Protective Effect of Minocycline Against Ketamine-Induced Injury in Neural Stem Cell: Involvement of PI3K/Akt and Gsk-3 Beta Pathway

Lu, Yang; Shan, Lei; Wang, Ning; Lü, Ping; Li, Weisong; Zheng, Juan; Giri, Praveen Kumar; Lü, Haixia; Chen, Xinlin; Zuo, Zhiyi; Liu, Yong

doi:10.3389/fnmol.2016.00135

Cited by 31 publications

(15 citation statements)

References 40 publications

(51 reference statements)

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“…Interestingly, we found that minocycline alleviates cellular proliferating changes induced by midazolam in neurogenetic regions of neonatal rats, indicating that minocycline might enhance NSC proliferation following midazolam exposure during the brain development which is benefit for the neurogenesis. The finding about the neuroprotection of minocycline on brain development is in consistency with our recent study, which reported the protective effect of minocycline against ketamine-induced injury in NSCs 17 . Whether minocycline can mitigate midazolam-induced neuroapoptosis needs to be determined further.…”

Section: Discussionsupporting

confidence: 92%

“…The positive outcome of minocycline is associated with inhibition of microglia activation 14 , inhibition of caspase-1 and caspase-3 15 , and cytochrome c release 16 . Recently, we reported that minocycline attenuated ketamine-induced injury in neural stem cells (NSCs) 17 and restores neurogenesis in the subventricular zone (SVZ) and the subgranular zone (SGZ) of the hippocampus after ketamine exposure in neonatal rats 18 . However, whether minocycline can attenuate the developmental neurotoxicity of midazolam remains unclear.…”

Section: Introductionmentioning

confidence: 99%

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Pretreatment with minocycline improves neurogenesis and behavior performance after midazolam exposure in neonatal rats

Giri

Shan

et al. 2018

NeuroReport

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Laboratory studies suggested that general anesthetics induce neuroapoptosis and inhibit neurogenesis in developing brains of animals. Minocycline exerts neuroprotection against a wide range of toxic insults in neurodegenerative diseases models. Here, we investigate whether minocycline can alleviate neurogenetic damage and improve cognition following midazolam exposure in neonatal rats. Postnatal 7 days rats were divided randomly into three groups: control group (C), midazolam group (M), and minocycline pretreatment group (MP). After exposure to midazolam, the cell proliferation in the subventricular zone (SVZ) and the subgranular zone (SGZ) of the hippocampus in pups was analyzed by bromodeoxyuridine immunochemistry at 7 days after the administration of anesthesia. Cognitive function was assessed using the Morris water-maze test at 35 days after midazolam exposure. Compared with the control, midazolam reduced cell proliferation both in the SVZ and in the SGZ of the hippocampus of neonatal rats, and decreased spatial learning and memory ability of rats in adulthood significantly. Pretreatment with minocycline increased cell proliferation both in the SVZ and in the SGZ of the hippocampus and improved spatial learning and memory ability compared with midazolam, but it did not mitigate the changes to the normal levels compared with the controls. Our results indicated that pretreatment with minocycline can alleviate midazolam-induced damage in neural stem cell proliferation of neonatal rats and improve spatial learning and memory ability of rats in adulthood.

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Section: Discussionsupporting

confidence: 92%

Section: Introductionmentioning

confidence: 99%

Pretreatment with minocycline improves neurogenesis and behavior performance after midazolam exposure in neonatal rats

Giri

Shan

et al. 2018

NeuroReport

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“…In vitro , Res up-regulated the expression of p-Akt and p-p300, which were co-localized in the PC-12 cells ( p < 0.01 ). LY294002, an inhibitor of Akt signaling (Lu et al, 2016 ), down-regulated the expression of p-p300 ( p < 0.05 , Figures 3D–F ), suggesting that the Res-induced phosphorylation of p300 was mediated via Akt signaling. In addition, these results may indicate that Res enhanced the activity of p300 acetyltransferase, as the phosphorylation of p300 at Ser-1834 is believed to be essential for this activity (Huang and Chen, 2005 ; Liu et al, 2006 ; Chen et al, 2015 ).…”

Section: Resultsmentioning

confidence: 90%

Resveratrol Promotes Nerve Regeneration via Activation of p300 Acetyltransferase-Mediated VEGF Signaling in a Rat Model of Sciatic Nerve Crush Injury

et al. 2018

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Peripheral nerve injuries are generally associated with incomplete restoration of motor function. The slow rate of nerve regeneration after injury may account for this. Although many benefits of resveratrol have been shown in the nervous system, it is not clear whether resveratrol could promote fast nerve regeneration and motor repair after peripheral nerve injury. This study showed that the motor deficits caused by sciatic nerve crush injury were alleviated by daily systematic resveratrol treatment within 10 days. Resveratrol increased the number of axons in the distal part of the injured nerve, indicating enhanced nerve regeneration. In the affected ventral spinal cord, resveratrol enhanced the expression of several vascular endothelial growth factor family proteins (VEGFs) and increased the phosphorylation of p300 through Akt signaling, indicating activation of p300 acetyltransferase. Inactivation of p300 acetyltransferase reversed the resveratrol-induced expression of VEGFs and motor repair in rats that had undergone sciatic nerve crush injury. The above results indicated that daily systematic resveratrol treatment promoted nerve regeneration and led to rapid motor repair. Resveratrol activated p300 acetyltransferase-mediated VEGF signaling in the affected ventral spinal cord, which may have thus contributed to the acceleration of nerve regeneration and motor repair.

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“…Lu et al [18]aimed to elucidate a possible mechanism underlying the neuroprotective effect of minocycline by using LY294002 to inhibit the PI3K pathway. Immunoblotting revealed that minocycline enhanced phosphorylation/activation of Akt and phosphorylation/inactivation of GSK3β.…”

Section: Discussionmentioning

confidence: 99%

Hydrogen-Rich Saline Attenuates Brain Injury Induced by Cardiopulmonary Bypass and Inhibits Microvascular Endothelial Cell Apoptosis Via the PI3K/Akt/GSK3β Signaling Pathway in Rats

Chen¹,

Wang²,

Diao³

et al. 2017

Cell Physiol Biochem

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Background/Aims: Cardiopulmonary bypass (CPB) is prone to inducing brain injury during open heart surgery. A hydrogen-rich solution (HRS) can prevent oxidation and apoptosis, and inhibit inflammation. This study investigated effects of HRS on brain injury induced by CPB and regulatory mechanisms of the PI3K/Akt/GSK3β signaling pathway. Methods: A rat CPB model and an in vitro cell hypoxia model were established. After HRS treatment, Rat behavior was measured using neurological deficit score; Evans blue (EB) was used to assess permeability of the blood-brain barrier (BBB); HE staining was used to observe pathological changes; Inflammatory factors and brain injury markers were detected by ELISA; the PI3K/Akt/GSK3β pathway-related proteins and apoptosis were assessed by western blot, immunohistochemistry and qRT –PCR analyses of brain tissue and neurons. Results: After CPB, brain tissue anatomy was disordered, and cell structure was abnormal. Brain tissue EB content increased. There was an increase in the number of apoptotic cells, an increase in expression of Bax and caspase-3, a decrease in expression of Bcl2, and increases in levels of Akt, GSK3β, P-Akt, and P-GSK3β in brain tissue. HRS treatment attenuated the inflammatory reaction ,brain tissue EB content was significantly reduced and significantly decreased expression levels of Bax, caspase-3, Akt, GSK3β, P-Akt, and P-GSK3β in the brain. After adding the PI3K signaling pathway inhibitor, LY294002, to rat cerebral microvascular endothelial cells (CMECs), HRS could reduce activated Akt expression and downstream regulatory gene phosphorylation of GSK3β expression, and inhibit CMEC apoptosis. Conclusion: The PI3K/Akt/GSK3β signaling pathway plays an important role in the mechanism of CPB-induced brain injury. HRS can reduce CPB-induced brain injury and inhibit CMEC apoptosis through the PI3K/Akt/GSK3β signaling pathway.

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Protective Effect of Minocycline Against Ketamine-Induced Injury in Neural Stem Cell: Involvement of PI3K/Akt and Gsk-3 Beta Pathway

Cited by 31 publications

References 40 publications

Pretreatment with minocycline improves neurogenesis and behavior performance after midazolam exposure in neonatal rats

Pretreatment with minocycline improves neurogenesis and behavior performance after midazolam exposure in neonatal rats

Resveratrol Promotes Nerve Regeneration via Activation of p300 Acetyltransferase-Mediated VEGF Signaling in a Rat Model of Sciatic Nerve Crush Injury

Hydrogen-Rich Saline Attenuates Brain Injury Induced by Cardiopulmonary Bypass and Inhibits Microvascular Endothelial Cell Apoptosis Via the PI3K/Akt/GSK3β Signaling Pathway in Rats

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