Melatonin ameliorates cerebral ischemia/reperfusion injury through SIRT3 activation.

07:00 EST 4th November 2019 | BioPortfolio

Summary of "Melatonin ameliorates cerebral ischemia/reperfusion injury through SIRT3 activation."

Previous literature has shown that melatonin plays a critical role in protecting against cerebral ischemia/reperfusion (I/R) injury. Sirtuin3(SIRT3), as one member of the sirtuin family, protects against oxidative stress-related diseases. However, the association between melatonin and SIRT3 in cerebral I/R injury is not well understood. Our experiment was planned to investigate whether melatonin protects against cerebral I/R injury through SIRT3 activation.


Journal Details

This article was published in the following journal.

Name: Life sciences
ISSN: 1879-0631
Pages: 117036


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Medical and Biotech [MESH] Definitions

Adverse functional, metabolic, or structural changes in ischemic tissues resulting from the restoration of blood flow to the tissue (REPERFUSION), including swelling; HEMORRHAGE; NECROSIS; and damage from FREE RADICALS. The most common instance is MYOCARDIAL REPERFUSION INJURY.

Generally, restoration of blood supply to heart tissue which is ischemic due to decrease in normal blood supply. The decrease may result from any source including atherosclerotic obstruction, narrowing of the artery, or surgical clamping. Reperfusion can be induced to treat ischemia. Methods include chemical dissolution of an occluding thrombus, administration of vasodilator drugs, angioplasty, catheterization, and artery bypass graft surgery. However, it is thought that reperfusion can itself further damage the ischemic tissue, causing MYOCARDIAL REPERFUSION INJURY.

Restoration of blood supply to tissue which is ischemic due to decrease in normal blood supply. The decrease may result from any source including atherosclerotic obstruction, narrowing of the artery, or surgical clamping. It is primarily a procedure for treating infarction or other ischemia, by enabling viable ischemic tissue to recover, thus limiting further necrosis. However, it is thought that reperfusion can itself further damage the ischemic tissue, causing REPERFUSION INJURY.

Softening or loss of brain tissue following CEREBRAL INFARCTION; cerebral ischemia (see BRAIN ISCHEMIA), infection, CRANIOCEREBRAL TRAUMA, or other injury. The term is often used during gross pathologic inspection to describe blurred cortical margins and decreased consistency of brain tissue following infarction. Multicystic encephalomalacia refers to the formation of multiple cystic cavities of various sizes in the cerebral cortex of neonates and infants following injury, most notably perinatal hypoxia-ischemic events. (From Davis et al., Textbook of Neuropathology, 2nd ed, p665; J Neuropathol Exp Neurol, 1995 Mar;54(2):268-75)

Exposure of myocardial tissue to brief, repeated periods of vascular occlusion in order to render the myocardium resistant to the deleterious effects of ISCHEMIA or REPERFUSION. The period of pre-exposure and the number of times the tissue is exposed to ischemia and reperfusion vary, the average being 3 to 5 minutes.

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