山东大学学报 (医学版) ›› 2021, Vol. 59 ›› Issue (6): 16-24.doi: 10.6040/j.issn.1671-7554.0.2021.0295
李敏启1,2,杜娟1,3,杨盼盼1,2,寇雨莹1,2,柳珊珊1,2
LI Minqi1,2, DU Juan1,3, YANG Panpan1,2, KOU Yuying1,2, LIU Shanshan1,2
摘要： 骨质疏松症是一种骨量降低、骨组织微结构破坏、骨脆性增加,导致患者容易出现骨折的全身代谢性疾病。伴随着老龄化社会的到来,骨质疏松目前已成为我国中老年人群的重要健康问题。骨质疏松症的发病因素是多方面的,增龄、衰老造成的器官功能减退是主要因素,而“氧化应激衰老理论”迄今仍然是最有据可循的衰老机制假说。综述将围绕氧化应激与骨形成、氧化应激与骨吸收以及抗氧化剂与骨稳态维持等方面,回顾氧化应激诱导骨质疏松症发生发展的相关研究进展。
中图分类号:
| [1] Atashi F, Modarressi A, Pepper MS. The role of reactive oxygen species in mesenchymal stem cell adipogenic and osteogenic differentiation: a review [J]. Stem Cells Dev, 2015, 24(10): 1150-1163. [2] Li Q, Gao Z, Chen Y, et al. The role of mitochondria in osteogenic, adipogenic and chondrogenic differentiation of mesenchymal stem cells [J]. Protein Cell, 2017, 8(6): 439-445. [3] Tan J, Xu X, Tong Z, et al. Decreased osteogenesis of adult mesenchymal stem cells by reactive oxygen species under cyclic stretch: a possible mechanism of age related osteoporosis [J]. Bone Res, 2015, 3: 15003. doi: 10.1038/boneres.2015.3. [4] Wang L, Zhao X, Wei BY, et al. Insulin improves osteogenesis of titanium implants under diabetic conditions by inhibiting reactive oxygen species overproduction via the PI3K-Akt pathway [J]. Biochimie, 2015, 108: 85-93. doi: 10.1016/j.biochi.2014.10.004. [5] Nastase MV, Janicova A, Wygrecka M, et al. Signaling at the Crossroads: matrix-derived proteoglycan and reactive oxygen species signaling [J]. Antioxid Redox Signal, 2017, 27(12): 855-873. [6] Shi C, Wu J, Yan Q, et al. Bone marrow ablation demonstrates that estrogen plays an important role in osteogenesis and bone turnover via an antioxidative mechanism [J]. Bone, 2015, 79: 94-104. doi: 10.1016/j.bone.2015.05.034. [7] Gómez-Puerto MC, Verhagen LP, Braat AK, et al. Activation of autophagy by FOXO3 regulates redox homeostasis during osteogenic differentiation [J]. Autophagy, 2016, 12(10): 1804-1816. [8] Wang Z, Yang X, Yang S, et al. Sodium fluoride suppress proliferation and induce apoptosis through decreased insulin-like growth factor-I expression and oxidative stress in primary cultured mouse osteoblasts [J]. Arch Toxicol, 2011, 85(11): 1407-1417. [9] Chen CT, Shih YR, Kuo TK, et al. Coordinated changes of mitochondrial biogenesis and antioxidant enzymes during osteogenic differentiation of human mesenchymal stem cells [J]. Stem Cells, 2008, 26(4): 960-968. [10] Zhang Y, Yang JH. Activation of the PI3K/Akt pathway by oxidative stress mediates high glucose-induced increase of adipogenic differentiation in primary rat osteoblasts [J]. J Cell Biochem, 2013, 114(11): 2595-2602. [11] Kalyanaraman H, Schwaerzer G, Ramdani G, et al. Protein kinase G activation reverses oxidative stress and restores osteoblast function and bone formation in male mice with type 1 diabetes [J]. Diabetes, 2018, 67(4): 607-623. [12] Wang YN, Jia TT, Feng Y, et al. Hyperlipidemia impairs osseointegration via the ROS/wnt/β-catenin pathway [J]. J Dent Res, 2021: 22034520983245. doi: 10.1177/0022034520983245. [13] James AW. Review of signaling pathways governing MSC osteogenic and adipogenic differentiation [J]. Scientifica(Cairo), 2013, 2013: 684736. doi: 10.1155/2013/684736. [14] O&apos, Donnell VB, Azzi A. High rates of extracellular superoxide generation by cultured human fibroblasts: involvement of a lipid-metabolizing enzyme [J]. Biochem J, 1996, 318(Pt 3): 805-812. [15] Kim WK, Meliton V, Bourquard N, et al. Hedgehog signaling and osteogenic differentiation in multipotent bone marrow stromal cells are inhibited by oxidative stress [J]. J Cell Biochem, 2010, 111(5): 1199-1209. [16] Zhang B, Xie QY, Quan Y, et al. Reactive oxygen species induce cell death via Akt signaling in rat osteoblast-like cell line ROS 17/2.8 [J]. Toxicol Ind Health, 2015, 31(12): 1236-1242. [17] Wauquier F, Leotoing L, Coxam V, et al. Oxidative stress in bone remodelling and disease [J]. Trends Mol Med, 2009, 15(10): 468-477. [18] Domazetovic V, Marcucci G, Iantomasi T, et al. Oxidative stress in bone remodeling: role of antioxidants [J]. Clin Cases Miner Bone Metab, 2017, 14(2): 209-216. [19] Bellanti F, Matteo M, Rollo T, et al. Sex hormones modulate circulating antioxidant enzymes: impact of estrogen therapy [J]. Redox Biol, 2013, 1: 340-346. doi: 10.1016/j.redox.2013.05.003. [20] Grassi F, Tell G, Robbie-Ryan M, et al. Oxidative stress causes bone loss in estrogen-deficient mice through enhanced bone marrow dendritic cell activation[J]. PNAS, 2007, 104(38): 15087-15092. [21] Wang X, Chen B, Sun J, et al. Iron-induced oxidative stress stimulates osteoclast differentiation via NF-κB signaling pathway in mouse model [J]. Metabolism, 2018, 83: 167-176. doi: 10.1016/j.metabol.2018.01.005. [22] Almeida M, Han L, Martin-Millan M, et al. Skeletal involution by age-associated oxidative stress and its acceleration by loss of sex steroids [J]. J Biol Chem, 2007, 282(37): 27285-27297. [23] An Y, Zhang H, Wang C, et al. Activation of ROS/MAPKs/NF-κB/NLRP3 and inhibition of efferocytosis in osteoclast-mediated diabetic osteoporosis [J]. FASEB J, 2019, 33(11): 12515-12527. [24] Henriksen K, Neutzsky-Wulff AV, Bonewald LF, et al. Local communication on and within bone controls bone remodeling [J]. Bone, 2009, 44(6): 1026-1033. [25] Mulcahy LE, Taylor D, Lee TC, et al. RANKL and OPG activity is regulated by injury size in networks of osteocyte-like cells [J]. Bone, 2011, 48(2): 182-188. [26] Romagnoli C, Marcucci G, Favilli F, et al. Role of GSH/GSSG redox couple in osteogenic activity and osteoclastogenic markers of human osteoblast-like SaOS-2 cells [J]. FEBS J, 2013, 280(3): 867-879. [27] Filaire E, Toumi H. Reactive oxygen species and exercise on bone metabolism: friend or enemy? [J]. Joint Bone Spine, 2012, 79(4): 341-346. [28] Chen JR, Shankar K, Nagarajan S, et al. Protective effects of estradiol on ethanol-induced bone loss involve inhibition of reactive oxygen species generation in osteoblasts and downstream activation of the extracellular signal-regulated kinase/signal transducer and activator of transcription 3/receptor activator of nuclear factor-kappaB ligand signaling cascade [J]. J Pharmacol Exp Ther, 2008, 324(1): 50-59. [29] Qin D, Zhang H, Zhang H, et al. Anti-osteoporosis effects of osteoking via reducing reactive oxygen species [J]. J Ethnopharmacol, 2019, 244: 112045. doi: 10.1016/j.jep.2019.112045. [30] Fontani F, Marcucci G, Iantomasi T, et al. Glutathione, N-acetylcysteine and lipoic acid down-regulate starvation-induced apoptosis, RANKL/OPG ratio and sclerostin in osteocytes: involvement of JNK and ERK1/2 signalling [J]. Calcif Tissue Int, 2015, 96(4): 335-346. [31] Schreck R, Rieber P, Baeuerle PA. Reactive oxygen intermediates as apparently widely used messengers in the activation of the NF-kappa B transcription factor and HIV-1 [J]. EMBO J, 1991, 10(8): 2247-2258. [32] Oliveira-Marques V, Marinho HS, Cyrne L, et al. Role of hydrogen peroxide in NF-kappaB activation: from inducer to modulator [J]. Antioxid Redox Signal, 2009, 11(9): 2223-2243. [33] Sies H, Berndt C, Jones DP. Oxidative Stress [J]. Annu Rev Biochem, 2017, 86: 715-748. doi: 10.1146/annurev-biochem-061516-045037. [34] Ghonime MG, Shamaa OR, Das S, et al. Inflammasome priming by lipopolysaccharide is dependent upon ERK signaling and proteasome function [J]. J Immunol, 2014, 192(8): 3881-3888. [35] Ha H, Kwak HB, Lee SW, et al. Reactive oxygen species mediate RANK signaling in osteoclasts [J]. Exp Cell Res, 2004, 301(2): 119-127. [36] Lee SY, Lee KS, Yi SH, et al. Acteoside suppresses RANKL-mediated osteoclastogenesis by inhibiting c-Fos induction and NF-κB pathway and attenuating ROS production [J]. PLoS One, 2013, 8(12): e80873. [37] Callaway DA, Jiang JX. Reactive oxygen species and oxidative stress in osteoclastogenesis, skeletal aging and bone diseases [J]. J Bone Miner Metab, 2015, 33(4): 359-370. [38] Decuypere JP, Monaco G, Missiaen L, et al. IP(3)receptors, mitochondria, and Ca signaling: implications for aging [J]. J Aging Res, 2011, 2011: 920178. doi: 10.4061/2011/920178. [39] Kim MS, Yang YM, Son A, et al. RANKL-mediated reactive oxygen species pathway that induces long lasting Ca2+oscillations essential for osteoclastogenesis [J]. J Biol Chem, 2010, 285(10): 6913-6921. [40] Almeida M, Porter RM. Sirtuins and FoxOs in osteoporosis and osteoarthritis [J]. Bone, 2019, 121: 284-292. doi: 10.1016/j.bone.2019.01.018. [41] Tothova Z, Kollipara R, Huntly BJ, et al. FoxOs are critical mediators of hematopoietic stem cell resistance to physiologic oxidative stress [J]. Cell, 2007, 128(2): 325-339. [42] de Keizer PL, Burgering BM, Dansen TB. Forkhead box o as a sensor, mediator, and regulator of redox signaling [J]. Antioxid Redox Signal, 2011, 14(6): 1093-1106. [43] Zainabadi K, Liu CJ, Caldwell ALM, et al. SIRT1 is a positive regulator of in vivo bone mass and a therapeutic target for osteoporosis [J]. PLoS One, 2017,12(9): e0185236. [44] Edwards JR, Perrien DS, Fleming N, et al. Silent information regulator(Sir)T1 inhibits NF-κB signaling to maintain normal skeletal remodeling [J]. J Bone Miner Res, 2013, 28(4): 960-969. [45] Bartell SM, Kim HN, Ambrogini E, et al. FoxO proteins restrain osteoclastogenesis and bone resorption by attenuating H2O2 accumulation [J]. Nat Commun, 2014, 5: 3773. doi: 10.1038/ncomms4773. [46] Thummuri D, Naidu VGM, Chaudhari P. Carnosic acid attenuates RANKL-induced oxidative stress and osteoclastogenesis via induction of Nrf2 and suppression of NF-κB and MAPK signalling [J]. J Mol Med(Berl), 2017, 95(10): 1065-1076. [47] Kanzaki H, Shinohara F, Itohiya K, et al. RANKL induces Bach1 nuclear import and attenuates Nrf2-mediated antioxidant enzymes, thereby augmenting intracellular reactive oxygen species signaling and osteoclastogenesis in mice [J]. Faseb J, 2017, 31(2): 781-792. [48] Chen Y, Sun J, Dou C, et al. Alliin Attenuated RANKL-Induced Osteoclastogenesis by Scavenging Reactive Oxygen Species through Inhibiting Nox1 [J]. Int J Mol Sci, 2016, 17(9): 1516. [49] Gao Y, Ge W. The histone methyltransferase DOT1L inhibits osteoclastogenesis and protects against osteoporosis [J]. Cell Death Dis, 2018, 9(2): 33. [50] Kim BJ, Ahn SH, Bae SJ, et al. Iron overload accelerates bone loss in healthy postmenopausal women and middle-aged men: a 3-year retrospective longitudinal study [J]. J Bone Miner Res, 2012, 27(11): 2279-2290. [51] Chen B, Yan YL, Liu C, et al. Therapeutic effect of deferoxamine on iron overload-induced inhibition of osteogenesis in a zebrafish model [J]. Calcif Tissue Int, 2014, 94(3): 353-360. [52] Chen D, Ye Z, Wang C, et al. Arctiin abrogates osteoclastogenesis and bone resorption via suppressing RANKL-induced ROS and NFATc1 activation [J]. Pharmacol Res, 2020, 159: 104944. doi: 10.1016/j.phrs.2020.104944. [53] Sun X, Xie Z, Hu B, et al. The Nrf2 activator RTA-408 attenuates osteoclastogenesis by inhibiting STING dependent NF-κb signaling [J]. Redox Biol, 2020, 28: 101309. doi: 10.1016/j.redox.2019.101309. [54] Chen K, Qiu P, Yuan Y, et al. Pseurotin A inhibits osteoclastogenesis and prevents ovariectomized-induced bone loss by suppressing reactive oxygen species [J]. Theranostics, 2019, 9(6): 1634-1650. [55] Li DZ, Zhang QX, Dong XX, et al. Treatment with hydrogen molecules prevents RANKL-induced osteoclast differentiation associated with inhibition of ROS formation and inactivation of MAPK, AKT and NF-kappa B pathways in murine RAW264.7 cells [J]. J Bone Miner Metab, 2014, 32(5): 494-504. [56] Circu ML, Aw TY. Reactive oxygen species, cellular redox systems, and apoptosis [J]. Free Radic Biol Med, 2010, 48(6): 749-762. [57] Romagnoli C, Marcucci G, Favilli F, et al. Role of GSH/GSSG redox couple in osteogenic activity and osteoclastogenic markers of human osteoblast-like SaOS-2 cells [J]. Febs J, 2013, 280(3): 867-879. [58] Lean JM, Jagger CJ, Kirstein B, et al. Hydrogen peroxide is essential for estrogen-deficiency bone loss and osteoclast formation [J]. Endocrinology, 2005, 146(2): 728-735. [59] Mainini G, Rotondi M, Di Nola K, et al. Oral supplementation with antioxidant agents containing alpha lipoic acid: effects on postmenopausal bone mass [J]. Clin Exp Obstet Gynecol, 2012, 39(4): 489-493. [60] Sanders KM, Kotowicz MA, Nicholson GC. Potential role of the antioxidant N-acetylcysteine in slowing bone resorption in early post-menopausal women: a pilot study [J]. Transl Res, 2007, 150(4): 215. [61] Polat B, Halici Z, Cadirci E, et al. The effect of alpha-lipoic acid in ovariectomy and inflammation-mediated osteoporosis on the skeletal status of rat bone [J]. Eur J Pharmacol, 2013, 718(1-3): 469-474. [62] Ostman B, Michaëlsson K, Helmersson J, et al. Oxidative stress and bone mineral density in elderly men: antioxidant activity of alpha-tocopherol [J]. Free Radic Biol Med, 2009, 47(5): 668-673. [63] Shuid AN, Mohamad S, Muhammad N, et al. Effects of α-tocopherol on the early phase of osteoporotic fracture healing [J]. J Orthop Res, 2011, 29(11): 1732-1738. [64] Koh JM, Lee YS, Byun CH, et al. Alpha-lipoic acid suppresses osteoclastogenesis despite increasing the receptor activator of nuclear factor kappaB ligand/osteoprotegerin ratio in human bone marrow stromal cells [J]. J Endocrinol, 2005, 185(3): 401-413. [65] Feng H, Li Z, Du J, et al. Dual function of peroxiredoxin I in lipopolysaccharide-induced osteoblast apoptosis via reactive oxygen species and the apoptosis signal-regulating kinase 1 signaling pathway [J]. Cell Death Discov, 2018, 4: 47. doi: 10.1038/s41420-018-0050-9. [66] Du J, Feng W, Sun J, et al. Ovariectomy upregulated the expression of Peroxiredoxin 1 & 5 in osteoblasts of mice [J]. Sci Rep, 2016, 6: 35995. doi: 10.1038/srep35995. [67] Xu GP, Li X, Zhu ZY, et al. Iron overload induces apoptosis and cytoprotective autophagy regulated by ROS generation in Mc3t3-E1 cells [J]. Biol Trace Elem Res, 2021: 1-12. doi: 10.1007/s12011-020-02508-x. [68] Soares MPR, Silva DP, Uehara IA, et al. The use of apocynin inhibits osteoclastogenesis [J]. Cell Biol Int, 2019, 43(5): 466-475. [69] Byun CH, Koh JM, Kim DK, et al. Alpha-lipoic acid inhibits TNF-alpha-induced apoptosis in human bone marrow stromal cells [J]. J Bone Miner Res, 2005, 20(7): 1125-1135. [70] Jiang Y, Luo W, Wang B, et al. Resveratrol promotes osteogenesis via activating SIRT1/FoxO1 pathway in osteoporosis mice [J]. Life Sci, 2020, 246: 117422. doi: 10.1016/j.lfs.2020.117422. [71] Kim EN, Kim GR, Yu JS, et al. Inhibitory Effect of(2R)-4-(4-hydroxyphenyl)-2-butanol 2-O-β-d-apiofuranosyl-(1→6)-β-d-glucopyranoside on RANKL-Induced Osteoclast Differentiation and ROS Generation in Macrophages [J]. Int J Mol Sci, 2020, 22(1): 222. [72] Ferlazzo N, Andolina G, Cannata A, et al. Is Melatonin the Cornucopia of the 21st Century? [J]. Antioxidants(Basel), 2020, 9(11): 1088. [73] Li X, Chen Y, Mao Y, et al. Curcumin protects osteoblasts from oxidative stress-induced dysfunction via GSK3β-Nrf2 signaling pathway [J]. Front Bioeng Biotechnol, 2020, 8: 625. doi: 10.3389/fbioe.2020.00625. [74] Pinna A, Torki Baghbaderani M, Vigil Hernández V, et al. Nanoceria provides antioxidant and osteogenic properties to mesoporous silica nanoparticles for osteoporosis treatment [J]. Acta Biomater, 2021, 122: 365-376. doi: 10.1016/j.actbio.2020.12.029. [75] Huang HT, Cheng TL, Lin SY, et al. Osteoprotective Roles of Green Tea Catechins [J]. Antioxidants(Basel), 2020, 9(11): 1136. [76] Devareddy L, Hooshmand S, Collins JK, et al. Blueberry prevents bone loss in ovariectomized rat model of postmenopausal osteoporosis [J]. J Nutr Biochem, 2008, 19(10): 694-699. [77] Zhang J, Lazarenko OP, Blackburn ML, et al. Blueberry consumption prevents loss of collagen in bone matrix and inhibits senescence pathways in osteoblastic cells [J]. Age(Dordr), 2013, 35(3): 807-820. [78] Jin H, Du J, Ren H, et al. Astragaloside IV protects against iron loading-induced abnormal differentiation of bone marrow mesenchymal stem cells(BMSCs)[J]. FEBS Open Bio, 2021, 11(4): 1223-1236. [79] Chen L, Hu SL, Xie J, et al. Proanthocyanidins-mediated nrf2 activation ameliorates glucocorticoid-induced oxidative stress and mitochondrial dysfunction in osteoblasts [J]. Oxid Med Cell Longev, 2020, 2020: 9102012. doi: 10.1155/2020/9102012. [80] Li M, Hao L, Li L, et al. Cinnamtannin B-1 prevents ovariectomy-induced osteoporosis via attenuating osteoclastogenesis and ROS generation [J]. Front Pharmacol, 2020, 11: 1023. doi: 10.3389/fphar.2020.01023. [81] Rhee SG, Kang SW, Chang TS, et al. Peroxiredoxin, a novel family of peroxidases [J]. IUBMB Life, 2001, 52(1/2): 35-41. [82] Rhee SG, Woo HA. Multiple functions of peroxiredoxins: peroxidases, sensors and regulators of the intracellular messenger H2O2, and protein chaperones [J]. Antioxid Redox Signal, 2011, 15(3): 781-794. [83] Hall A, Nelson K, Poole LB, et al. Structure-based insights into the catalytic power and conformational dexterity of peroxiredoxins [J]. Antioxid Redox Signal, 2011, 15(3): 795-815. [84] Yang KS, Kang SW, Woo HA, et al. Inactivation of human peroxiredoxin I during catalysis as the result of the oxidation of the catalytic site cysteine to cysteine-sulfinic acid [J]. J Biol Chem, 2002, 277(41): 38029-38036. [85] Park MH, Jo M, Kim YR, et al. Roles of peroxiredoxins in cancer, neurodegenerative diseases and inflammatory diseases [J]. Pharmacol Ther, 2016, 163: 1-23. doi: 10.1016/j.pharmthera.2016.03.018. [86] Jeong SJ, Kim S, Park JG, et al. Prdx1(peroxiredoxin 1)deficiency reduces cholesterol efflux via impaired macrophage lipophagic flux [J]. Autophagy, 2018, 14(1): 120-133. [87] Bolduc JA, Collins JA, Loeser RF. Reactive oxygen species, aging and articular cartilage homeostasis [J]. Free Radic Biol Med, 2019, 132: 73-82. doi: 10.1016/j.freeradbiomed.2018.08.038. [88] Román F, Urra C, Porras O, et al. Real-time H2O2 measurements in bone marrow mesenchymal stem cells(MSCs)show increased antioxidant capacity in cells from osteoporotic women [J]. J Cell Biochem, 2017, 118(3): 585-593. [89] Park KR, Yun HM, Yeo IJ, et al. Peroxiredoxin 6 inhibits osteogenic differentiation and bone formation through human dental pulp stem cells and induces delayed bone development [J]. Antioxid Redox Signal, 2019, 30(17): 1969-1982. [90] Du J, Feng W, Sun J, et al. Ovariectomy upregulated the expression of Peroxiredoxin 1 & 5 in osteoblasts of mice [J]. Sci Rep, 2016, 6: 35995. doi: 10.1038/srep35995. [91] Feng H, Li Z, Du J, et al. Dual function of peroxiredoxin I in lipopolysaccharide-induced osteoblast apoptosis via reactive oxygen species and the apoptosis signal-regulating kinase 1 signaling pathway [J]. Cell Death Discov, 2018, 4: 47. doi: 10.1038/s41420-018-0050-9. |
| [1] | 陈杨,冯莹,卢晓,郑蓉. 半乳糖凝集素-3通过PI3K/Akt/mTOR通路促进巨噬细胞自噬分化[J]. 山东大学学报 (医学版), 2026, 64(4): 14-22. |
| [2] | 于昊志,史桂东,徐国鹏,姜云鹏,冯世庆,刘新宇,祁磊. 抗氧化碳点纳米酶调控神经再生微环境的研究进展[J]. 山东大学学报 (医学版), 2026, 64(2): 44-49. |
| [3] | 李响,张艺,王雪纯,徐梦超,王月兰. 氧化应激在创伤性脑损伤诱发急性肺损伤中的研究进展[J]. 山东大学学报 (医学版), 2025, 63(2): 118-124. |
| [4] | 王璐瑶,胡晓琳,孙佩,董振华,逄曙光. 青年合并骨质疏松的Gitelman综合征1例[J]. 山东大学学报 (医学版), 2024, 62(2): 120-124. |
| [5] | 扈艳雯,赵蕙琛,马小莉,刘元涛,张玉超. GLP-1通过细胞色素P450表氧化酶途径抑制氧化应激[J]. 山东大学学报 (医学版), 2023, 61(8): 10-16. |
| [6] | 闫丛丛,陈辰,谢倩,王亚楠,张鑫璐,张迎春,武斌. 双酚A暴露对KGN细胞m6A修饰水平的影响[J]. 山东大学学报 (医学版), 2023, 61(8): 17-23. |
| [7] | 刘洋,陈贵海. 寒痉汤对冷刺激诱导主动脉平滑肌细胞氧化应激的影响及机制[J]. 山东大学学报 (医学版), 2023, 61(8): 24-30. |
| [8] | 祁少俊,唐延金,张正铎,吴虹,张佳程,秦川,刘锐,高希宝. 补充多种微量元素对高糖饮食大鼠的保护作用[J]. 山东大学学报 (医学版), 2023, 61(7): 19-26. |
| [9] | 刘凤祺,高峰,薛彩彩,乔秀梅,王金红. 高糖诱导PC12细胞损伤的影响因素及梓醇的保护作用[J]. 山东大学学报 (医学版), 2023, 61(7): 34-39. |
| [10] | 张嘉颖,宿荣允,王英惠,王洪刚,柳刚. ACE2基因通过调控Nrf2/HO-1通路改善肾缺血再灌注损伤[J]. 山东大学学报 (医学版), 2023, 61(4): 1-9. |
| [11] | 朱超,孙超,刘绪昌,夏大伟,马春骋,丰荣杰. 3D打印椎间融合器在37例单节段腰椎手术中的应用[J]. 山东大学学报 (医学版), 2023, 61(3): 134-140. |
| [12] | 吴虹,张正铎,唐延金,祁少俊,高希宝. 5-甲基四氢叶酸对大鼠动脉粥样硬化的潜在干预作用[J]. 山东大学学报 (医学版), 2022, 60(8): 6-13. |
| [13] | 陈诗鸿,姜冬青,庄向华,李晓博,潘喆,孙爱丽,娄能俊,王殿辉,杜娇娇,宋玉文. 以骨痛为首发表现的原发性胆汁性胆管炎1例[J]. 山东大学学报 (医学版), 2022, 60(8): 98-102. |
| [14] | 包舒晴,杨明月,刘端瑞,汪运山,郏雁飞. NOX4在幽门螺旋杆菌诱导胃癌细胞ROS中的作用[J]. 山东大学学报 (医学版), 2022, 60(6): 19-25. |
| [15] | 刘敏,张玉超,马小莉,刘昕宇,孙露,左丹,刘元涛. 孤核受体NR4A1在H2O2诱导小鼠肾脏足细胞损伤中的作用[J]. 山东大学学报 (医学版), 2022, 60(5): 16-21. |
|
||
