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Neuroprotective Effects of Inhibiting Fyn S-Nitrosylation on Cerebral Ischemia/Reperfusion-Induced Damage to CA1 Hippocampal Neurons
Open AccessArticle

Neuroprotective Effect of Salvianolic Acids against Cerebral Ischemia/Reperfusion Injury

1
Department of Neurology and Neuroscience Center, the First Hospital of Jilin University, Changchun 130021, China
2
Department of Neurology, the Center Hospital of Jilin City, Jilin 132000, China
3
Department of Neurology, Xuzhou Center Hospital, Xuzhou 221000, China
*
Author to whom correspondence should be addressed.
Academic Editors: Katalin Prokai-Tatrai and Anthony Lemarié
Int. J. Mol. Sci. 2016, 17(7), 1190; https://doi.org/10.3390/ijms17071190
Received: 9 May 2016 / Revised: 18 July 2016 / Accepted: 18 July 2016 / Published: 22 July 2016
(This article belongs to the Special Issue Neuroprotective Strategies 2016)
This study investigated the neuroprotective effect of salvianolic acids (SA) against ischemia/reperfusion (I/R) injury, and explored whether the neuroprotection was dependent on mitochondrial connexin43 (mtCx43) via the phosphatidylinositol 3-kinase/protein kinase B (PI3K/AKT) pathway. In vitro, we measured astrocyte apoptosis, mitochondrial membrane potential, and also evaluated the morphology of astrocyte mitochondria with transmission electron microscopy. In vivo, we determined the cerebral infarction volume and measured superoxide dismutase (SOD) activity and malondialdehyde (MDA) content. Additionally, mtCx43, p-mtCx43, AKT, and p-AKT levels were determined. In vitro, we found that I/R injury induced apoptosis, decreased cell mitochondrial membrane potential (MMP), and damaged mitochondrial morphology in astrocytes. In vivo, we found that I/R injury resulted in a large cerebral infarction, decreased SOD activity, and increased MDA expression. Additionally, I/R injury reduced both the p-mtCx43/mtCx43 and p-AKT/AKT ratios. We reported that both in vivo and in vitro, SA ameliorated the detrimental outcomes of the I/R. Interestingly, co-administering an inhibitor of the PI3K/AKT pathway blunted the effects of SA. SA represents a potential treatment option for cerebral infarction by up-regulating mtCx43 through the PI3K/AKT pathway. View Full-Text
Keywords: salvianolic acid; mitochondrial connexin43; phosphatidylinositol 3-kinase/protein kinase B; cerebral ischemia/reperfusion; astrocyte salvianolic acid; mitochondrial connexin43; phosphatidylinositol 3-kinase/protein kinase B; cerebral ischemia/reperfusion; astrocyte
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Hou, S.; Zhao, M.-M.; Shen, P.-P.; Liu, X.-P.; Sun, Y.; Feng, J.-C. Neuroprotective Effect of Salvianolic Acids against Cerebral Ischemia/Reperfusion Injury. Int. J. Mol. Sci. 2016, 17, 1190.

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