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6. Dihydromyricetin ameliorates social isolation-induced anxiety by modulating mitochondrial function, antioxidant enzymes, and BDNF

Author

Al Omran, Alzahra J, Watanabe, Saki, Hong, Ethan C, Skinner, Samantha G, Zhang, Mindy, Zhang, Jifeng, Shao, Xuesi M, and Liang, Jing

Subjects
Cognitive and Computational Psychology, Biomedical and Clinical Sciences, Neurosciences, Psychology, Mental Health, Brain Disorders, Mental Illness, Behavioral and Social Science, Mental health, Stress, Anxiety, Dihydromyricetin, Mitochondria, Antioxidative enzymes, Oxidative stress, Autophagy, BDNF, BDNF-TrkB, Social isolation, Repeated social isolation, Cognitive and computational psychology
Abstract

Stress has been implicated in the etiology of neurological and psychological illnesses. Chronic social isolation (SI) is a psychological stressor that provokes neurobehavioral changes associated with psychiatric disorders, including anxiety disorders. Mitochondria dysfunction and oxidative stress are hallmarks of anxiety pathogenesis. Here we demonstrate the effects of SI-induced stress on mitochondrial function, antioxidative enzymes, autophagy, and brain derivative neurotrophic factor (BDNF). SI induced a reduction in electron transport chain subunits C-I, C-II, and C-VI and an increase in hydrogen peroxide. Treatment with dihydromyricetin (DHM), extracted from Ampelopsis grossedentata, counteracted these changes. A dramatic increase in several primary mitochondrial antioxidative enzymes such as superoxide dismutase 2 (SOD2), heme oxygenase-1 (HO-1), peroxiredoxin-3 (PRDX3), and glutathione peroxidase 4 (GPX4) was observed after SI and a repeated episode of SI. Both SI and repeated SI induced a reduction in sequestosome 1 (SQSTM1/p62). However, only repeated SI modulated autophagy primary protein beclin-1 (Bcl-1). In addition, SI and repeated SI modulated the BDNF-TrkB signaling pathway and the phosphorylation of the downstream extracellular signal-regulated MAP kinase1/2 (p-Erk p42 and p-Erk p44) cascade. DHM treatment ameliorated these changes. Collectively, we demonstrated that DHM treatment counteracted the effects of SI and repeated SI on antioxidative enzymes, autophagy, and the BDNF-TrkB signaling pathway. These findings highlight the molecular mechanisms that partially explain the anxiolytic effects of DHM.

Published
2022

12. Genome-wide association meta-analysis identifies risk loci for abdominal aortic aneurysm and highlights PCSK9 as a therapeutic target

Author

Roychowdhury, Tanmoy, Klarin, Derek, Levin, Michael G., Spin, Joshua M., Rhee, Yae Hyun, Deng, Alicia, Headley, Colwyn A., Tsao, Noah L., Gellatly, Corry, Zuber, Verena, Shen, Fred, Hornsby, Whitney E., Laursen, Ina Holst, Verma, Shefali S., Locke, Adam E., Einarsson, Gudmundur, Thorleifsson, Gudmar, Graham, Sarah E., Dikilitas, Ozan, Pattee, Jack W., Judy, Renae L., Pauls-Verges, Ferran, Nielsen, Jonas B., Wolford, Brooke N., Brumpton, Ben M., Dilmé, Jaume, Peypoch, Olga, Juscafresa, Laura Calsina, Edwards, Todd L., Li, Dadong, Banasik, Karina, Brunak, Søren, Jacobsen, Rikke L., Garcia-Barrio, Minerva T., Zhang, Jifeng, Rasmussen, Lars M., Lee, Regent, Handa, Ashok, Wanhainen, Anders, Mani, Kevin, Lindholt, Jes S., Obel, Lasse M., Strauss, Ewa, Oszkinis, Grzegorz, Nelson, Christopher P., Saxby, Katie L., van Herwaarden, Joost A., van der Laan, Sander W., van Setten, Jessica, Camacho, Mercedes, Davis, Frank M., Wasikowski, Rachael, Tsoi, Lam C., Gudjonsson, Johann E., Eliason, Jonathan L., Coleman, Dawn M., Henke, Peter K., Ganesh, Santhi K., Chen, Y. Eugene, Guan, Weihua, Pankow, James S., Pankratz, Nathan, Pedersen, Ole B., Erikstrup, Christian, Tang, Weihong, Hveem, Kristian, Gudbjartsson, Daniel, Gretarsdottir, Solveig, Thorsteinsdottir, Unnur, Holm, Hilma, Stefansson, Kari, Ferreira, Manuel A., Baras, Aris, Kullo, Iftikhar J., Ritchie, Marylyn D., Christensen, Alex H., Iversen, Kasper K., Eldrup, Nikolaj, Sillesen, Henrik, Ostrowski, Sisse R., Bundgaard, Henning, Ullum, Henrik, Burgess, Stephen, Gill, Dipender, Gallagher, Katherine, Sabater-Lleal, Maria, Surakka, Ida, Jones, Gregory T., Bown, Matthew J., Tsao, Philip S., Willer, Cristen J., and Damrauer, Scott M.

Published
2023
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21. Social isolation induces neuroinflammation and microglia overactivation, while dihydromyricetin prevents and improves them

Author

Al Omran, Alzahra J, Shao, Amy S, Watanabe, Saki, Zhang, Zeyu, Zhang, Jifeng, Xue, Chen, Watanabe, Junji, Davies, Daryl L, Shao, Xuesi M, and Liang, Jing

Subjects
Pharmacology and Pharmaceutical Sciences, Biomedical and Clinical Sciences, Mental Health, Brain Disorders, Behavioral and Social Science, Prevention, Good Health and Well Being, Animals, Anxiety, Flavonols, Inflammation Mediators, Male, Maze Learning, Mice, Mice, Inbred C57BL, Microglia, Social Isolation, Dihydromyricetin, GABAAR, Neuroinflammation, Social isolation, Clinical Sciences, Immunology, Neurosciences, Neurology & Neurosurgery
Abstract

BackgroundAnxiety disorders are the most prevalent mental illnesses in the U.S. and are estimated to consume one-third of the country's mental health treatment cost. Although anxiolytic therapies are available, many patients still exhibit treatment resistance, relapse, or substantial side effects. Further, due to the COVID-19 pandemic and stay-at-home order, social isolation, fear of the pandemic, and unprecedented times, the incidence of anxiety has dramatically increased. Previously, we have demonstrated dihydromyricetin (DHM), the major bioactive flavonoid extracted from Ampelopsis grossedentata, exhibits anxiolytic properties in a mouse model of social isolation-induced anxiety. Because GABAergic transmission modulates the immune system in addition to the inhibitory signal transmission, we investigated the effects of short-term social isolation on the neuroimmune system.MethodsEight-week-old male C57BL/6 mice were housed under absolute social isolation for 4 weeks. The anxiety-like behaviors after DHM treatment were examined using elevated plus-maze and open field behavioral tests. Gephyrin protein expression, microglial profile changes, NF-κB pathway activation, cytokine level, and serum corticosterone were measured.ResultsSocially isolated mice showed increased anxiety levels, reduced exploratory behaviors, and reduced gephyrin levels. Also, a dynamic alteration in hippocampal microglia were detected illustrated as a decline in microglia number and overactivation as determined by significant morphological changes including decreases in lacunarity, perimeter, and cell size and increase in cell density. Moreover, social isolation induced an increase in serum corticosterone level and activation in NF-κB pathway. Notably, DHM treatment counteracted these changes.ConclusionThe results suggest that social isolation contributes to neuroinflammation, while DHM has the ability to improve neuroinflammation induced by anxiety.

Published
2022

22. Dihydromyricetin improves social isolation-induced cognitive impairments and astrocytic changes in mice

Author

Watanabe, Saki, Omran, Alzahra Al, Shao, Amy S, Xue, Chen, Zhang, Zeyu, Zhang, Jifeng, Davies, Daryl L, Shao, Xuesi M, Watanabe, Junji, and Liang, Jing

Subjects
Biological Psychology, Psychology, Brain Disorders, Basic Behavioral and Social Science, Acquired Cognitive Impairment, Behavioral and Social Science, Neurosciences, Mental Health, Neurological, Mental health, Animals, Astrocytes, Cognitive Dysfunction, Flavonols, Hippocampus, Mice, Social Isolation
Abstract

Social isolation induces stress, anxiety, and mild cognitive impairment that could progress towards irreversible brain damage. A probable player in the mechanism of social isolation-induced anxiety is astrocytes, specialized glial cells that support proper brain function. Using a social isolation mouse model, we observed worsened cognitive and memory abilities with reductions of Object Recognition Index (ORI) in novel object recognition test and Recognition Index (RI) in novel context recognition test. Social isolation also increased astrocyte density, reduced astrocyte size with shorter branches, and reduced morphological complexity in the hippocampus. Dihydromyricetin, a flavonoid that we previously demonstrated to have anxiolytic properties, improved memory/cognition and restored astrocyte plasticity in these mice. Our study indicates astrocytic involvement in social isolation-induced cognitive impairment as well as anxiety and suggest dihydromyricetin as an early-stage intervention against anxiety, cognitive impairment, and potential permanent brain damage.

Published
2022

23. Sarcoidosis

Author

Li, Ping, Zhang, Jifeng, Li, Hongjun, editor, Liu, Jingzhe, editor, and Li, Li, editor

Published
2023
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32. Serine synthesis via reversed SHMT2 activity drives glycine depletion and acetaminophen hepatotoxicity in MASLD

Author

Ghrayeb, Alia, Finney, Alexandra C., Agranovich, Bella, Peled, Daniel, Anand, Sumit Kumar, McKinney, M. Peyton, Sarji, Mahasen, Yang, Dongshan, Weissman, Natan, Drucker, Shani, Fernandes, Sara Isabel, Fernández-García, Jonatan, Mahan, Kyle, Abassi, Zaid, Tan, Lin, Lorenzi, Philip L., Traylor, James, Zhang, Jifeng, Abramovich, Ifat, Chen, Y. Eugene, Rom, Oren, Mor, Inbal, and Gottlieb, Eyal

Published
2024
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40. Loss-of-function genomic variants highlight potential therapeutic targets for cardiovascular disease.

Author

Nielsen, Jonas B, Rom, Oren, Surakka, Ida, Graham, Sarah E, Zhou, Wei, Roychowdhury, Tanmoy, Fritsche, Lars G, Gagliano Taliun, Sarah A, Sidore, Carlo, Liu, Yuhao, Gabrielsen, Maiken E, Skogholt, Anne Heidi, Wolford, Brooke, Overton, William, Zhao, Ying, Chen, Jin, Zhang, He, Hornsby, Whitney E, Acheampong, Akua, Grooms, Austen, Schaefer, Amanda, Zajac, Gregory JM, Villacorta, Luis, Zhang, Jifeng, Brumpton, Ben, Løset, Mari, Rai, Vivek, Lundegaard, Pia R, Olesen, Morten S, Taylor, Kent D, Palmer, Nicholette D, Chen, Yii-Der, Choi, Seung H, Lubitz, Steven A, Ellinor, Patrick T, Barnes, Kathleen C, Daya, Michelle, Rafaels, Nicholas, Weiss, Scott T, Lasky-Su, Jessica, Tracy, Russell P, Vasan, Ramachandran S, Cupples, L Adrienne, Mathias, Rasika A, Yanek, Lisa R, Becker, Lewis C, Peyser, Patricia A, Bielak, Lawrence F, Smith, Jennifer A, Aslibekyan, Stella, Hidalgo, Bertha A, Arnett, Donna K, Irvin, Marguerite R, Wilson, James G, Musani, Solomon K, Correa, Adolfo, Rich, Stephen S, Guo, Xiuqing, Rotter, Jerome I, Konkle, Barbara A, Johnsen, Jill M, Ashley-Koch, Allison E, Telen, Marilyn J, Sheehan, Vivien A, Blangero, John, Curran, Joanne E, Peralta, Juan M, Montgomery, Courtney, Sheu, Wayne H-H, Chung, Ren-Hua, Schwander, Karen, Nouraie, Seyed M, Gordeuk, Victor R, Zhang, Yingze, Kooperberg, Charles, Reiner, Alexander P, Jackson, Rebecca D, Bleecker, Eugene R, Meyers, Deborah A, Li, Xingnan, Das, Sayantan, Yu, Ketian, LeFaive, Jonathon, Smith, Albert, Blackwell, Tom, Taliun, Daniel, Zollner, Sebastian, Forer, Lukas, Schoenherr, Sebastian, Fuchsberger, Christian, Pandit, Anita, Zawistowski, Matthew, Kheterpal, Sachin, Brummett, Chad M, Natarajan, Pradeep, Schlessinger, David, Lee, Seunggeun, Kang, Hyun Min, Cucca, Francesco, and Holmen, Oddgeir L

Subjects
Liver, Humans, Cardiovascular Diseases, Lipids, Receptors, LDL, Gene Targeting, Gene Silencing, Genome, Human, Biological Specimen Banks, Genome-Wide Association Study, Molecular Targeted Therapy, United Kingdom, Loss of Function Mutation, Phenomics
Abstract

Pharmaceutical drugs targeting dyslipidemia and cardiovascular disease (CVD) may increase the risk of fatty liver disease and other metabolic disorders. To identify potential novel CVD drug targets without these adverse effects, we perform genome-wide analyses of participants in the HUNT Study in Norway (n = 69,479) to search for protein-altering variants with beneficial impact on quantitative blood traits related to cardiovascular disease, but without detrimental impact on liver function. We identify 76 (11 previously unreported) presumed causal protein-altering variants associated with one or more CVD- or liver-related blood traits. Nine of the variants are predicted to result in loss-of-function of the protein. This includes ZNF529:p.K405X, which is associated with decreased low-density-lipoprotein (LDL) cholesterol (P = 1.3 × 10-8) without being associated with liver enzymes or non-fasting blood glucose. Silencing of ZNF529 in human hepatoma cells results in upregulation of LDL receptor and increased LDL uptake in the cells. This suggests that inhibition of ZNF529 or its gene product should be prioritized as a novel candidate drug target for treating dyslipidemia and associated CVD.

Published
2020

45. Predicting Consumers’ Coupon-usage in E-commerce with Capsule Network

Author

Jiang, Wenjun, Tan, Zhenqiong, He, Jiawei, Zhang, Jifeng, Wang, Tian, Chen, Shuhong, Goos, Gerhard, Founding Editor, Hartmanis, Juris, Founding Editor, Bertino, Elisa, Editorial Board Member, Gao, Wen, Editorial Board Member, Steffen, Bernhard, Editorial Board Member, Woeginger, Gerhard, Editorial Board Member, Yung, Moti, Editorial Board Member, Lai, Yongxuan, editor, Wang, Tian, editor, Jiang, Min, editor, Xu, Guangquan, editor, Liang, Wei, editor, and Castiglione, Aniello, editor

Published
2022
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