Adiponectin Protects against Glutamate‐Induced Excitotoxicity via Activating SIRT1‐Dependent PGC‐1α Expression in HT22 Hippocampal Neurons

Liang, Yue; Zhao, Lei; Liu, Haixiao; Li, Xia; Wang, Bodong; Guo, Hao; Li, Gao; Feng, Dayun; Qu, Yan

doi:10.1155/2016/2957354

Cited by 42 publications

(25 citation statements)

References 49 publications

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“…The present study indicated that aPn increased the expression of lc3ii and Beclin-1 in the brain tissue simultaneously with inhibition of caspase-3 activation. To the best of the authors' knowledge, the present study is the first to demonstrate that aPn protected the neuron from Gcir injury-induced excessive apoptosis following ca-cPr by promoting autophagy, although Yue et al (41) reported that aPn increases the expression of lc3ii and Beclin-1 in the skeletal muscle of diabetic mice to reduce apoptotic cells in a diabetic mouse model. The mechanisms of how aPn regulates the crosstalk between apoptosis and autophagy in brain tissues injured by Gcir following ca-cPr remain to be elucidated.…”

Section: Discussionmentioning

confidence: 49%

Adiponectin inhibits cardiac arrest/cardiopulmonary resuscitation‑induced apoptosis in brain by increasing autophagy involved in AdipoR1‑AMPK signaling

et al. 2020

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emerging evidence suggests that both apoptosis and autophagy contribute to global cerebral ischemia-reperfusion (Gcir)-induced neuronal death, which results from cardiac arrest (ca). However, the mechanism of how Gcir may affect the balance between apoptosis and autophagy resulting from ca remains to be elucidated. additionally, the role of adiponectin (aPn) in reversing the apoptosis and autophagy induced by Gcir following cardiac arrest-cardiopulmonary resuscitation (ca-cPr) is unclear. Thus, the aim of the present study was to investigate how Gcir affect the apoptosis and autophagy in response to ca and to clarify whether aPn may alter the apoptosis and autophagy of neuronal death in Gcir-injured brain post-ca-cPr. using normal controls (Sham group) and two experimental groups [ca-cPr-induced Gcir injury (PcaS) group and exogenous treatment with adiponectin post-ca-cPr (aPn group)], it was demonstrated that both apoptosis and autophagy were observed simultaneously in the brain subjected to Gcir, but apoptosis appeared to be more apparent. exogenous administration of aPn significantly reduced the formation of malondialdehyde, a marker of oxidative stress and increased the expression of superoxide dismutase, an anti-oxidative enzyme, resulting in the stimulation of autophagy, inhibition of apoptosis and reduced brain tissue injury (P<0.05 vs. PcaS). aPn treatment increased the expression of aPn receptor 1 (adipr1) and the phosphorylation of aMP-activated protein kinase (aMPK; Ser182) in brain tissues. in conclusion, Gcir induced apoptosis and inhibited autophagy, contributing to brain injury in ca-cPr. By contrast, aPn reduced the brain injury by reversing the changes of neuronal autophagy and apoptosis induced by Gcir. The possible mechanism might owe to its effects on the activation of aMPK after combining with adipr1 on neurons, which suggests a novel intervention against Gcir injury in ca-cPr conditions.

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Section: Discussionmentioning

confidence: 49%

Adiponectin inhibits cardiac arrest/cardiopulmonary resuscitation‑induced apoptosis in brain by increasing autophagy involved in AdipoR1‑AMPK signaling

et al. 2020

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“…Similarly, adiponectin has been shown to have a neuroprotective effect by inhibiting NMDA-mediated excitotoxicity [ 128 ]. In addition, adiponectin and memantine play a protective role in glutamate-induced excitotoxicity (shown in both animal/in-vitro models) [ 129 , 130 ]. Furthermore, memantine also has the ability to attenuate insulin resistance and improve brain function in high-fat diet-induced models.…”

Section: Adiponectin-associated Therapeutic Strategy Against Ad Inmentioning

confidence: 99%

Adiponectin: The Potential Regulator and Therapeutic Target of Obesity and Alzheimer’s Disease

Kim

Barua

Jeong

et al. 2020

IJMS

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Animal and human mechanistic studies have consistently shown an association between obesity and Alzheimer’s disease (AD). AD, a degenerative brain disease, is the most common cause of dementia and is characterized by the presence of extracellular amyloid beta (Aβ) plaques and intracellular neurofibrillary tangles disposition. Some studies have recently demonstrated that Aβ and tau cannot fully explain the pathophysiological development of AD and that metabolic disease factors, such as insulin, adiponectin, and antioxidants, are important for the sporadic onset of nongenetic AD. Obesity prevention and treatment can be an efficacious and safe approach to AD prevention. Adiponectin is a benign adipokine that sensitizes the insulin receptor signaling pathway and suppresses inflammation. It has been shown to be inversely correlated with adipose tissue dysfunction and may enhance the risk of AD because a range of neuroprotection adiponectin mechanisms is related to AD pathology alleviation. In this study, we summarize the recent progress that addresses the beneficial effects and potential mechanisms of adiponectin in AD. Furthermore, we review recent studies on the diverse medications of adiponectin that could possibly be related to AD treatment, with a focus on their association with adiponectin. A better understanding of the neuroprotection roles of adiponectin will help clarify the precise underlying mechanism of AD development and progression.

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“…Both SIRT1 and PGC‐1α are involved in the mitochondrial biogenesis and inflammatory processes. It has been reported that reduction of SIRT1 activity results in inhibition of PGC‐1α . In human GCs, the exact roles of resveratrol in terms of its cytoprotective effects and ability to improve mitochondrial quantity in a hypoxic condition remain unclear.…”

Section: Introductionmentioning

confidence: 99%

Resveratrol protects mitochondrial quantity by activating SIRT1/PGC‐1α expression during ovarian hypoxia

Nishigaki

Kido

Kida

et al. 2020

Reprod Medicine & Biology

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Purpose Resveratrol is a well‐known potent activator of sirtuin‐1 (SIRT1). We investigated the direct effects of hypoxia and resveratrol on SIRT1/ peroxisome proliferator‐activated receptor‐gamma coactivator 1α (PGC‐1α) pathways, vascular endothelial growth factor (VEGF), hypoxia‐inducible factor (HIF)‐1α, and mitochondrial quantity in a steroidogenic human ovarian granulosa‐like tumor cell line (KGN) cells. Methods KGN cells were cultured with cobalt chloride (CoCl2; a hypoxia‐mimicking agent) and/or resveratrol. The mRNA and protein levels, protein secretion, and intracellular localization were assessed by real‐time PCR, Western blot analysis, ELISA, and immunofluorescence staining, respectively. Mitochondrial quantity was measured based on the mitochondrial DNA (mtDNA) copy number. Results CoCl2 simultaneously attenuated the levels of SIRT1 and mtDNA expression, and induced the levels of VEGF protein production. In contrast, resveratrol significantly increased the levels of SIRT1 and mtDNA copy number, but reduced VEGF production in normoxia. Resveratrol could recover CoCl2‐suppressed SIRT1 and mtDNA expression and antagonize CoCl2‐induced VEGF production. CoCl2 treatment resulted in a downregulation of PGC‐1α expression, and this effect was recovered by resveratrol. Resveratrol significantly suppressed the production of the CoCl2‐induced HIF‐1α and VEGF proteins. Conclusion These results suggest that resveratrol improves mitochondrial quantity by activating the SIRT1/PGC‐1α pathway and inhibits VEGF induction through HIF‐1α under hypoxic conditions.

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Adiponectin Protects against Glutamate‐Induced Excitotoxicity via Activating SIRT1‐Dependent PGC‐1α Expression in HT22 Hippocampal Neurons

Cited by 42 publications

References 49 publications

Adiponectin inhibits cardiac arrest/cardiopulmonary resuscitation‑induced apoptosis in brain by increasing autophagy involved in AdipoR1‑AMPK signaling

Adiponectin inhibits cardiac arrest/cardiopulmonary resuscitation‑induced apoptosis in brain by increasing autophagy involved in AdipoR1‑AMPK signaling

Adiponectin: The Potential Regulator and Therapeutic Target of Obesity and Alzheimer’s Disease

Resveratrol protects mitochondrial quantity by activating SIRT1/PGC‐1α expression during ovarian hypoxia

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