A novel free radical scavenger, NSP-116, ameliorated the brain injury in both ischemic and hemorrhagic stroke models
Reperfusion injury is a serious problem in ischemic stroke therapy, which leads to neuronal damage and intracranial hemorrhage (ICH). A novel free radical scavenger, NSP-116, has anti-oxidative effect and may ameliorate reperfusion injury. The purpose of this study was to investigate the effects of...
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2019-11-01T00:00:00Z.
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LEADER | 00000 am a22000003u 4500 | ||
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001 | doaj_8c7d2c524c5b4af0a61ba28b3732b68a | ||
042 | |a dc | ||
100 | 1 | 0 | |a Takahiko Imai |e author |
700 | 1 | 0 | |a Sena Iwata |e author |
700 | 1 | 0 | |a Daisuke Miyo |e author |
700 | 1 | 0 | |a Shinsuke Nakamura |e author |
700 | 1 | 0 | |a Masamitsu Shimazawa |e author |
700 | 1 | 0 | |a Hideaki Hara |e author |
245 | 0 | 0 | |a A novel free radical scavenger, NSP-116, ameliorated the brain injury in both ischemic and hemorrhagic stroke models |
260 | |b Elsevier, |c 2019-11-01T00:00:00Z. | ||
500 | |a 1347-8613 | ||
500 | |a 10.1016/j.jphs.2019.09.012 | ||
520 | |a Reperfusion injury is a serious problem in ischemic stroke therapy, which leads to neuronal damage and intracranial hemorrhage (ICH). A novel free radical scavenger, NSP-116, has anti-oxidative effect and may ameliorate reperfusion injury. The purpose of this study was to investigate the effects of NSP-116 on both ischemic and hemorrhagic stroke models.First, we assessed whether NSP-116 has protective effects in vitro. Pre-treatment of NSP-116 decreased neuronal cell damage induced by H2O2 or LPS. Moreover, NSP-116 also suppressed mitochondria damage and apoptosis in H2O2-induced neuronal injury model. Based on these results, we used a middle cerebral artery occlusion (MCAO)-induced ischemic stroke model or a collagenase-induced ICH model. Using the MCAO model, we evaluated the cerebral blood flow (CBF), neurological deficit, and infarct volume. Hematoma volume was assessed at 3 days after ICH. In the MCAO model, oral administration of NSP-116 at 30 mg/kg attenuated the reduction of CBF, neurological deficits, and infarct formation. Interestingly, NSP-116 also ameliorated hematoma expansion and neurological deficits in the ICH model. Additionally, pre-treatment of NSP-116 suppressed the brain microvascular endothelial cell death induced by collagenase treatment.Collectively, our findings indicated that oral administration of NSP-116 attenuates both ischemic and hemorrhagic brain injuries after stroke. Keywords: Brain hemorrhage, Brain ischemia, Oxidative stress, A free radical scavenger, Stroke | ||
546 | |a EN | ||
690 | |a Therapeutics. Pharmacology | ||
690 | |a RM1-950 | ||
655 | 7 | |a article |2 local | |
786 | 0 | |n Journal of Pharmacological Sciences, Vol 141, Iss 3, Pp 119-126 (2019) | |
787 | 0 | |n http://www.sciencedirect.com/science/article/pii/S1347861319357159 | |
787 | 0 | |n https://doaj.org/toc/1347-8613 | |
856 | 4 | 1 | |u https://doaj.org/article/8c7d2c524c5b4af0a61ba28b3732b68a |z Connect to this object online. |