan disfungsi neuron dan apoptosis (20). Protein iNOS yang dihasilkan secara berlebihan akan mengaktivasi mikroglia dan selanjutnya akan membangkitkan proses kaskade inflamasi.…”