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urolithin a alleviates blood-brain barrier disruption and attenuates neuronal apoptosis following traumatic brain injury in mice

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Neural Regeneration Research 2022年第9期17卷 2007-2013页

作者： Qiu-Yuan Gong Lin Cai Yao Jing Wei Wang Dian-Xu Yang Shi-Wen Chen Heng-Li Tian Department of Neurosurgery Shanghai Jiao Tong University Affiliated Sixth People’s HospitalShanghaiChina

urolithin a(UA)is a natural metabolite produced from polyphenolics in foods such as pomegranates,berries,and nuts.UA is neuroprotective against Parkinson’s disease,Alzheimer’s disease,and cerebral hemorrhage.However,its effect against traumatic brain injury remains unknown.In this study,we established adult C57BL/6J mouse models of traumatic brain injury by controlled cortical impact and then intraperitoneally administered UA.We found that UA greatly reduced brain edema;increased the expression of tight junction proteins in injured cortex;increased the immunopositivity of two neuronal autophagy markers,microtubule-associated protein 1A/B light chain 3A/B(LC3)and p62;downregulated protein kinase B(Akt)and mammalian target of rapamycin(mTOR),two regulators of the phosphatidylinositol 3-kinase(PI3K)/Akt/mTOR signaling pathway;decreased the phosphorylation levels of inhibitor of NFκB(IκB)kinase alpha(IKKα)and nuclear factor kappa B(NFκB),two regulators of the neuroinflammation-related Akt/IKK/NFκB signaling pathway;reduced blood-brain barrier permeability and neuronal apoptosis in injured cortex;and improved mouse neurological function.These findings suggest that UA may be a candidate drug for the treatment of traumatic brain injury,and its neuroprotective effects may be mediated by inhibition of the PI3K/Akt/mTOR and Akt/IKK/NFκB signaling pathways,thus reducing neuroinflammation and enhancing autophagy.

关键词： autophagy blood-brain barrier cerebral edema controlled cortical impact model neuronal apoptosis neuropharmacology neuroprotection tight junction protein traumatic brain injury urolithin a

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urolithin a alleviates oxidative stress-induced senescence in nucleus pulposus-derived mesenchymal stem cells through SIRT1/PGC-1α pathway

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World Journal of Stem Cells 2021年第12期13卷 1928-1946页

作者： Peng-Zhi Shi Jun-Wu Wang Ping-Chuan Wang Bo Han Xu-Hua Lu Yong-Xin Ren Xin-Min Feng Xiao-Fei Cheng Liang Zhang Department of Orthopedic Dalian Medical UniversityDalian 116000Liaoning ProvinceChina Department of Orthopedics Clinical Medical College of Yangzhou UniversityYangzhou 225000Jiangsu ProvinceChina Department of Orthopedic Beijing Chaoyang HospitalCapital Medical UniversityBeijing 100020China Department of Orthopedics Changzheng Hospital of The Second Military Medical UniversityShanghai 200003China Department of Orthopedics First Affiliated Hospital of Nanjing Medical UniversityNanjing 210029Jiangsu ProvinceChina Department of Orthopedic Surgery Shanghai Key Laboratory of Orthopedics ImplantsShanghai Ninth People’s HospitalShanghai JiaoTong University School of MedicineShanghai 200011China

BACKGROUND In degenerative intervertebral disc(IVD),an unfavorable IVD environment leads to increased senescence of nucleus pulposus(NP)-derived mesenchymal stem cells(NPMSCs)and the inability to complete the differentiation from NPMSCs to NP cells,leading to further aggravation of IVD degeneration(IDD).urolithin a(UA)has been proven to have obvious effects in delaying cell senescence and resisting oxidative stress.AIM To explore whether UA can alleviate NPMSCs senescence and to elucidate the underlying mechanism.METHODS In vitro,we harvested NPMSCs from rat tails,and divided NPMSCs into four groups:the control group,H2O2 group,H2O2+UA group,and H2O2+UA+SR-18292 group.Senescence-associatedβ-Galactosidase(SA-β-Gal)activity,cell cycle,cell proliferation ability,and the expression of senescence-related and silent information regulator of transcription 1/PPAR gamma coactivator-1α(SIRT1/PGC-1α)pathway-related proteins and mRNA were used to evaluate the protective effects of UA.In vivo,an animal model of IDD was constructed,and Xrays,magnetic resonance imaging,and histological analysis were used to assess whether UA could alleviate IDD in vivo.RESULTS We found that H2O2 can cause NPMSCs senescence changes,such as cell cycle arrest,reduced cell proliferation ability,increased SA-β-Gal activity,and increased expression of senescence-related proteins and mRNA.After UA pretreatment,the abovementioned senescence indicators were significantly alleviated.To further demonstrate the mechanism of UA,we evaluated the mitochondrial membrane potential and the SIRT1/PGC-1αpathway that regulates mitochondrial function.UA protected mitochondrial function and delayed NPMSCs senescence by activating the SIRT1/PGC-1αpathway.In vivo,we found that UA treatment alleviated an animal model of IDD by assessing the disc height index,Pfirrmann grade and the histological score.CONCLUSION In summary,UA could activate the SIRT1/PGC-1αsignaling pathway to protect mitochondrial function and alleviate cell senescence and IDD in vivo and vitro.

关键词： urolithin a Mitochondrial function Oxidative stress Senescence Nucleus pulposus-derived Mesenchymal stem cells The silent information regulator of transcription 1/PPAR gamma coactivator-1αpathway

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Potential of the ellagic acid-derived gut microbiota metabolite–urolithin a in gastrointestinal protection

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World Journal of Gastroenterology 2020年第23期26卷 3170-3181页

作者： Malgorzata Kujawska Jadwiga Jodynis-Liebert Department of Toxicology Poznan University of Medical SciencesPoznan 60631Poland

urolithin a(UA)is a metabolic compound generated during the biotransformation of ellagitannins by the intestinal bacteria.The physiologically relevant micromolar concentrations of UA,achieved in the plasma and gastrointestinal tract(GI)after consumption of its dietary precursors,have been revealed to offer GI protection.The health benefit has been demonstrated to be principally related to anticancer and anti-inflammatory effects.UA has been shown to possess the capability to regulate multiple tumor and inflammatory signaling pathways and to modulate enzyme activity,including those involved in carcinogen biotransformation and antioxidant defense.The purpose of this review is to gather evidence from both in vitro and in vivo studies showing the potential of UA in GI protection alongside suggested mechanisms by which UA can protect against cancer and inflammatory diseases of the digestive tract.The data presented herein,covering both studies on the pure compound and in vivo generated UA form its natural precursor,support the potential of this metabolite in treatment interventions against GI ailments.

关键词： urolithin a Colonic metabolite Gut microbiota Colorectal cancer Inflammatory bowel diseases Hepatocellular carcinoma Pancreatic ductal adenocarcinoma Barrett's esophagus Ellagitannins

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urolithin a protects dopaminergic neurons in experimental models of Parkinson disease by promoting mitochondrial biogenesis through SIRT1/PGC-1αsignaling pathway

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中国药理学与毒理学杂志 2021年第9期35卷 648-649页

作者： LIU Jia QIU jing-ru WANG Bao-zhu SUN De-qing YU Shu-yan LOU Hai-yan Department of Pharmacology School of Basic Medical SciencesCheeloo College of MedicineShandong UniversityJinan 250012China

OBJECTIVE Mitochondrial dys⁃function contributes to the pathogenesis of neuro⁃degenerative diseases such as Parkinson dis⁃ease(PD).Therapeutic strategies targeting mito⁃chondrial dysfunction hold considerable promise for the treatment of PD.urolithin a(UA)is a gut metabolite produced from ellagic acid-containing foods such as pomegranates,berries,and wal⁃nuts.Recent reports have highlighted the protec⁃tive role of UA in several neurological disorders including Alzheimer disease and ischemic stroke.However,the potential role of UA in PD has not been characterized.In this study,the role of UA in 6-OHDA-induced neurotoxicity in cell cultures and mouse model of PD was investi⁃gated.METHODS In vitro,PC12 cells were exposed to 6-OHDA in the presence or absence of UA.For in vivo study,C57BL/6 mice were ste⁃reotactic injected with 6-OHDA to induce experi⁃mental PD model.UA(10 mg·kg-1)was intraperi⁃toneal injected for 7 d before surgery.RESULTS UA protected against 6-OHDA cytotoxicity and apoptosis in PC12 cells.Prior administration of UA to 6-OHDA lesioned mice ameliorated both motor deficits and nigral-straital dopaminergic neurotoxicity.Moreover,UA attenuated 6-OHDA-induced mitochondrial dysfunction in PC12 cells accompanied by enhanced mitochondrial biogen⁃esis.Mechanically,the neuroprotective effects of UA were mediated by SIRT1-PGC-1αsignaling-mediated mitochondrial biogenesis.CONCLU⁃SION These data provide new insights into the novel role of UA in promoting mitochondria bio⁃genesis and suggest that UA may have potential therapeutic applications for PD.

关键词： urolithin a Parkinson disease mito⁃chondrial biogenesis

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