Article(id=1304388157219299701, tenantId=1146029695717560320, journalId=1302319053441957962, issueId=1304388135723496407, articleNumber=null, orderNo=null, doi=10.7501/j.issn.0253-2670.2026.13.014, pmid=null, cstr=null, oa=null, hot=0, price=null, onlineType=0, articleFormat=0, articleType=null, articleTypeStr=null, receivedDate=1767110400000, receivedDateStr=2025-12-31, revisedDate=null, revisedDateStr=null, acceptedDate=null, acceptedDateStr=null, onlineDate=1788919971041, onlineDateStr=2026-09-09, pubDate=null, pubDateStr=null, doiRegisterDate=null, doiRegisterDateStr=null, onlineIssueDate=1788919971041, onlineIssueDateStr=2026-09-09, onlineJustAcceptDate=null, onlineJustAcceptDateStr=null, onlineFirstDate=null, onlineFirstDateStr=null, sourceXml=null, magXml=null, createTime=1788919971041, creator=13701087609, updateTime=1788919971041, updator=13701087609, issue=Issue{id=1304388135723496407, tenantId=1146029695717560320, journalId=1302319053441957962, year='2026', volume='57', issue='13', pageStart='4949', pageEnd='5352', issueExtLink='null', onlineDate='null', pubDate='1783785600000', pubDateStr='2026-07-12', beforeIssueId=null, nextIssueId=null, price=null, status=1, issueComplete=1, articleOrder=1, issueType=-1, specialIssue=null, createTime=1788919965916, creator='13701087609', updateTime=1788923489765, updator='13701087609', preIssue=null, nextIssue=null, articleTotal=null, ext={EN=IssueExt(id=1304402915871977875, tenantId=1146029695717560320, journalId=1302319053441957962, issueId=1304388135723496407, language=EN, specialIssueTitle=, coverIllustrator=null, specialIssueEditor=, specialIssueAbout=), CN=IssueExt(id=1304402915871977876, tenantId=1146029695717560320, journalId=1302319053441957962, issueId=1304388135723496407, language=CN, specialIssueTitle=, coverIllustrator=null, specialIssueEditor=, specialIssueAbout=)}, issueFiles=null, downloadFileDto=null}, startPage=5109, endPage=5119, ext={EN=ArticleExt(id=1304388157798113655, articleId=1304388157219299701, tenantId=1146029695717560320, journalId=1302319053441957962, language=EN, title=Mechanism of tannic acid in promoting mitochondrial autophagy in chondrocytes and improving knee osteoarthritis in mice based on PINK1/Parkin signaling pathway, columnId=null, journalTitle=Chinese Traditional and Herbal Drugs, columnName=null, runingTitle=null, highlight=null, articleAbstract=Objective To investigate the mechanism of tannic acid in promoting mitochondrial autophagy in chondrocytes and improving knee osteoarthritis (KOA) in mice based on PINK1/Parkin signaling pathway. Methods A mouse KOA model was established via destabilization of medial meniscus surgery. Sham group, model group and tannic acid low-, high-dose (25, 50 mg/kg) groups were set up, drugs were given for intervention for eight weeks. Joint cartilage pathology was assessed by imaging, safranin O-fast green staining and toluidine blue staining. Immunohistochemistry was used to detect the expressions of collagen II (Col-II), matrix metalloproteinase 13 (MMP13), interleukin-1β (IL-1β), PINK1, Parkin, p62 and microtubule-associated protein light chain 3B (LC3B) in cartilage tissue. ATDC5 mouse chondrocytes were stimulated with IL-1β and then treated with tannic acid. Cell viability was measured by CCK-8 assay. Western blotting and qRT-PCR were used to detect the protein and mRNA expressions of Col-II, MMP13 and IL-1β. Western blotting was used to detect the expressions of mitophagy-related proteins PINK1, Parkin, p62 and LC3-II/I. Changes in reactive oxygen species (ROS) and mitochondrial membrane potential were detected by immunofluorescence. Mitochondrial autophagy level was observed by transmission electron microscopy. And reverse mechanism validation was performed using the mitochondrial autophagy inhibitor Mdivi-1. Results Compared with sham group, the cartilage of mice in model group was severely worn, OARSI score was significantly increased (P < 0.01), the protein expression levels of Col-II, PINK1, Parkin and LC3B in cartilage tissue were significantly reduced (P < 0.01), while the protein expression levels of IL-1β, MMP13 and p62 were significantly increased (P < 0.01). Compared with model group, the cartilage morphology of mice in tannic acid group was improved, OARSI score was significantly reduced (P < 0.05), the protein expression levels of Col-II, PINK1, Parkin and LC3B in cartilage tissue were significantly increased (P < 0.01), while the protein expression levels of IL-1β, MMP13 and p62 were significantly decreased (P < 0.01). The cell experiment results showed that IL-1β-induced chondrocyte viability was significantly reduced (P < 0.01), IL-1β, MMP13 protein and mRNA expression levels were significantly increased (P < 0.01), Col-II protein and mRNA expression levels were significantly reduced (P < 0.01), LC3-II/I, PINK1, Parkin protein expression levels were significantly reduced (P < 0.05, 0.01), p62 protein expression level was significantly increased (P < 0.05), intracellular ROS accumulation was increased (P < 0.01), mitochondrial membrane potential was decreased (P < 0.01), and autophagosome was decreased. Compared with model group, cell viability in tannic acid group was significantly increased (P < 0.05, 0.01), ROS accumulation significantly was decreased (P < 0.01), mitochondrial membrane potential was recovered (P < 0.05), IL-1β, MMP13 protein and mRNA expression levels were significantly decreased (P < 0.05, 0.01), Col-II protein and mRNA expression levels were significantly increased (P < 0.05, 0.01), p62 protein expression level was significantly decreased (P < 0.01), LC3-II/I, PINK1 and Parkin protein expression levels were significantly increased (P < 0.01). After the combined use of mitochondrial autophagy inhibitor Mdivi-1, the therapeutic effect of tannic acid on chondrocytes was reversed (P < 0.05, 0.01). Conclusion Tannic acid alleviates articular cartilage damage and delays the progression of KOA by promoting chondrocyte mitophagy through PINK1/Parkin signaling pathway., authors=GAN Chun, FU Danqing, DAI Haoqiang, XIA Chenjie, authorsList=GAN Chun, FU Danqing, DAI Haoqiang, XIA Chenjie, authorCompany=null, correspAuthors=null, authorNote=null, correspAuthorsNote=null, copyrightStatement=null, copyrightOwner=null, extLink=null, articleAbsUrl=null, sourceXml=null, magXml=null, pdfUrl=null, pdf=null, pdfFileSize=null, pdfExtLink=null, richHtmlUrl=null, mobilePdfUrl=null, reviewReport=null, pdfFirstPage=null, abstractGraph=null, abstractGraphContent=null, abstractVideo=null, citation=null, cebUrl=null, magXmlContent=null, mapNumber=null, fund=null), CN=ArticleExt(id=1304388157718421878, articleId=1304388157219299701, tenantId=1146029695717560320, journalId=1302319053441957962, language=CN, title=基于PINK1/Parkin信号通路研究鞣酸促进软骨细胞线粒体自噬改善小鼠膝骨关节炎的机制, columnId=1304140191707456168, journalTitle=中草药, columnName=药理与临床, runingTitle=null, highlight=null, articleAbstract=目的 基于PTEN诱导激酶1（PTEN induced putative kinase 1，PINK1）/帕金蛋白（Parkin）通路探讨鞣酸促进软骨细胞线粒体自噬并减轻小鼠膝骨关节炎（knee osteoarthritis，KOA）的作用机制。方法 采用内侧半月板失稳手术构建小鼠KOA模型，设置假手术组、模型组和鞣酸低、高剂量（25、50 mg/kg）组，给药干预8周。通过影像学、番红O-固绿染色和甲苯胺蓝染色观察关节软骨病理变化；免疫组化检测软骨组织中Ⅱ型胶原蛋白（collagen II，Col-II）、基质金属蛋白酶13（matrix metallopeptidase 13，MMP13）、白细胞介素-1β（interleukin-1β，IL-1β）、PINK1、Parkin、p62和微管相关蛋白轻链3B（microtubule - associated protein light chain 3B，LC3B）蛋白表达。采用IL-1β刺激小鼠ATDC5软骨细胞，给予鞣酸干预后，CCK-8法检测细胞活力；Western blotting和qRT-PCR检测Col-II、MMP13和IL-1β蛋白及mRNA表达；Western blotting检测线粒体自噬相关蛋白PINK1、Parkin、p62和LC3-II/I蛋白表达；免疫荧光检测活性氧（reactive oxygen species，ROS）和线粒体膜电位变化；透射电镜观察线粒体自噬水平；并利用线粒体自噬抑制剂Mdivi-1进行反向机制验证。结果 与假手术组比较，模型组小鼠软骨严重磨损，OARSI评分显著升高（P ＜0.01），软骨组织Col-II、PINK1、Parkin和LC3B蛋白表达水平显著降低（P ＜0.01）、IL-1β、MMP13和p62蛋白表达水平显著升高（P ＜0.01）；与模型组比较，鞣酸组小鼠软骨形态得到改善，OARSI评分显著降低（P ＜0.05），软骨组织Col-II、PINK1、Parkin和LC3B蛋白表达水平显著升高（P ＜0.01），IL-1β、MMP13和p62蛋白表达水平显著降低（P ＜0.01）。细胞实验结果显示，IL-1β诱导的软骨细胞活力显著降低（P ＜0.01），IL-1β、MMP13蛋白和mRNA表达水平显著升高（P ＜0.01），Col-II蛋白和mRNA表达水平显著降低（P ＜0.01），LC3-II/I、PINK1、Parkin蛋白表达水平显著降低（P ＜0.05、0.01），p62蛋白表达水平显著升高（P ＜0.05），细胞内ROS积累增加（P ＜0.01），线粒体膜电位下降（P ＜0.01），自噬小体减少；与模型组比较，鞣酸组细胞活力升高（P ＜0.05、0.01），ROS积累显著减少（P ＜0.01），线粒体膜电位恢复（P ＜0.05），IL-1β、MMP13蛋白和mRNA表达水平显著降低（P ＜0.05、0.01），Col-II蛋白和mRNA表达水平显著升高（P ＜0.05、0.01），p62蛋白表达水平显著降低（P ＜0.01），LC3-II/I、PINK1、Parkin蛋白表达水平显著升高（P ＜0.01）；联合使用线粒体自噬抑制剂Mdivi-1后，鞣酸对软骨细胞的作用被逆转（P ＜0.05、0.01）。结论 鞣酸通过PINK1/Parkin信号通路促进软骨细胞线粒体自噬，缓解关节软骨退变，从而延缓KOA进展。, authors=甘纯1 , 傅丹青2 , 戴浩强1 , 夏臣杰1 , authorsList=甘纯, 傅丹青, 戴浩强, 夏臣杰, authorCompany=1 宁波大学附属李惠利医院 关节与运动医学科, 浙江 宁波 315040; et al . Na(v)1.7 as a chondrocyte regulator and therapeutic target for osteoarthritis [J]. Nature , 2024, 625(7995): 557-565.et al . Mitophagy in cell death regulation: Insights into mechanisms and disease implications [J]. Biomolecules , 2024, 14(10): 1270.et al . Urolithin A improves mitochondrial health, reduces cartilage degeneration, and alleviates pain in osteoarthritis [J]. Aging Cell , 2022, 21(8): e13662.Nat Cell Biol , 2024, 26(10): 1639-1651.et al . Treating osteoarthritis pain: Mechanisms of action of acetaminophen, nonsteroidal anti-inflammatory drugs, opioids, and nerve growth factor antibodies [J]. Postgrad Med , 2021, 133(8): 879-894.et al . Prevention and treatment of inflammatory arthritis with traditional Chinese medicine: Underlying mechanisms based on cell and molecular targets [J]. Ageing Res Rev , 2023, 89: 101981.et al . Quercetin alleviates rat osteoarthritis by inhibiting inflammation and apoptosis of chondrocytes, modulating synovial macrophages polarization to M2 macrophages [J]. Free Radic Biol Med , 2019, 145: 146-160.et al . Curcumin exerts chondroprotective effects against osteoarthritis by promoting AMPK/PINK1/Parkin-mediated mitophagy [J]. Biomed Pharmacother , 2022, 151: 113092.et al . Icariin inhibits chondrocyte ferroptosis and alleviates osteoarthritis by enhancing the SLC7A11/GPX4 signaling [J]. Int Immunopharmacol , 2024, 133: 112010.et al . Pharmacological effects and mechanisms of tannic acid [J]. Biomed Pharmacother , 2022, 154: 113561.et al . Tannic acid exhibits anti-inflammatory effects on formalin-induced paw edema model of inflammation in rats [J]. Hum Exp Toxicol , 2019, 38(11): 1296-1301.et al . Tannic acid-cerium nanoenzymes serve as broad-spectrum antioxidants to alleviate acute kidney injury by modulating macrophage polarization, mitophagy and endoplasmic reticulum stress [J]. J Control Release , 2025, 380: 892-909.et al . Punicalagin prevents inflammation in LPS-induced RAW264.7 macrophages by inhibiting FoxO3a/autophagy signaling pathway [J]. Nutrients , 2019, 11(11): 2794.et al . Multi-targeted protection of acetaminophen-induced hepatotoxicity in mice by tannic acid [J]. Int Immunopharmacol , 2017, 47: 95-105.Ann Intern Med , 2024, 177(9): ITC129-ITC144.et al . Mitochondrial quality control in cartilage damage and osteoarthritis: New insights and potential therapeutic targets [J]. Osteoarthr Cartil , 2022, 30(3): 395-405.et al . The role of mitochondrial autophagy in osteoarthritis [J]. iScience , 2024, 27(9): 110741.et al . The physiological metabolite α-ketoglutarate ameliorates osteoarthritis by regulating mitophagy and oxidative stress [J]. Redox Biol , 2023, 62: 102663.et al . Mitophagy in degenerative joint diseases [J]. Autophagy , 2021, 17(9): 2082-2092.et al . Koumine inhibits IL-1β-induced chondrocyte inflammation and ameliorates extracellular matrix degradation in osteoarthritic cartilage through activation of PINK1/Parkin-mediated mitochondrial autophagy [J]. Biomed Pharmacother , 2024, 173: 116273.et al . Tannic acid suppresses HBV replication via the regulation of NF-κB, MAPKs, and autophagy in HepG2.2.15 cells [J]. J Agric Food Chem , 2023, 71(29): 11069-11079.et al . Molecular mechanisms and physiological functions of mitophagy [J]. EMBO J , 2021, 40(3): EMBJ2020104705.et al . MFN2 contributes to metabolic disorders and inflammation in the aging of rat chondrocytes and osteoarthritis [J]. Osteoarthr Cartil , 2020, 28(8): 1079-1091.et al . Mitochondrial respiratory activity is altered in osteoarthritic human articular chondrocytes [J]. Arthritis Rheum , 2003, 48(3): 700-708.)
中草药
|药理与临床
2026
, 57
(13) :
5109
-5119
基于PINK1/Parkin信号通路研究鞣酸促进软骨细胞线粒体自噬改善小鼠膝骨关节炎的机制
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作者信息
通讯作者:
夏臣杰
作者简介:
甘纯: 甘纯，硕士研究生，从事骨关节疾病治疗研究。E-mail:2311140034@nbu.edu.cn
Mechanism of tannic acid in promoting mitochondrial autophagy in chondrocytes and improving knee osteoarthritis in mice based on PINK1/Parkin signaling pathway
Affiliations
doi: 10.7501/j.issn.0253-2670.2026.13.014
文章导航
目的 基于PTEN诱导激酶1（PTEN induced putative kinase 1，PINK1）/帕金蛋白（Parkin）通路探讨鞣酸促进软骨细胞线粒体自噬并减轻小鼠膝骨关节炎（knee osteoarthritis，KOA）的作用机制。方法 采用内侧半月板失稳手术构建小鼠KOA模型，设置假手术组、模型组和鞣酸低、高剂量（25、50 mg/kg）组，给药干预8周。通过影像学、番红O-固绿染色和甲苯胺蓝染色观察关节软骨病理变化；免疫组化检测软骨组织中Ⅱ型胶原蛋白（collagen II，Col-II）、基质金属蛋白酶13（matrix metallopeptidase 13，MMP13）、白细胞介素-1β（interleukin-1β，IL-1β）、PINK1、Parkin、p62和微管相关蛋白轻链3B（microtubule - associated protein light chain 3B，LC3B）蛋白表达。采用IL-1β刺激小鼠ATDC5软骨细胞，给予鞣酸干预后，CCK-8法检测细胞活力；Western blotting和qRT-PCR检测Col-II、MMP13和IL-1β蛋白及mRNA表达；Western blotting检测线粒体自噬相关蛋白PINK1、Parkin、p62和LC3-II/I蛋白表达；免疫荧光检测活性氧（reactive oxygen species，ROS）和线粒体膜电位变化；透射电镜观察线粒体自噬水平；并利用线粒体自噬抑制剂Mdivi-1进行反向机制验证。结果 与假手术组比较，模型组小鼠软骨严重磨损，OARSI评分显著升高（P ＜0.01），软骨组织Col-II、PINK1、Parkin和LC3B蛋白表达水平显著降低（P ＜0.01）、IL-1β、MMP13和p62蛋白表达水平显著升高（P ＜0.01）；与模型组比较，鞣酸组小鼠软骨形态得到改善，OARSI评分显著降低（P ＜0.05），软骨组织Col-II、PINK1、Parkin和LC3B蛋白表达水平显著升高（P ＜0.01），IL-1β、MMP13和p62蛋白表达水平显著降低（P ＜0.01）。细胞实验结果显示，IL-1β诱导的软骨细胞活力显著降低（P ＜0.01），IL-1β、MMP13蛋白和mRNA表达水平显著升高（P ＜0.01），Col-II蛋白和mRNA表达水平显著降低（P ＜0.01），LC3-II/I、PINK1、Parkin蛋白表达水平显著降低（P ＜0.05、0.01），p62蛋白表达水平显著升高（P ＜0.05），细胞内ROS积累增加（P ＜0.01），线粒体膜电位下降（P ＜0.01），自噬小体减少；与模型组比较，鞣酸组细胞活力升高（P ＜0.05、0.01），ROS积累显著减少（P ＜0.01），线粒体膜电位恢复（P ＜0.05），IL-1β、MMP13蛋白和mRNA表达水平显著降低（P ＜0.05、0.01），Col-II蛋白和mRNA表达水平显著升高（P ＜0.05、0.01），p62蛋白表达水平显著降低（P ＜0.01），LC3-II/I、PINK1、Parkin蛋白表达水平显著升高（P ＜0.01）；联合使用线粒体自噬抑制剂Mdivi-1后，鞣酸对软骨细胞的作用被逆转（P ＜0.05、0.01）。结论 鞣酸通过PINK1/Parkin信号通路促进软骨细胞线粒体自噬，缓解关节软骨退变，从而延缓KOA进展。
鞣酸
/
膝骨关节炎
/
软骨细胞
/
线粒体自噬
/
PINK1/Parkin通路
Objective To investigate the mechanism of tannic acid in promoting mitochondrial autophagy in chondrocytes and improving knee osteoarthritis (KOA) in mice based on PINK1/Parkin signaling pathway. Methods A mouse KOA model was established via destabilization of medial meniscus surgery. Sham group, model group and tannic acid low-, high-dose (25, 50 mg/kg) groups were set up, drugs were given for intervention for eight weeks. Joint cartilage pathology was assessed by imaging, safranin O-fast green staining and toluidine blue staining. Immunohistochemistry was used to detect the expressions of collagen II (Col-II), matrix metalloproteinase 13 (MMP13), interleukin-1β (IL-1β), PINK1, Parkin, p62 and microtubule-associated protein light chain 3B (LC3B) in cartilage tissue. ATDC5 mouse chondrocytes were stimulated with IL-1β and then treated with tannic acid. Cell viability was measured by CCK-8 assay. Western blotting and qRT-PCR were used to detect the protein and mRNA expressions of Col-II, MMP13 and IL-1β. Western blotting was used to detect the expressions of mitophagy-related proteins PINK1, Parkin, p62 and LC3-II/I. Changes in reactive oxygen species (ROS) and mitochondrial membrane potential were detected by immunofluorescence. Mitochondrial autophagy level was observed by transmission electron microscopy. And reverse mechanism validation was performed using the mitochondrial autophagy inhibitor Mdivi-1. Results Compared with sham group, the cartilage of mice in model group was severely worn, OARSI score was significantly increased (P < 0.01), the protein expression levels of Col-II, PINK1, Parkin and LC3B in cartilage tissue were significantly reduced (P < 0.01), while the protein expression levels of IL-1β, MMP13 and p62 were significantly increased (P < 0.01). Compared with model group, the cartilage morphology of mice in tannic acid group was improved, OARSI score was significantly reduced (P < 0.05), the protein expression levels of Col-II, PINK1, Parkin and LC3B in cartilage tissue were significantly increased (P < 0.01), while the protein expression levels of IL-1β, MMP13 and p62 were significantly decreased (P < 0.01). The cell experiment results showed that IL-1β-induced chondrocyte viability was significantly reduced (P < 0.01), IL-1β, MMP13 protein and mRNA expression levels were significantly increased (P < 0.01), Col-II protein and mRNA expression levels were significantly reduced (P < 0.01), LC3-II/I, PINK1, Parkin protein expression levels were significantly reduced (P < 0.05, 0.01), p62 protein expression level was significantly increased (P < 0.05), intracellular ROS accumulation was increased (P < 0.01), mitochondrial membrane potential was decreased (P < 0.01), and autophagosome was decreased. Compared with model group, cell viability in tannic acid group was significantly increased (P < 0.05, 0.01), ROS accumulation significantly was decreased (P < 0.01), mitochondrial membrane potential was recovered (P < 0.05), IL-1β, MMP13 protein and mRNA expression levels were significantly decreased (P < 0.05, 0.01), Col-II protein and mRNA expression levels were significantly increased (P < 0.05, 0.01), p62 protein expression level was significantly decreased (P < 0.01), LC3-II/I, PINK1 and Parkin protein expression levels were significantly increased (P < 0.01). After the combined use of mitochondrial autophagy inhibitor Mdivi-1, the therapeutic effect of tannic acid on chondrocytes was reversed (P < 0.05, 0.01). Conclusion Tannic acid alleviates articular cartilage damage and delays the progression of KOA by promoting chondrocyte mitophagy through PINK1/Parkin signaling pathway.
tannic acid
/
knee osteoarthritis
/
chondrocyte
/
mitophagy
/
PINK1/Parkin pathway
甘纯, 傅丹青, 戴浩强, 夏臣杰.
基于PINK1/Parkin信号通路研究鞣酸促进软骨细胞线粒体自噬改善小鼠膝骨关节炎的机制.
中草药,
2026
, 57
(13)
: 5109
-5119
.
DOI: 10.7501/j.issn.0253-2670.2026.13.014
GAN Chun, FU Danqing, DAI Haoqiang, XIA Chenjie.
Mechanism of tannic acid in promoting mitochondrial autophagy in chondrocytes and improving knee osteoarthritis in mice based on PINK1/Parkin signaling pathway[J].
Chinese Traditional and Herbal Drugs ,
2026
, 57
(13)
: 5109
-5119
.
DOI: 10.7501/j.issn.0253-2670.2026.13.014
国家自然科学基金资助项目 (82104885); 浙江省自然科学基金资助项目 (ZCLQN25H2701); 宁波市自然科学基金资助项目 (2023J215); 宁波市医学重点学科“运动医学”项目 (2026-A01); 宁波市医疗卫生高端团队重大攻坚项目 (2022020102)
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Fu W Y, Vasylyev D, Bi Y F, et al . Na(v)1.7 as a chondrocyte regulator and therapeutic target for osteoarthritis [J]. Nature , 2024, 625(7995): 557-565.et al . Mitophagy in cell death regulation: Insights into mechanisms and disease implications [J]. Biomolecules , 2024, 14(10): 1270.et al . Urolithin A improves mitochondrial health, reduces cartilage degeneration, and alleviates pain in osteoarthritis [J]. Aging Cell , 2022, 21(8): e13662.Nat Cell Biol , 2024, 26(10): 1639-1651.et al . Treating osteoarthritis pain: Mechanisms of action of acetaminophen, nonsteroidal anti-inflammatory drugs, opioids, and nerve growth factor antibodies [J]. Postgrad Med , 2021, 133(8): 879-894.et al . Prevention and treatment of inflammatory arthritis with traditional Chinese medicine: Underlying mechanisms based on cell and molecular targets [J]. Ageing Res Rev , 2023, 89: 101981.et al . Quercetin alleviates rat osteoarthritis by inhibiting inflammation and apoptosis of chondrocytes, modulating synovial macrophages polarization to M2 macrophages [J]. Free Radic Biol Med , 2019, 145: 146-160.et al . Curcumin exerts chondroprotective effects against osteoarthritis by promoting AMPK/PINK1/Parkin-mediated mitophagy [J]. Biomed Pharmacother , 2022, 151: 113092.et al . Icariin inhibits chondrocyte ferroptosis and alleviates osteoarthritis by enhancing the SLC7A11/GPX4 signaling [J]. Int Immunopharmacol , 2024, 133: 112010.et al . Pharmacological effects and mechanisms of tannic acid [J]. Biomed Pharmacother , 2022, 154: 113561.et al . Tannic acid exhibits anti-inflammatory effects on formalin-induced paw edema model of inflammation in rats [J]. Hum Exp Toxicol , 2019, 38(11): 1296-1301.et al . Tannic acid-cerium nanoenzymes serve as broad-spectrum antioxidants to alleviate acute kidney injury by modulating macrophage polarization, mitophagy and endoplasmic reticulum stress [J]. J Control Release , 2025, 380: 892-909.et al . Punicalagin prevents inflammation in LPS-induced RAW264.7 macrophages by inhibiting FoxO3a/autophagy signaling pathway [J]. Nutrients , 2019, 11(11): 2794.et al . Multi-targeted protection of acetaminophen-induced hepatotoxicity in mice by tannic acid [J]. Int Immunopharmacol , 2017, 47: 95-105.Ann Intern Med , 2024, 177(9): ITC129-ITC144.et al . Mitochondrial quality control in cartilage damage and osteoarthritis: New insights and potential therapeutic targets [J]. Osteoarthr Cartil , 2022, 30(3): 395-405.et al . The role of mitochondrial autophagy in osteoarthritis [J]. iScience , 2024, 27(9): 110741.et al . The physiological metabolite α-ketoglutarate ameliorates osteoarthritis by regulating mitophagy and oxidative stress [J]. Redox Biol , 2023, 62: 102663.et al . Mitophagy in degenerative joint diseases [J]. Autophagy , 2021, 17(9): 2082-2092.et al . Koumine inhibits IL-1β-induced chondrocyte inflammation and ameliorates extracellular matrix degradation in osteoarthritic cartilage through activation of PINK1/Parkin-mediated mitochondrial autophagy [J]. Biomed Pharmacother , 2024, 173: 116273.et al . Tannic acid suppresses HBV replication via the regulation of NF-κB, MAPKs, and autophagy in HepG2.2.15 cells [J]. J Agric Food Chem , 2023, 71(29): 11069-11079.et al . Molecular mechanisms and physiological functions of mitophagy [J]. EMBO J , 2021, 40(3): EMBJ2020104705.et al . MFN2 contributes to metabolic disorders and inflammation in the aging of rat chondrocytes and osteoarthritis [J]. Osteoarthr Cartil , 2020, 28(8): 1079-1091.et al . Mitochondrial respiratory activity is altered in osteoarthritic human articular chondrocytes [J]. Arthritis Rheum , 2003, 48(3): 700-708.
2026年第57卷第13期
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doi: 10.7501/j.issn.0253-2670.2026.13.014
接收时间：2025-12-31
首发时间：2026-09-09
https://castjournals.cast.org.cn/joweb/zcy/CN/10.7501/j.issn.0253-2670.2026.13.014
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2种不同金属材料的力学参数
科 属数 种数 占总种数比例 属 种数 占总种数比例 鹅膏菌科Amanitaceae 2 11 5.26 鹅膏菌属 Amanita 10 4.78 小菇科 Mycenaceae 2 12 5.74 丝盖伞属 Inocybe 5 2.39 多孔菌科 Polyporaceae 8 14 6.70 蜡蘑属 Laccaria 5 2.39 红菇科 Russulaceae 3 23 11.00 小皮伞属 Marasmius 6 2.87 小菇属 Mycena 11 5.26 光柄菇属 Pluteus 5 2.39 红菇属 Russula 17 8.13 栓菌属 Trametes 5 2.39
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