Anesthetic effects on autophagy

Yuan, Fan; Zuo, Zhiyi

doi:10.4103/2045-9912.215751

Cited by 7 publications

(3 citation statements)

References 57 publications

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“…In some cases, upregulated autophagy was beneficial, whereas in others the opposite is true. The vast majority of studies demonstrate that anesthetic modulation of autophagy is beneficial for cell survival (Ye & Zuo, 2017 ). For example, (Zhou et al 2016 ) showed that sevoflurane treatment activates autophagy, which antagonizes sevoflurane-induced apoptosis in H4 human neuroglioma cells.…”

Section: Discussionmentioning

confidence: 99%

Propofol inhibited autophagy through Ca2+/CaMKKβ/AMPK/mTOR pathway in OGD/R-induced neuron injury

Sun

Ren

et al. 2018

Mol Med

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BackgroundThe neuroprotective role of propofol (PPF) in cerebral ischemia-reperfusion (I/R) has recently been highlighted. This study aimed to explore whether the neuroprotective mechanisms of PPF were linked to its regulation of Ca2+/CaMKKβ (calmodulin-dependent protein kinase kinase β)/AMPK (AMP-activated protein kinase)/mTOR (mammalian target of rapamycin)/autophagy pathway.MethodsCultured primary rat cerebral cortical neurons were treated with oxygen-glucose deprivation and re-oxygenation (OGD/R) to mimic cerebral I/R injury in vitro.ResultsCompared with the control neurons, OGD/R exposure successfully induced neuronal I/R injury. Furthermore, OGD/R exposure notably caused autophagy induction, reflected by augmented LC3-II/LC3-I ratio and Beclin 1 expression, decreased p62 expression, and increased LC3 puncta formation. Moreover, OGD/R exposure induced elevation of intracellular Ca2+ concentration ([Ca2+]i). However, PPF treatment significantly antagonized OGD/R-triggered cell injury, autophagy induction, and [Ca2+]i elevation. Further investigation revealed that both autophagy induction by rapamycin and [Ca2+]i elevation by the Ca2+ ionophore ionomycin significantly reversed the PPF-mediated amelioration of OGD/R-triggered cell injury. Importantly, ionomycin also significantly abrogated the PPF-mediated suppression of autophagy and CaMKKβ/AMPK/mTOR signaling in OGD/R-exposed neurons. Additionally, activation of CaMKKβ/AMPK/mTOR signaling abrogated the PPF-mediated autophagy suppression.ConclusionOur findings demonstrate that PPF antagonized OGD/R-triggered neuronal injury, which might be mediated, at least in part, via inhibition of autophagy through Ca2+/CaMKKβ/AMPK/mTOR pathway.Electronic supplementary materialThe online version of this article (10.1186/s10020-018-0054-1) contains supplementary material, which is available to authorized users.

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Section: Discussionmentioning

confidence: 99%

Propofol inhibited autophagy through Ca2+/CaMKKβ/AMPK/mTOR pathway in OGD/R-induced neuron injury

Sun

Ren

et al. 2018

Mol Med

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“…Autophagy is a physiological process to remove the faulty/degraded proteins from the cells; 7 however, excessive activation of autophagy during pathological conditions may also produce deleterious effects due to induction of apoptosis and degradation of essential proteins of the cell. [11][12][13] Accordingly, autophagy inhibitors including 3-methyladenine have been reported to produce beneficial effects in different disease states. 47,48 The role of autophagy in the present study was delineated by assessing the alterations in the levels of a specific marker of autophagy, LC3II.…”

Section: Discussionmentioning

confidence: 99%

“…Although there have been studies showing the beneficial effects of autophagy in neurodegenerative diseases, 9,10 yet excessive activation of autophagy has been documented to produce deleterious effects due to induction of apoptosis and degradation of essential proteins of the cell. [11][12][13] A distinct role of autophagy has been identified to be a maladaptive response to hemodynamic stress on myocytes which accentuates pathological remodeling. 14 Excessive activation of autophagy is shown to induce neuronal death in ischemia-reperfusion induced injury in the PC12 cells and hippocampus region of rats.…”

Section: Introductionmentioning

confidence: 99%

Ameliorative Effects of 3-methyladenine and Chloroquine in 3-nitropropionic-induced Huntington’s Disease like Symptoms in Mice

Virdi¹,

Kulshrestha²,

Jaggi³

2021

IJPER

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Aim:To study the effect of 3-methyladenine and chloroquine phosphate on 3-nitropropionic acid induced Huntington's disease-like symptoms in mice. Materials and Methods: 3-Nitropropionic acid was administered at the dose of 50 mg/kg, i.p. twice daily for 5 days for inducing Huntington's disease like symptoms. 3-Methyladenine (15 and 30 mg/kg, i.p.) and chloroquine phosphate (25 and 50 mg/kg, i.p.) were administered 30 min before each 3-nitropropionic acid administration. The motor tests including, rota-rod, beam walking, lateral push test and open-field test, along with memory/cognitive test using object recognition test were performed on day 0, 3 and 6. The role of autophagy was assessed by measuring the levels of LC3II in the brain. Histopathological studies using H&E, nissl staining; and immunohistochemistry of neuron specific enolase and caspase-3 were also performed. Results: Administration of 3-nitropropionic acid caused a decline in the motor functions and cognitive abilities of the animals. The histopathological studies also indicated neuronal injury and neuronal loss in the striatal region. Treatment with 3-methyladenine and chloroquine ameliorated motor and cognitive parameters induced by 3-nitropropionic acid along with prevention of neuronal loss. Moreover, these pharmacological agents ameliorated altered levels of LC3II with 3-methyladenine and chloroquine administration indicated involvement of autophagy. Conclusion: Treatment with 3-methyladenine and chloroquine may improve the symptoms related with Huntington's disease by preventing 3-nitropropionic acid-induced neurodegeneration possibly by inhibiting autophagy.

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MicroRNA-20b-5p regulates propofol-preconditioning-induced inhibition of autophagy in hypoxia-and-reoxygenation-stimulated endothelial cells

et al. 2020

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Anesthetic effects on autophagy

Cited by 7 publications

References 57 publications

Propofol inhibited autophagy through Ca2+/CaMKKβ/AMPK/mTOR pathway in OGD/R-induced neuron injury

Propofol inhibited autophagy through Ca2+/CaMKKβ/AMPK/mTOR pathway in OGD/R-induced neuron injury

Ameliorative Effects of 3-methyladenine and Chloroquine in 3-nitropropionic-induced Huntington’s Disease like Symptoms in Mice

MicroRNA-20b-5p regulates propofol-preconditioning-induced inhibition of autophagy in hypoxia-and-reoxygenation-stimulated endothelial cells

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