Nitric oxide substitution during ischemia/reperfusion improves hemodynamic and metabolic outcome of explanted rabbit hearts after long-term ischemia

Aim: The aim of the present study is to explore the neuroprotective effects of remote ischemic preconditioning in long term cognitive impairment after global cerebral ischemia induced-vascular dementia in mice. Material and methods: The mice were subjected to global cerebral ischemia by occluding the bilateral common carotid arteries for 12 minutes followed by the 24 hours of the reperfusion. The remote ischemic preconditioning stimulus was delivered in the form of 4 cycles of ischemia/reperfusion for 5 minutes each. The cerebral ischemic injury induced-long term cognitive impairment-related learning and memory alterations was assessed using morris water maze, the motor performances of the animals were evaluated using rota-rod test and neurological severity score. The cerebral infract size of the brain were quantified using triphenyltetrazolium chloride staining. Results: Global cerebral ischemia causes long term memory impairment, decreases motor performances and increases the brain infract size in animals. The delivery of remote ischemic preconditioning stimulus significantly abolished the long-term cognitive impairment and ameliorates the motor performances as well as cerebral infract size in brain. Conclusion: The remote ischemic preconditioning mediates neuro protection against global cerebral ischemic injury induced long-term cognitive impairment.

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The Role of Reactive Oxygen Species, Kinases, Hydrogen Sulfide, and Nitric Oxide in the Regulation of Autophagy and Their Impact on Ischemia and Reperfusion Injury in the Heart

Current Cardiology Reviews ◽

10.2174/1573403x16666201014142446 ◽

2020 ◽

Vol 16 ◽

Author(s):

Andrey Krylatov ◽

Leonid Maslov ◽

Sergey Y. Tsibulnikov ◽

Nikita Voronkov ◽

Alla Boshchenko ◽

...

Keyword(s):

Nitric Oxide ◽

Reactive Oxygen Species ◽

Hydrogen Sulfide ◽

Ischemia Reperfusion ◽

Reactive Oxygen ◽

Ischemia And Reperfusion ◽

Oxygen Species ◽

Ischemia And Reperfusion Injury ◽

Adaptive Process

: There is considerable evidence in the heart that autophagy in cardiomyocytes is activated by hypoxia/reoxygenation (H/R) or in hearts by ischemia/reperfusion (I/R). Depending upon the experimental model and duration of ischemia, increases in autophagy in this setting maybe beneficial (cardioprotective) or deleterious (exacerbate I/R injury). Aside from the conundrum as to whether or not autophagy is an adaptive process, it is clearly regulated by a number of diverse molecules including reactive oxygen species (ROS), various kinases, hydrogen sulfide (H2S) and nitric oxide (NO). The purpose this review is to address briefly the controversy regarding the role of autophagy in this setting and to examine a variety of disparate molecules that are involved in its regulation.

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Hydrogen Sulfide in Physiological and Pathological Mechanisms in Brain

CNS & Neurological Disorders - Drug Targets ◽

10.2174/1871527317666180605072018 ◽

2018 ◽

Vol 17 (9) ◽

pp. 654-670 ◽

Cited By ~ 16

Author(s):

Mohit Kumar ◽

Rajat Sandhir

Keyword(s):

Nitric Oxide ◽

Traumatic Brain Injury ◽

Hydrogen Sulfide ◽

Neurodegenerative Disorders ◽

Neurological Disorders ◽

Scientific Community ◽

Molecular Targets ◽

Long Term Potentiation ◽

Term Potentiation

Background & Objective: Hydrogen sulfide [H2S] has been widely known as a toxic gas for more than 300 years in the scientific community. However, the understanding about this small molecule has changed after the discovery of involvement of H2S in physiological and pathological mechanisms in brain. H2S is a third gasotransmitter and neuromodulator after carbon monoxide [CO] and nitric oxide [NO]. H2S plays an important role in memory and cognition by regulating long-term potentiation [LTP] and calcium homeostasis in neuronal cells. The disturbances in endogenous H2S levels and trans-sulfuration pathway have been implicated in neurodegenerative disorders like Alzheimer’s disease, Parkinson disease, stroke and traumatic brain injury. According to the results obtained from various studies, H2S not only behaves as neuromodulator but also is a potent antioxidant, anti-inflammatory and anti-apoptotic molecule suggesting its neuroprotective potential. Conclusion: Recently, there is an increased interest in developing H2S releasing pharmaceuticals to target various neurological disorders. This review covers the information about the involvement of H2S in neurodegenerative diseases, its molecular targets and its role as potential therapeutic molecule.

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