Delayed neuronal death prevented by inhibition of increased hydroxyl radical formation in a transient cerebral ischemia

Yamamoto, Toshihiro; Yuki, Satoshi; Watanabe, Toshiaki; Mitsuka, Masayuki; Saitô, Kenichi; Kogure, Kyuya

doi:10.1016/s0006-8993(97)00490-3

Cited by 197 publications

(127 citation statements)

References 13 publications

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“…The importance of antioxidant treatment in preventing neuronal damage has recently been emphasized (23,(59)(60)(61). Vitamin E (62) and a novel free radical scavenger (59) protect against changes in membrane permeability caused by peroxidation and attenuate ischemic and postischemic brain swelling.…”

Section: Discussionmentioning

confidence: 99%

Dehydroepiandrosterone prevents oxidative injury induced by transient ischemia/reperfusion in the brain of diabetic rats.

et al. 2000

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Both chronic hyperglycemia and ischemia/reperfusion (IR) cause an imbalance in the oxidative state of tissues. Normoglycemic and streptozotocin (STZ)-diabetic rats were subjected to bilateral carotid artery occlusion for 30 min followed by reperfusion for 60 min. Rats had either been treated with dehydroepiandrosterone (DHEA) for 7, 14, or 21 days (2 or 4 mg/day per rat) or left untreated. Oxidative state, antioxidant balance, and membrane integrity were evaluated in isolated synaptosomes. IR increased the levels of reactive species and worsened the synaptic function, affecting membrane Na/K-ATPase activity and lactate dehydrogenase release in all rats. The oxidative imbalance was much severer when transient IR was induced in STZ-diabetic rats. DHEA treatment restored H 2 O 2 , hydroxyl radical, and reactive oxygen species to close to control levels in normoglycemic rats and significantly reduced the level of all reactive species in STZ-diabetic rats. Moreover, DHEA treatment counteracted the detrimental effect of IR on membrane integrity and function: the increase of lactate dehydrogenase release and the drop in Na/K-ATPase activity were significantly prevented in both normoglycemic and STZ-diabetic rats. The results confirm that DHEA, an adrenal steroid that is synthesized de novo by brain neurons and astrocytes, possesses a multitargeted antioxidant effect. They also show that DHEA treatment is effective in preventing both derangement of the oxidative state and neuronal damage induced by IR in experimental diabetes. Diabetes

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Section: Discussionmentioning

confidence: 99%

Dehydroepiandrosterone prevents oxidative injury induced by transient ischemia/reperfusion in the brain of diabetic rats.

et al. 2000

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“…This pyrazolin containing molecule undergoes keto-enol tautomerization and generates phenolic structure [51]. Half of edaravone exists in an anionic form at physiological pH, which is the form that strongly reacts with the ROS in the brain [52]. The products of the reaction Fig.…”

Section: Edaravonementioning

confidence: 99%

Clinical and pharmacological aspects of bath salt use: A review of the literature and case reports

Miotto¹,

Striebel²,

Cho

et al. 2013

Drug and Alcohol Dependence

120

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Abstract:Reactive oxygen species (ROS) are widely believed to cause or aggravate several human pathologies such as neurodegenerative diseases, cancer, stroke and many other ailments. Antioxidants are assumed to counteract the harmful effects of ROS and therefore prevent or treat oxidative stress-related diseases. In this report, recent human studies exploring the efficiency of antioxidants in prevention and treatment of various diseases are reviewed. Few antioxidants including edaravone (for ischemic stroke in Japan), Nacetylcysteine (for acetaminophen toxicity), alfa-lipoic acid (for diabetic neuropathy) and some flavonoids (polyphenolic compounds present in dietary plants), such as micronized purified flavonoid fraction (diosmin and hesperidin) and oxerutins (for chronic venous insufficiency) as well as baicalein and catechins (for osteoarthritis) have found accepted clinical use. However, despite much enthusiasm in the 1980s and 1990s, many well-known agents such as antioxidant vitamins and also more recently developed compounds such as nitrones have not successfully passed the scrutiny of clinical trials for prevention and treatment of various diseases. This has given rise to a pessimistic view of antioxidant therapy, however, the evidence from human epidemiological studies about the beneficial effects of dietary antioxidants and preclinical in vitro and animal data are compelling. We have probably wasted too much time on agents like antioxidant vitamins instead of focusing on more disease specific, target-directed, highly bioavailable antioxidants. We here discuss possible reasons for the lack of success in some clinical trials and seek to provide some suggestions to be considered if antioxidant therapy is to succeed as an effective therapeutic strategy.

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“…However, edaravone is recommended by the American Heart Association in the guidelines for the early management of adults with AIS (21). Edaravone exerts antioxidant effects by inhibiting hydroxyl radical-dependent and -independent lipid peroxidation (22,23). This antioxidant activity, the main suggested action mechanism, may protect against free radical-related injuries following AIS (24).…”

Section: Edaravonementioning

confidence: 99%

Edaravone (Radicut), a free radical scavenger, is a potentially useful addition to thrombolytic therapy in patients with acute ischemic stroke

et al. 2012

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Delayed neuronal death prevented by inhibition of increased hydroxyl radical formation in a transient cerebral ischemia

Cited by 197 publications

References 13 publications

Dehydroepiandrosterone prevents oxidative injury induced by transient ischemia/reperfusion in the brain of diabetic rats.

Dehydroepiandrosterone prevents oxidative injury induced by transient ischemia/reperfusion in the brain of diabetic rats.

Clinical and pharmacological aspects of bath salt use: A review of the literature and case reports

Edaravone (Radicut), a free radical scavenger, is a potentially useful addition to thrombolytic therapy in patients with acute ischemic stroke

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