Green tea polyphenols improve isoflurane-induced cognitive impairment via modulating oxidative stress

Song, Yuting; Li, Xiuxiu; Gong, Xiangdan; Zhao, Xin; Ma, Zhengliang; Xia, Tianjiao; Gu, Xiaoping

doi:10.1016/j.jnutbio.2019.07.004

Cited by 25 publications

(26 citation statements)

References 29 publications

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“…Further, accumulating clinical and experimental evidence suggest that surgery under general anesthesia increases the risk of developing Alzheimer’s disease (AD) and other forms of dementia ( James, 2020 ). Our previous studies confirmed that long-term isoflurane exposure can induce cognitive impairment in adult mice, providing an experimental model to investigate the underlying pathogenesis ( Xia et al, 2016 ; Song et al, 2019 ).…”

Section: Introductionsupporting

confidence: 76%

Amelioration of Hippocampal Insulin Resistance Reduces Tau Hyperphosphorylation and Cognitive Decline Induced by Isoflurane in Mice

Peng

Fang

et al. 2021

Front. Aging Neurosci.

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General anesthetics can induce cognitive impairments and increase the risk of Alzheimer’s disease (AD). However, the underlying mechanisms are still unknown. Our previous studies shown that long-term isoflurane exposure induced peripheral and central insulin resistance (IR) in adult mice and aggravated IR in type 2 diabetes mellitus (T2DM) mice. Clinical and preclinical studies revealed an association between impaired insulin signaling and tau pathology in AD and other tauopathies. We investigated if alleviation of hippocampal IR by the antidiabetic agent metformin could reduce tau hyperphosphorylation and cognitive decline induced by isoflurane in mice. The effects of prolonged (6 h) isoflurane anesthesia on hippocampal IR, hippocampal tau hyperphosphorylation, and hippocampus-dependent cognitive function were evaluated in wild type (WT) adult mice and the high-fat diet plus streptozotocin (HFD/STZ) mouse model of T2DM. Here we shown that isoflurane and HFD/STZ dramatically and synergistically induced hippocampal IR and fear memory impairment. Metformin pretreatment strongly ameliorated hippocampal IR and cognitive dysfunction caused by isoflurane in WT mice, but was less effective in T2DM mice. Isoflurane also induced hippocampal tau hyperphosphorylation and metformin reversed this effect. In addition, isoflurane significantly increased blood glucose levels in both adult and T2DM mice, and metformin reversed this effect as well. Administration of 25% glucose to metformin-pretreated mice induced hyperglycemia, but surprisingly did not reverse the benefits of metformin on hippocampal insulin signaling and fear memory following isoflurane anesthesia. Our findings show hippocampal IR and tau hyperphosphorylation contribute to acute isoflurane-induced cognitive dysfunction. Brief metformin treatment can mitigate these effects through a mechanism independent of glycemic control. Future studies are needed to investigate whether long-term metformin treatment can also prevent T2DM-induced hippocampal IR and cognitive decline.

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Section: Introductionsupporting

confidence: 76%

Amelioration of Hippocampal Insulin Resistance Reduces Tau Hyperphosphorylation and Cognitive Decline Induced by Isoflurane in Mice

Peng

Fang

et al. 2021

Front. Aging Neurosci.

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“…The fear-conditioning paradigm was also assessed [ 49 , 50 ]. Briefly, mice were trained to associate cage context or an audiovisual cue with an aversive stimulus (foot-shock).…”

Section: Methodsmentioning

confidence: 99%

Pyruvate kinase isoform M2 impairs cognition in systemic lupus erythematosus by promoting microglial synaptic pruning via the β-catenin signaling pathway

Lü

Wang

et al. 2021

J Neuroinflammation

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Background Neuropsychiatric systemic lupus erythematosus (NPSLE) is a severe complication, which involves pathological damage to the brain and cognitive function. However, its exact mechanism of action still remains unclear. In this study, we explored the role of microglia in the cognitive dysfunction of NPSLE mice. We also analyzed and compared the metabolites in the hippocampal tissues of the lupus model and control mice. Methods MRL/MpJ-Faslpr (MRL/lpr) female mice were used as the NPSLE mouse model. Metabolomics was used to assess hippocampal glycolysis levels. Glucose, lactic acid, IL-6, and IL-1β of the hippocampus were detected by ELISA. Based on the glycolysis pathway, we found that pyruvate kinase isoform M2 (PKM2) in the hippocampus was significantly increased. Thus, the expression of PKM2 was detected by qRT-PCR and Western blotting, and the localization of PKM2 in microglia (IBA-1+) or neurons (NeuN+) was assessed by immunofluorescence staining. Flow cytometry was used to detect the number and phenotype of microglia; the changes in microglial phagocytosis and the β-catenin signaling pathway were detected in BV2 cells overexpressing PKM2. For in vivo experiments, MRL/lpr mice were treated with AAV9-shPKM2. After 2 months, Morris water maze and conditional fear tests were applied to investigate the cognitive ability of mice; H&E and immunofluorescence staining were used to evaluate brain damage; flow cytometry was used to detect the phenotype and function of microglia; neuronal synapse damage was monitored by qRT-PCR, Western blotting, and immunofluorescence staining. Results Glycolysis was elevated in the hippocampus of MRL/lpr lupus mice, accompanied by increased glucose consumption and lactate production. Furthermore, the activation of PKM2 in hippocampal microglia was observed in lupus mice. Cell experiments showed that PKM2 facilitated microglial activation and over-activated microglial phagocytosis via the β-catenin signaling pathway. In vivo, AAV9-shPKM2-treated mice showed decreased microglial activation and reduced neuronal synapses loss by blocking the β-catenin signaling pathway. Furthermore, the cognitive impairment and brain damage of MRL/lpr mice were significantly relieved after microglial PKM2 inhibition. Conclusion These data indicate that microglial PKM2 have potential to become a novel therapeutic target for treating lupus encephalopathy.

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“…The medium dose of GJE treatment showed the most effective inhibition of neuronal necrosis in different brain regions of the rat model of chronic cerebral ischemia ( Figure 7 ) ( Zhang et al, 2016 ). Green tea polyphenols have been demonstrated to play a neuroprotective role due to their antioxidant and anti-inflammatory properties ( Sutherland et al, 2006 ; Song et al, 2019 ). Zhang et al (2010) showed that a 30-days treatment with green tea polyphenols (200 mg/kg, twice a day) prominently restored blood-brain barrier permeability, rescued cerebral infarction and improved neurological functions in rats underwent cerebral ischemia.…”

Section: Bioactivity Of Polyphenolsmentioning

confidence: 99%

Insight in the Recent Application of Polyphenols From Biomass

Yan

Chen

et al. 2021

Front. Bioeng. Biotechnol.

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Biomass polyphenols are bio-active macromolecules with distinct chemical structures in a variety of biomass. In recent years, the study of biomass polyphenols and their application in food and medicine fields has become a research hotspot, which predominantly focuses on the preparation, purification, structural identifications, and measurements of biological activities. Many studies describe methodologies for extraction and application of polyphenols, but comprehensive work to review its physiological activities like drugs and health products are lacking. This paper comprehensively unlocks the bioactivities of antioxidant, antibacterial, antitumor, anticancer, neuroprotection, control of blood sugar, regulation of blood fat, and promotion of gastrointestinal health functions of polyphenols from different biomass sources. This review will serve as an illuminating resource for the global scientific community, especially for those who are actively working to promote the advances of the polyphenols research field.

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Green tea polyphenols improve isoflurane-induced cognitive impairment via modulating oxidative stress

Cited by 25 publications

References 29 publications

Amelioration of Hippocampal Insulin Resistance Reduces Tau Hyperphosphorylation and Cognitive Decline Induced by Isoflurane in Mice

Amelioration of Hippocampal Insulin Resistance Reduces Tau Hyperphosphorylation and Cognitive Decline Induced by Isoflurane in Mice

Pyruvate kinase isoform M2 impairs cognition in systemic lupus erythematosus by promoting microglial synaptic pruning via the β-catenin signaling pathway

Insight in the Recent Application of Polyphenols From Biomass

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