mTOR‐mediated autophagy in the hippocampus is involved in perioperative neurocognitive disorders in diabetic rats

Chen, Xiaohui; Gao, Fei; Lin, Cuicui; Chen, Andi; Deng, Jianhui; Chen, Pinzhong; Lin, Mingxue; Xie, Bingxin; Liao, Yanling; Gong, Cansheng; Zheng, Xiaochun

doi:10.1111/cns.13762

Cited by 23 publications

(15 citation statements)

References 59 publications

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“…In fact, in CNS disorders an altered autophagy is seminal to promote chronic degenerative conditions (Ravikumar and Rubinsztein, 2004;Rubinsztein et al, 2005;Fornai et al, 2008a;2008b;Castino et al, 2008;Ferrucci et al, 2008;Isidoro et al, 2009;Madeo et al, 2009), while sustaining maturation phenomena following acute brain injury as it happens during brain ischemia and epilepsyinduced brain damage (Wang et al, 2022a;2022b;Zhang et al, 2021;Biagioni et al, 2021;Xiao et al, 2021). This is also the case of those area, which surround a trauma within the CNS, which integrity is recovered also depending on the autophagy status (Aruri et al, 2022;Chen et al, 2022). In fact, the nervous tissue, which surrounds an acute brain injury represents a sort of penumbra, where cells are borderline to recover or degenerate.…”

Section: Introductionmentioning

confidence: 99%

Combined pulses of light and sound in the retina with nutraceuticals may enhance the recovery of foveal holes

Pinelli¹,

Berti²,

Scaffidi³

et al. 2022

Archives Italiennes De Biologie

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The present manuscript stems from evidence, which indicates that specific wavelength produce an activation of the autophagy pathway in the retina. These effects were recently reported to synergize with the autophagy-inducing properties of specific phytochemicals. The combined administration of photo-modulation and phytochemicals was recently shown to have a strong potential in eliciting the recovery in the course of retinal degeneration and it was suggested as a non-invasive approach named "Lugano protocol" to treat age-related macular degeneration (AMD). Recent translational findings indicate that the protective role of autophagy may extend also to acute neuronal injuries including traumatic neuronal damage. At the same time, very recent investigations indicate that autophagy activation and retinal anatomical recovery may benefit from sound exposure. Therefore, in the present study, the anatomical rescue of a traumatic neuronal loss at macular level was investigated in a patient with idiopathic macular hole by using a combined approach of physical and chemical non-invasive treatments. In detail, light exposure was administered in combination with sound pulses to the affected retina. This treatment was supplemented by phytochemicals known to act as autophagy inducers, which were administered orally for 6 months. This combined administration of light and sound with nutraceuticals reported here as Advanced Lugano's Protocol (ALP) produced a remarkable effect in the anatomical architecture of the retina affected by the macular hole. The anatomical recovery was almost complete at roughly one year after diagnosis and beginning of treatment. The structural healing of the macular hole was concomitant with a strong improvement of visual acuity and the disappearance of metamorphopsia. The present findings are discussed in the light of a synergism shown at neuronal level between light and sound in the presence of phytochemicals to stimulate autophagy and promote proliferation and neuronal differentiation of retinal stem cells.

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Section: Introductionmentioning

confidence: 99%

Combined pulses of light and sound in the retina with nutraceuticals may enhance the recovery of foveal holes

Pinelli¹,

Berti²,

Scaffidi³

et al. 2022

Archives Italiennes De Biologie

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“…Autophagy is regulated by autophagy-related proteins, with LC3 II/I as one of the important proteins that mediate the process. Beclin-1 is not only an important autophagy-related protein, it also mediates apoptosis by interacting with Bcl-2 lentinus edodes [12].…”

Section: Discussionmentioning

confidence: 99%

Sevoflurane induces ho-1-mrna expression by regulating P13K/Akt/P70S6K signaling pathway and affects neuronal apoptosis

Li¹,

Yan²,

Xu³

et al. 2022

Trop. J. Pharm Res

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Purpose: To determine the effect of sevoflurane (SE) on neuronal apoptosis, and the mechanism involved.Methods: Sixty healthy male Sprague-Dawley rats were assigned to control, model and SE groups. Sham surgery was performed in control group, while middle cerebral artery infarction (MCAO) was established in model group. The expression of HO-1 mRNA was determined by quantitative real-time polymerase chain reaction (qRT-PCR). Apoptosis, autophagy and protein content of P13K/Akt/P70S6K signaling pathway were assessed by Western blot assay.Results: Apoptosis was significantly lower in SE rats, relative to model rats. There were markedly higher protein levels of LC3 II / I, beclin-1, bad, Bcl-2 and caspase-3 in model and SE groups than in control rats (p < 0.05). The HO-1 mRNA was significantly up-regulated in model and SE groups, relative to controls, but it was significantly up-regulated in SE group, relative to model rats (p < 0.05). The expression levels of phosphorylated proteins of the P13K/Akt /P70S6K signal-related proteins in model and SE groups were significantly up-regulated, relative to control, but elevated in SE mice, when compared to model mice (p < 0.05).Conclusion: SE improves the behavior of MCAO rats, reduces cerebral infarction, and inhibits apoptosis and autophagy of nerve cells by regulating autophagy and apoptosis-related proteins through a mechanism that may be related to the induction of HO-1-mRNA expression by regulating P13K/Akt /P70S6K signal pathway. This provides new insights for the development of anti-neuronal apoptosis drugs.

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“…Western blotting was carried out as described previously (Chen X. et al, 2022). Tissues from the left brain hemisphere were collected on day 2 after HI treatment and homogenized using lysis buffer supplemented with protease and phosphatase inhibitors on ice.…”

Section: Western Blot Analysismentioning

confidence: 99%

Dexmedetomidine alleviates olfactory cognitive dysfunction by promoting neurogenesis in the subventricular zone of hypoxic-ischemic neonatal rats

Chen

Deng

et al. 2022

Front. Pharmacol.

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Background: Hypoxic-ischemic brain damage (HIBD) is the main cause of neurological dysfunction in neonates. Olfactory cognitive function is important for feeding, the ability to detect hazardous situations and social relationships. However, only a few studies have investigated olfactory cognitive dysfunction in neonates with HIBD; furthermore, the specific mechanisms involved are yet to be elucidated. It has been reported that neurogenesis in the subventricular zone (SVZ) is linked to olfactory cognitive function. Recently, dexmedetomidine (DEX) has been shown to provide neuroprotection in neonates following HIBD. In the present study, we investigated whether DEX could improve olfactory cognitive dysfunction in neonatal rats following HIBD and attempted to determine the underlying mechanisms.Methods: We induced HIBD in rats using the Rice–Vannucci model, and DEX (25 μg/kg, i.p.) was administered immediately after the induction of HIBD. Next, we used triphenyl tetrazolium chloride (TTC) staining and the Zea-longa score to assess the success of modelling. The levels of BDNF, TNF-α, IL-1β and IL-6 were determined by western blotting. Immunofluorescence staining was used to detect microglial activation and microglial M1/M2 polarization as well as to evaluate the extent of neurogenesis in the SVZ. To evaluate the olfactory cognitive function, the rats in each group were raised until post-natal days 28–35; then, we performed the buried food test and the olfactory memory test.Results: Analysis showed that HIBD induced significant brain infarction, neurological deficits, and olfactory cognitive dysfunction. Furthermore, we found that DEX treatment significantly improved olfactory cognitive dysfunction in rat pups with HIBD. DEX treatment also increased the number of newly formed neuroblasts (BrdU/DCX) and neurons (BrdU/NeuN) in the SVZ by increasing the expression of BDNF in rat pups with HIBD. Furthermore, analysis showed that the neurogenic effects of DEX were possibly related to the inhibition of inflammation and the promotion of M1 to M2 conversion in the microglia.Conclusion: Based on the present findings, DEX treatment could improve olfactory cognitive dysfunction in neonatal rats with HIBD by promoting neurogenesis in the SVZ and enhancing the expression of BDNF in the microglia. It was possible associated that DEX inhibited neuroinflammation and promoted M1 to M2 conversion in the microglia.

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mTOR‐mediated autophagy in the hippocampus is involved in perioperative neurocognitive disorders in diabetic rats

Abstract: This is an open access article under the terms of the Creative Commons Attribution License, which permits use, distribution and reproduction in any medium, provided the original work is properly cited.

Cited by 23 publications

References 59 publications

Combined pulses of light and sound in the retina with nutraceuticals may enhance the recovery of foveal holes

Combined pulses of light and sound in the retina with nutraceuticals may enhance the recovery of foveal holes

Sevoflurane induces ho-1-mrna expression by regulating P13K/Akt/P70S6K signaling pathway and affects neuronal apoptosis

Dexmedetomidine alleviates olfactory cognitive dysfunction by promoting neurogenesis in the subventricular zone of hypoxic-ischemic neonatal rats

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