参考文献/References:
[1] Miao Y, Wu Y L, Jin Y J, et al. Benzoquinone derivativeswith antioxidant activity inhibit activated hepatic stellatecells and attenuate liver fibrosis in TAA-induced mice[J].Chemico-Biological Interactions, 2020, 317: 108945.[2] Popper H, Uenfriend S, Hepatic F. Correlation of biochemicaland morphologic investigations[J]. The American Journalof Medicine, 1970, 49: 707-721.[3] Chen R J, Wu H H, Wang Y J. Strategies to prevent andreverse liver fibrosis in humans and laboratory animals[J].Archives of Toxicology, 2015, 89(10): 1727-1750.[4] Li J S, Wang W J, Sun Y, et al. Ursolic acid inhibits thedevelopment of nonalcoholic fatty liver disease byattenuating endoplasmic reticulum stress[J]. Food andFunction, 2015, 6(5): 1643-1651.[5] 李顶春,李武. TGF-β/Smad、MAPK/ERK、NF-κB 信号通路对肝纤维化的影响[J]. 现代免疫学,2017,37(5):427-432.[6] Zhang J Q, Han C, Song K, et al. The long-noncodingRNA MALAT1 regulates TGF-β/Smad signaling throughformation of a lncRNA-protein complex with Smads,SETD2 and PPM1A in hepatic cells[J]. PLoS One, 2020,15(1): e0228160 .[7] Ojiaku C A, Cao G, Zhu W, et al. TGF-β1 evokes humanair-way smooth muscle cell shortening andhyperresponsiveness via Smad3[J]. American Journal ofRespiratory Cell and Molecular Biology, 2018, 58(5):575-584.[8] 颜小明,张立婷,李敏,等. TGF-β1/Smad 信号通路在肝纤维化中的研究进展[J]. 现代生物医学进展,2016,16(9): 1778-1781,1752.[9] Xu Y T, Sun X L, Zhang R L, et al. A positive feedbackloop of TET3 and TGF-β1 promotes liver fibrosis[J]. CellReports, 2020, 30(5): 1310-1318.[10] Yu S S, Chen B, Huang C K, et al. Ursolic acid suppressesTGF-β1-induced quiescent HSC activation andtransformation by inhibiting NADPH oxidase expressionand Hedgehog signaling[J]. Experimental and TherapeuticMedicine, 2017, 14(4): 3577-3582.[11] 欧阳灿晖,朱萱,张焜和,等. 熊果酸对肝纤维化大鼠肝组织TGF-β1和α-SMA表达的影响[J]. 世界华人消化杂志,2009,17(22): 2237-2243.[12] Gaestel M. MAPK-Activated Protein Kinases (MKs):Novel Insights and Challenges[J]. Frontiers in Cell andDevelopmental Biology, 2016, 3: 00088.[13] 叶平,杨波,吴晓玲,等. P38 MAPK 信号通路主要功能及对肝纤维化的作用[J]. 世界华人消化杂志,2011,19(32): 3353-3358.[14] 张新华,何文华,朱萱,等. 熊果酸(UA)对大鼠活化型肝星状细胞(HSC)的 NADPH 氧化酶(NOX)亚基及PI3K/Akt、P38MAPK 信号通路活化的影响[J]. 第二军医大学学报,2012,33(6): 590-594.[15] Ma J Q, Ding J, Zhang L, et al. Ursolic acid protects mouseliver against CCl4-induced oxidative stress andinflammation by the MAPK/NF-κB pathway[J].- 36 -Environmental toxicology and pharmacology, 2014, 37(3):975-983.[16] He W, Shi F, Zhou Z W, et al. A bioinformatic andmechanistic study elicits the antifibrotic effect of ursolicacid through the attenuation of oxidative stress with theinvolvement of ERK,PI3K/Akt, and p38 MAPK signalingpathways in human hepatic stellate cells and rat liver[J].Drug Design, Development and Therapy, 2015, 9: 3989-4104.[17] Pompura S L, Dominguez-Villar M. The PI3K/AKTsignaling pathway in regulatory T-cell development,stability, and function[J]. Journal of Leukocyte Biology,2018, 103(6): 1065-1076.[18] Shimon R, Alon L, Lindquist J N, et al. The role of focaladhesion kinase-phosphatidylinositol 3-kinase-akt signalingin hepatic stellate cell proliferation and type I collagenexpression[J]. The Journal of Biological Chemistry 2003,278(10): 8083-8090.[19] 崔永佳,徐军全,王美娇,等. PI3K/Akt/mTOR 信号通路在脂多糖诱导的大鼠肝星状细胞自噬中的作用[J].中国细胞生物学学报,2019(9): 1724-1729.[20] 陈涛. 熊果酸对血管紧张素Ⅱ诱导肝星状细胞 NADPH氧化酶的活化及 PI3K/Akt、P38MAPK 信号通路的影响[D]. 南昌: 南昌大学,2014.[21] Sang B, Zhang YY, Guo ST, et al. Dual functions forOVAAL in initiation of RAF/MEK/ERK prosurvivalsignals and evasion of p27-mediated cellular senescence[J]. Proceedings of the National Academy of Sciences,2018, 115(50): E11661-E11670.[22] Lennartsson J, Burovic F, Witek B, et al. Erk 5 is necessaryfor sustained PDGF-induced Akt phosphorylation andinhibition of apoptosis[J]. Cell Signalling, 2010, 22(6):955-960.[23] Mendoza MC, Blenis J. The Ras-ERK and PI3K-mTORpathways: cross-talk and compensation[J]. TrendsBiochemical Sciences, 2011, 36(6): 320-328.[24] 黄雯. 熊果酸对 PDGF 诱导的活化型肝星状细胞内NOX 信号通路的影响[D]. 南昌: 南昌大学,2014.[25] Lee J J, von Kessler D P, Parks S, et al. Secretion andlocalized transcription suggest a role in positionalsignaling for products of the segmentation gene hedgehog[J]. Cell, 1992, 71(1): 33-50.[26] Shen X, Peng Y, Li H M. The injury-related activation ofhedgehog signaling pathway modulates the repair-associated inflammation in liver fibrosis[J]. Frontiers inImmunology, 2017, 8: 1450.[27] 陈标. 熊果酸对原代肝星状细胞活化过程中 NOX-Hedgehog 信号网络的影响[D]. 南昌: 南昌大学,2015.[28] 陈璐,何文华,朱萱,等. 熊果酸对肝星状细胞 NADPH氧化酶-Hedgehog 信号通路的影响[J]. 第三军医大学学报,2014,36(5): 427-431.[29] Crosas-Molist E, Fabregat I. Role of NADPH oxidases inthe redox biology of liver fibrosis[J]. Redox Biology,2015, 6: 106-111.[30] 陈涛,何文华,黄雯,等. 熊果酸对肝星状细胞内 AP-1、NF-κB 表达的影响[J]. 广东医学,2016,37(17): 2545-2548.[31] 黄晨恺,甘达凯,张望,等. 熊果酸对肝纤维化大鼠NOX2/ROS/NLRP3 炎性小体活化的影响[J]. 基础医学与临床,2018(4): 485-491.[32] Gan D K, Zhang W, Huang C K, et al. Ursolic acidameliorates CCl4-induced liver fibrosis through theNOXs/ROS pathway[J]. Journal of Cellular Physiology,2017, 233(5): 6799-6813.[33] 罗方云. NOX4/ROS和RhoA/ROCK1信号通路在肝纤维化中的作用及熊果酸的干预靶点[D]. 南昌: 南昌大学,2019.[34] 周娟娟. 熊果酸对大鼠肝纤维化过程中肝细胞的保护作用及其可能机制[D]. 南昌: 南昌大学,2016.[35] Huang C K, Gan D K, Luo F Y, et al. Interactionmechanisms between the NOX4/ROS and RhoA/ROCK1signaling pathways as new anti-fibrosis targets of ursolicacid in hepatic stellate cells[J]. Frontiers in Pharmacology,2019, 10: 431.[36] Wang X, Ikejima K, Kon K, et al. Ursolic acid ameliorateshepatic fibrosis in the rat by specific induction of apoptosisin hepatic stellate cells[J]. Journal of Hepatology, 2011,55(2): 379-387.[37] Higashi T, Friedman SL, Hoshida Y. Hepatic stellate cellsas key target in liver fibrosis[J]. Advanced drug deliveryreviews, 2017, 121: 27-42.[38] Poisson J, Lemoinne S, Boulanger C, et al. Liver sinusoidalendothelial cells: physiology and role in liver diseases[J].Journal of Hepatology, 2017, 66(1): 212-227.[39] Shen Y M, Zhu X, Zhang K H, et al. Effect of ursolic acidon proliferation and apoptosis of hepatic stellate cells invitro[J]. Chinese Journal of Hepatology, 2008, 16(4): 298-301.[40] Schnabl B, Brenner D A. Interactions between the intestinalmicrobiome and liver diseases[J]. Gastroenterology, 2014,146(6): 1513-1524.[41] Wan S Z, Liu C, Huang C K, et al. Ursolic acid improvesintestinal damage and bacterial dysbiosis in liver fibrosismice[J]. Frontiers in Pharmacology, 2019, 10: 1321.[42] Zhang W, Gan D, Jian J, et al. Protective effect of ursolicacid on the intestinal mucosal barrier in a rat model of liverfibrosis[J]. Frontiers in Physiology, 2019, 30: 956.[43] Liu B, Piao X, Guo L, et al. Ursolic acid protects againstulcerative colitis via anti-inflammatory and antioxidanteffects in mice[J]. Molecular Medicine Reports, 2016,13(6): 4779-4785.[44] Chun J, Lee C, Hwang S W, et al. Ursolic acid inhibitsnuclear factor-κB signaling in intestinal epithelial cellsand macrophages,and attenuates experimental colitis inmice[J]. Life Sciences. 2014, 110(1): 23-34.
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