Postconditioning-induced neuroprotection, mechanisms and applications in cerebral ischemia

Fan, Yanying; Hu, Weiwei; Fang, Nan; Chen, Zhong

doi:10.1016/j.neuint.2017.01.006

Cited by 41 publications

(20 citation statements)

References 153 publications

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“…The PI3K/AKT pathway has been documented as an essential pathway for cell survival in response to apoptosis and oxidative stress induced by a series of physiological and pathological or exogenous stimuli (53,54), while this pathway is also significantly involved in cerebral ischemia (55). To date, a number of studies have confirmed that the PI3K/AKT pathway serves an important role in the neuroprotective effects of curcumin by inhibiting apoptosis, oxidative stress and inflammation (56)(57)(58).…”

Section: Discussionmentioning

confidence: 99%

Curcumin exerts protective effects against hypoxia‑reoxygenation injury via the enhancement of apurinic/apyrimidinic endonuclease�1 in SH‑SY5Y cells: Involvement of the PI3K/AKT pathway

Cao²,

Kang

et al. 2020

Int J Mol Med

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Section: Discussionmentioning

confidence: 99%

Curcumin exerts protective effects against hypoxia‑reoxygenation injury via the enhancement of apurinic/apyrimidinic endonuclease�1 in SH‑SY5Y cells: Involvement of the PI3K/AKT pathway

Cao²,

Kang

et al. 2020

Int J Mol Med

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“…In particular, Uro‐A inhibited neuroinflammation and reduced oxidative stress in neuronal cells, which were highly relevant to ischemic neuronal injury. Autophagy suppresses neuroinflammation and attenuates oxidative stress in ischemic brains. Hence, it is likely that autophagy activation is the primary mechanism underlying the benefits of Uro‐A.…”

Section: Discussionmentioning

confidence: 99%

Urolithin A‐activated autophagy but not mitophagy protects against ischemic neuronal injury by inhibiting ER stress in vitro and in vivo

Ahsan

Zheng

et al. 2019

CNS Neurosci Ther

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Aim Mitochondrial autophagy (mitophagy) clears damaged mitochondria and attenuates ischemic neuronal injury. Urolithin A (Uro‐A) activates mitophagy in mammal cells and Caenorhabditis elegans. We explored neuroprotection of Uro‐A against ischemic neuronal injury. Methods Mice were subjected to middle cerebral artery occlusion. The brain infarct and neurological deficit scores were measured. The N2a cells and primary cultured mice cortical neurons were subjected to oxygen‐glucose deprivation and reperfusion (OGD/R). Uro‐A was incubated during OGD/R, and cell injury was determined by MTT and LDH. Autophagosomes were visualized by transfecting mCherry‐microtubule‐associated protein 1 light chain 3 (LC3). The protein levels of LC3‐II, p62, Translocase Of Inner Mitochondrial Membrane 23 (TIMM23), and cytochrome c oxidase subunit 4 isoform 1 (COX4I1) were detected by Western blot. The ER stress markers, activating transcription factor 6 (ATF6) and C/EBP homologous protein (CHOP), were determined by reverse transcription‐polymerase chain reaction (RT‐PCR). Results Urolithin A alleviated OGD/R‐induced injury in N2a cells and neurons and reduced ischemic brain injury in mice. Uro‐A reinforced ischemia‐induced autophagy. Furthermore, Uro‐A‐conferred protection was abolished by 3‐methyladenine, suggesting the requirement of autophagy for neuroprotection. However, mitophagy was not further activated by Uro‐A. Instead, Uro‐A attenuated OGD/R‐induced ER stress, which was abolished by 3‐methyladenosine. Additionally, neuroprotection was reversed by ER stress inducer. Conclusion Urolithin A protected against ischemic neuronal injury by reinforcing autophagy rather than mitophagy. Autophagy activation by Uro‐A attenuated ischemic neuronal death by suppressing ER stress.

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“…Several reports indicate that nAChR neuroprotective activity requires activation of protein kinase B (Akt) signaling, a critical cell survival pathway (Davis and Pennypacker 2016;Fan et al 2017). The α7 but not the α4 nAChR subunit interacts with the non-receptor-type tyrosine kinase Fyn and janus-activated kinase 2 (JAK2) (Kihara et al 2001;Shaw et al 2002), and α7 nAChR stimulation triggers activation of both kinases and subsequently upregulates phosphatidylinositol 3 kinase (PI3K) (Kihara et al 2001;Shaw et al 2002).…”

Section: Sak3 Is Neuroprotective Via Nachrsmentioning

confidence: 99%

SAK3-Induced Neuroprotection Is Mediated by Nicotinic Acetylcholine Receptors

Fukunaga

Yabuki

2018

Nicotinic Acetylcholine Receptor Signaling in Neuroprotection

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Cholinergic neurotransmission plays a critical role in neuronal plasticity and cell survival in the central nervous system (CNS). Two types of acetylcholine receptors (AChRs), muscarinic AChRs (mAChRs) and nicotinic AChRs (nAChRs), trigger intracellular signaling through G protein activity and ion influx, respectively. To assess mechanisms underlying neuroprotection through nAChRs, we developed SAK3, a novel modulator of nAChR activity. Recently, we found that SAK3 enhances T-type calcium channel activity, promoting ACh release in the hippocampal CA1 region of olfactory-bulbectomized mice. Here, we observed potent SAK3 neuroprotective activity in mice with 20-min bilateral common carotid artery occlusion (BCCAO) or hypothyroidism. Treatment of mice with the α7 nAChR-selective inhibitor methyllycaconitine (0.5 mg/kg/day, p.o.) antagonized SAK3-mediated neuroprotection and memory improvement in BCCAO mice. Single administration of the anti-Graves' disease therapeutic methimazole (MMI) to female mice disrupted olfactory bulb (OB) glomerular structure, and cholinergic neurons largely disappeared in the medial septum followed by memory loss. Chronic SAK3 (0.5-1 mg/kg, p.o.) administration significantly rescued the number of cholinergic medial septum neurons in MMI-treated mice and improved cognitive deficits seen in those mice. Overall, our study suggests that, in mice, the novel nAChR modulator SAK3 can rescue neurons impaired by transient ischemia and hypothyroidism. We also address mechanisms common to SAK3-induced neuroprotection in both conditions.

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Postconditioning-induced neuroprotection, mechanisms and applications in cerebral ischemia

Cited by 41 publications

References 153 publications

Curcumin exerts protective effects against hypoxia‑reoxygenation injury via the enhancement of apurinic/apyrimidinic endonuclease�1 in SH‑SY5Y cells: Involvement of the PI3K/AKT pathway

Curcumin exerts protective effects against hypoxia‑reoxygenation injury via the enhancement of apurinic/apyrimidinic endonuclease�1 in SH‑SY5Y cells: Involvement of the PI3K/AKT pathway

Urolithin A‐activated autophagy but not mitophagy protects against ischemic neuronal injury by inhibiting ER stress in vitro and in vivo

SAK3-Induced Neuroprotection Is Mediated by Nicotinic Acetylcholine Receptors

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