Sesamol supplementation prevents systemic inflammation‐induced memory impairment and amyloidogenesis via inhibition of nuclear factor kappaB

Liu, Zhigang; Chen, Yuwei; Qiao, Qinglian; Sun, Yali; Liu, Qian; Ren, Bo; Liu, Xuebo

doi:10.1002/mnfr.201600734

Cited by 45 publications

(67 citation statements)

References 43 publications

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“…Our lab has shown sesamol possessed cytotoxicity in hepatocellular carcinoma cells in a previous publication18. There have been numerous of reports in the literature that sesamol possesses curative role in various diseases due to its diverse bioactivities in vivo such as anti-inflammatory, lipid-lowering, neuroprotective, and chemopreventive19353637. Previous study have demonstrated that oral administration of sesamol was absorbed and metabolized in the liver, which are then excreted in the bile or urine.…”

Section: Discussionmentioning

confidence: 89%

Sesamol Induces Human Hepatocellular Carcinoma Cells Apoptosis by Impairing Mitochondrial Function and Suppressing Autophagy

Liu

Ren

Wang

et al. 2017

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Sesamol, a nutritional phenolic antioxidant compound enriched in sesame seeds, has been shown to have potential anticancer activities. This study aims at characterizing the antitumor efficacy of sesamol and unveiling the importance of mitochondria in sesamol-induced effects using a human hepatocellular carcinoma cell line, HepG2 cells. Results of this study showed that sesamol treatment suppressed colony formation, elicited S phase arrest during cell cycle progression, and induced both intrinsic and extrinsic apoptotic pathway in vitro with a dose-dependent manner. Furthermore, sesamol treatment elicited mitochondrial dysfunction by inducing a loss of mitochondrial membrane potential. Impaired mitochondria and accumulated H2O2 production resulted in disturbance of redox-sensitive signaling including Akt and MAPKs pathways. Mitochondrial biogenesis was inhibited as suggested by the decline in expression of mitochondrial complex I subunit ND1, and the upstream AMPK/PGC1α signals. Importantly, sesamol inhibited mitophagy and autophagy through impeding the PI3K Class III/Belin-1 pathway. Autophagy stimulator rapamycin reversed sesamol-induced apoptosis and mitochondrial respiration disorders. Moreover, it was also shown that sesamol has potent anti-hepatoma activity in a xenograft nude mice model. These data suggest that mitochondria play an essential role in sesamol-induced HepG2 cells death, and further research targeting mitochondria will provide more chemotherapeutic opportunities.

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Section: Discussionmentioning

confidence: 89%

Sesamol Induces Human Hepatocellular Carcinoma Cells Apoptosis by Impairing Mitochondrial Function and Suppressing Autophagy

Liu

Ren

Wang

et al. 2017

Sci Rep

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“…Western blotting was performed as previous study described 47 . Extractions solubilized in SDS sample buffer, were separated by Laemmli SDS/PAGE, and transferred onto PVDF membranes.…”

Section: Methodsmentioning

confidence: 99%

Effects of Lipoic Acid on High-Fat Diet-Induced Alteration of Synaptic Plasticity and Brain Glucose Metabolism: A PET/CT and 13C-NMR Study

Liu

Patil

Sancheti

et al. 2017

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High-fat diet (HFD)-induced obesity is accompanied by insulin resistance and compromised brain synaptic plasticity through the impairment of insulin-sensitive pathways regulating neuronal survival, learning, and memory. Lipoic acid is known to modulate the redox status of the cell and has insulin mimetic effects. This study was aimed at determining the effects of dietary administration of lipoic acid on a HFD-induced obesity model in terms of (a) insulin signaling, (b) brain glucose uptake and neuronal- and astrocytic metabolism, and (c) synaptic plasticity. 3-Month old C57BL/6J mice were divided into 4 groups exposed to their respective treatments for 9 weeks: (1) normal diet, (2) normal diet plus lipoic acid, (3) HFD, and (4) HFD plus lipoic acid. HFD resulted in higher body weight, development of insulin resistance, lower brain glucose uptake and glucose transporters, alterations in glycolytic and acetate metabolism in neurons and astrocytes, and ultimately synaptic plasticity loss evident by a decreased long-term potentiation (LTP). Lipoic acid treatment in mice on HFD prevented several HFD-induced metabolic changes and preserved synaptic plasticity. The metabolic and physiological changes in HFD-fed mice, including insulin resistance, brain glucose uptake and metabolism, and synaptic function, could be preserved by the insulin-like effect of lipoic acid.

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“…The Morris water maze test was performed as previously described, with minor modifications (5,32). The Morris water maze is a white circular pool (diameter, 150 cm; height, 35 cm) with a featureless inner surface (XR-XM101; Shanghai Xinruan Information Technology, Shanghai, China).…”

Section: Morris Water Maze Testmentioning

confidence: 99%

“…Total RNA was extracted from brain tissue by using an RNA extraction kit (MiniBEST Universal RNA Extraction Kit; TaKaRa, Dalian, China) as previously described (32). For quality control, RNA purity and integrity were evaluated by using the Quawell 5000 UV-Vis Spectrophotometer (Quawell Technology, San Jose, CA, USA).…”

Section: Rna Preparation and Quality Controlmentioning

confidence: 99%

EGCG ameliorates high‐fat– and high‐fructose‐induced cognitive defects by regulating the IRS/AKT and ERK/CREB/BDNF signaling pathways in the CNS

Fan

et al. 2017

FASEB j.

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113

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Obesity, which is caused by an energy imbalance between calorie intake and consumption, has become a major international health burden. Obesity increases the risk of insulin resistance and age-related cognitive decline, accompanied by peripheral inflammation. (-)-Epigallocatechin-3-gallate (EGCG), the major polyphenol in green tea, possesses antioxidant, anti-inflammatory, and cardioprotective activities; however, few reports have focused on its potential effect on cognitive disorders. In this study, our goal was to investigate the protective effects of EGCG treatment on insulin resistance and memory impairment induced by a high-fat and high-fructose diet (HFFD). We randomly assigned 3-mo-old C57BL/6J mice to 3 groups with different diets: control group, HFFD group, and HFFD plus EGCG group. Memory loss was assessed by using the Morris water maze test, during which EGCG was observed to prevent HFFD-elicited memory impairment and neuronal loss. Consistent with these results, EGCG attenuated HFFD-induced neuronal damage. Of note, EGCG significantly ameliorated insulin resistance and cognitive disorder by up-regulating the insulin receptor substrate-1 (IRS-1)/AKT and ERK/cAMP response element binding protein (CREB)/brain-derived neurotrophic factor (BDNF) signaling pathways. Long-term HFFD-triggered neuroinflammation was restored by EGCG supplementation by inhibiting the MAPK and NF-κB pathways, as well as the expression of inflammatory mediators, such as TNF-α. EGCG also reversed high glucose and glucosamine-induced insulin resistance in SH-SY5Y neuronal cells by improving the oxidized cellular status and mitochondrial function. To our knowledge, this study is the first to provide compelling evidence that the nutritional compound EGCG has the potential to ameliorate HFFD-triggered learning and memory loss.-Mi, Y., Qi, G., Fan, R., Qiao, Q., Sun, Y., Gao, Y., Liu, X. EGCG ameliorates high-fat- and high-fructose-induced cognitive defects by regulating the IRS/AKT and ERK/CREB/BDNF signaling pathways in the CNS.

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Sesamol supplementation prevents systemic inflammation‐induced memory impairment and amyloidogenesis via inhibition of nuclear factor kappaB

Abstract: These results indicated that sesamol mitigated LPS-induced amyloidogenesis and memory impairment via inhibiting NFκB signal pathway, suggesting that the compound might be plausible therapeutic intervention for neuroinflammation-related diseases such as AD.

Cited by 45 publications

References 43 publications

Sesamol Induces Human Hepatocellular Carcinoma Cells Apoptosis by Impairing Mitochondrial Function and Suppressing Autophagy

Sesamol Induces Human Hepatocellular Carcinoma Cells Apoptosis by Impairing Mitochondrial Function and Suppressing Autophagy

Effects of Lipoic Acid on High-Fat Diet-Induced Alteration of Synaptic Plasticity and Brain Glucose Metabolism: A PET/CT and 13C-NMR Study

EGCG ameliorates high‐fat– and high‐fructose‐induced cognitive defects by regulating the IRS/AKT and ERK/CREB/BDNF signaling pathways in the CNS

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