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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 *** To explore whether UA can alleviate NPMSCs senescence and to elucidate the underlying *** 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 ***-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 *** 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 *** 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 *** UA pretreatment,the abovementioned senescence indicators were significantly *** further demonstrate the mechanism of UA,we evaluated the mitochondrial membrane potential and the SIRT1/PGC-1αpathway that regulates mitochondrial *** protected mitochondrial function and delayed NPMSCs senescence by activating the SIRT1/PGC-1α*** vivo,we found that UA treatment alleviated an animal model of IDD by assessing the disc height index,Pfirrmann grade and the histological *** In summary,UA could activate the SIRT1/PGC-1αsignaling pathway to protect mitochondrial function and alleviate ce

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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Quercetin ameliorates oxidative stress-induced senescence in rat nucleus pulposus-derived mesenchymal stem cells via the miR-34a-5p/SIRT1 axis

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World Journal of stem cells 2023年第8期15卷 842-865页

作者： Wen-Jie Zhao Xin Liu Man Hu Yu Zhang Peng-Zhi Shi Jun-Wu Wang Xu-Hua Lu Xiao-Fei Cheng Yu-Ping Tao Xin-Min Feng Yong-Xiang Wang Liang Zhang Graduate School Dalian Medical UniversityDalian 116044Liaoning ProvinceChina Department of Orthopedics Clinical Medical CollegeYangzhou UniversityYangzhou 225001Jiangsu ProvinceChina Department of Orthopedics Changzheng Hospital of The Second Military Medical UniversityShanghai 200003China Department of Orthopedic Surgery Shanghai Key Laboratory of Orthopedics ImplantsShanghai Ninth People’s HospitalShanghai Jiaotong University School of MedicineShanghai 200011China

BACKGROUND Intervertebral disc degeneration(IDD)is a main contributor to low back *** stress,which is highly associated with the progression of IDD,increases senescence of nucleus pulposus-derived mesenchymal stem cells(NPMSCs)and weakens the differentiation ability of NPMSCs in degenerated intervertebral discs(IVDs).Quercetin(Que)has been demonstrated to reduce oxidative stress in diverse degenerative *** To investigate the role of Que in oxidative stress-induced NPMSC damage and to elucidate the underlying *** In vitro,NPMSCs were isolated from rat ***-associatedβ-galactosidase(SA-β-Gal)staining,cell cycle,reactive oxygen species(ROS),realtime quantitative polymerase chain reaction(RT-qPCR),immunofluorescence,and western blot analyses were used to evaluated the protective effects of *** the relationship between miR-34a-5p and Sirtuins 1(SIRT1)was evaluated by dual-luciferase reporter *** explore whether Que modulates tert-butyl hydroperoxide(TBHP)-induced senescence of NPMSCs via the miR-34a-5p/SIRT1 pathway,we used adenovirus vectors to overexpress and downregulate the expression of miR-34a-5p and used SIRT1 siRNA to knockdown SIRT1 *** vivo,a puncture-induced rat IDD model was constructed,and X rays and histological analysis were used to assess whether Que could alleviate IDD in *** We found that TBHP can cause NPMSCs senescence changes,such as reduced cell proliferation ability,increased SA-β-Gal activity,cell cycle arrest,the accumulation of ROS,and increased expression of senescence-related *** abovementioned senescence indicators were significantly alleviated by Que *** decreased the expression levels of senescence-related proteins(p16,p21,and p53)and senescence-associated secreted phenotype(SASP),including IL-1β,IL-6,and MMP-13,and it increased the expression of *** addition,the protective effects of Que on cell senescence were partially reversed by mi

关键词： Quercetin nucleus pulposus-derived mesenchymal stem cells Oxidative stress Senescence Intervertebral disc degeneration miR-34a-5p/SIRT1 pathway

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6-gingerol protects nucleus pulposus-derived mesenchymal stem cells from oxidative injury by activating autophagy

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World Journal of stem cells 2020年第12期12卷 1603-1622页

作者： Li-Ping Nan Feng Wang Yang Liu Zhong Wu Xin-Min Feng Jun-Jian Liu Liang Zhang Department of Orthopedic Tongji University School of MedicineShanghai Tenth People’s HospitalTenth People’s Hospital of Tongji UniversityShanghai 200072China Department of Spine Surgery Tongji University School of MedicineShanghai East HospitalShanghai 200120China Department of Orthopedic West China Hospital of Sichuan UniversityChengdu 610000Sichuan ProvinceChina Department of Orthopedics Shanghai Tenth People’s HospitalTongji University School of MedicineShanghai 200072China Department of Orthopedics Clinical Medical College of Yangzhou UniversityYangzhou 225000Jiangsu ProvinceChina

BACKGROUND To date,there has been no effective treatment for intervertebral disc degeneration(IDD).nucleus pulposus-derived mesenchymal stem cells(NPMSCs)showed encouraging results in IDD treatment,but the overexpression of reactive oxygen species(ROS)impaired the endogenous repair abilities of NPMSCs.6-gingerol(6-GIN)is an antioxidant and anti-inflammatory reagent that might protect NPMSCs from *** To investigate the effect of 6-GIN on NPMSCs under oxidative conditions and the potential *** The cholecystokinin-8 assay was used to evaluate the cytotoxicity of hydrogen peroxide and the protective effects of *** levels were measured by 2´7´-dichlorofluorescin diacetate *** metalloproteinase(MMP)was detected by the tetraethylbenzimidazolylcarbocyanine iodide *** assay and Annexin V/PI double-staining were used to determine the apoptosis ***,autophagy-related proteins(Beclin-1,LC-3,and p62),apoptosisassociated proteins(Bcl-2,Bax,and caspase-3),and PI3K/Akt signaling pathwayrelated proteins(PI3K and Akt)were evaluated by Western blot *** were detected by transmission electron microscopy in ***-3 was also detected by *** mRNA expression of collagen II and aggrecan was evaluated by real-time polymerase chain reaction(RT-PCR),and the changes in collagen II and MMP-13 expression were verified through an immunofluorescence *** 6-GIN exhibited protective effects against hydrogen peroxide-induced injury in NPMSCs,decreased hydrogen peroxide-induced intracellular ROS levels,and inhibited cell apoptosis.6-GIN could increase Bcl-2 expression and decrease Bax and caspase-3 *** MMP,Annexin V-FITC/PI flow cytometry and TUNEL assay results further confirmed that 6-GIN treatment significantly inhibited NPMSC apoptosis induced by hydrogen peroxide.6-GIN treatment promoted extracellular matrix(ECM)expression by reducing the oxidative stress injury-induced increas

关键词： nucleus pulposus-derived mesenchymal stem cells 6-Gingerol Intervertebral disc degeneration Oxidative stress Autophagy Apoptosis

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