• 文献检索
  • 文档翻译
  • 深度研究
  • 学术资讯
  • Suppr Zotero 插件Zotero 插件
  • 邀请有礼
  • 套餐&价格
  • 历史记录
应用&插件
Suppr Zotero 插件Zotero 插件浏览器插件Mac 客户端Windows 客户端微信小程序
定价
高级版会员购买积分包购买API积分包
服务
文献检索文档翻译深度研究API 文档MCP 服务
关于我们
关于 Suppr公司介绍联系我们用户协议隐私条款
关注我们

Suppr 超能文献

核心技术专利：CN118964589B侵权必究
粤ICP备2023148730 号-1Suppr @ 2026

文献检索

告别复杂PubMed语法，用中文像聊天一样搜索，搜遍4000万医学文献。AI智能推荐，让科研检索更轻松。

立即免费搜索

文件翻译

保留排版，准确专业，支持PDF/Word/PPT等文件格式，支持 12+语言互译。

免费翻译文档

深度研究

AI帮你快速写综述，25分钟生成高质量综述，智能提取关键信息，辅助科研写作。

立即免费体验

瘦素通过磷酸肌醇3激酶/蛋白激酶B/雷帕霉素哺乳动物靶标信号通路抑制自噬来保护软骨细胞。

Leptin protects chondrocytes by inhibiting autophagy via phosphoinositide 3 kinase/protein kinase B/mammalian target of rapamycin signaling pathway.

作者信息

Li Ping, Jiang Weiqian, Yang Qiming, Lu Yang, Zhang Jian

机构信息

Department of Orthopaedics, The First Affiliated Hospital of Chongqing Medical University, No.1, You-Yi Road, district of Yu-Zhong, Chongqing, 400016, China.

Department of Orthopaedics, Chongqing Hospital of Traditional Chinese Medicine, Chongqing, 400021, China.

出版信息

Heliyon. 2024 Aug 6;10(15):e35665. doi: 10.1016/j.heliyon.2024.e35665. eCollection 2024 Aug 15.

DOI:10.1016/j.heliyon.2024.e35665
PMID:39170379
原文链接:https://pmc.ncbi.nlm.nih.gov/articles/PMC11336819/
Abstract

Leptin has been widely studied and found to have a significant impact on the development of osteoarthritis (OA). However, there are conflicting findings regarding the impact of leptin on chondrocytes. The study aimed to examine the impact of leptin on human chondrocytes and rats with OA. In the in vitro experiment, cartilage tissue obtained from patients hospitalized for knee replacement due to OA was collected for primary culture of chondrocytes. The proliferation and apoptosis of chondrocytes were assessed using cell counting kit-8 and flow cytometry. Autophagy levels were evaluated through monodansylcadaverine staining, mRFP-GFP-LC3 fluorescence, and transmission electron microscopy. Additionally, the expression of autophagy-related genes and proteins was analyzed using qRT-PCR and western blotting. In the in vivo experiment, an OA rat model was established. Following treatment with leptin and leptin antagonists, the cartilage tissues were examined using histology analysis (hematoxylin-eosin and Safranin O/fast green staining) and immunohistochemical. Mankin's score was utilized to assess the severity of OA, while qRT-PCR and western blotting were employed to detect the expression of autophagy-related genes and proteins in the cartilage. The ability of leptin to protect chondrocytes is achieved through the inhibition of autophagy via phosphoinositide 3 kinase/protein kinase B/mammalian target of rapamycin signaling pathway.

摘要

瘦素已得到广泛研究，并发现其对骨关节炎（OA）的发展有重大影响。然而，关于瘦素对软骨细胞的影响存在相互矛盾的研究结果。该研究旨在探讨瘦素对人软骨细胞和OA大鼠的影响。在体外实验中，收集因OA住院接受膝关节置换手术患者的软骨组织用于软骨细胞原代培养。使用细胞计数试剂盒-8和流式细胞术评估软骨细胞的增殖和凋亡。通过单丹磺酰尸胺染色、mRFP-GFP-LC3荧光和透射电子显微镜评估自噬水平。此外，使用qRT-PCR和蛋白质免疫印迹法分析自噬相关基因和蛋白质的表达。在体内实验中，建立OA大鼠模型。在用瘦素和瘦素拮抗剂治疗后，使用组织学分析（苏木精-伊红和番红O/固绿染色）和免疫组织化学检查软骨组织。采用Mankin评分评估OA的严重程度，同时使用qRT-PCR和蛋白质免疫印迹法检测软骨中自噬相关基因和蛋白质的表达。瘦素保护软骨细胞的能力是通过磷脂酰肌醇3激酶/蛋白激酶B/雷帕霉素哺乳动物靶标信号通路抑制自噬来实现的。

https://cdn.ncbi.nlm.nih.gov/pmc/blobs/77ac/11336819/47d2caeb77a4/mmcfigs19.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/77ac/11336819/ccf6b2346259/gr1.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/77ac/11336819/2ff1e084d26c/gr2.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/77ac/11336819/e07e3106069d/gr3.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/77ac/11336819/c86a8c22ec1c/gr4.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/77ac/11336819/c51e0a238443/gr5.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/77ac/11336819/0b020111d54b/gr6.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/77ac/11336819/b28f6403c4f1/gr7.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/77ac/11336819/3e1e79419d07/mmcfigs1.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/77ac/11336819/39590282c6bb/mmcfigs2.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/77ac/11336819/9d819508d6f6/mmcfigs3.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/77ac/11336819/b70d5b8c1b72/mmcfigs4.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/77ac/11336819/e7ef941c7558/mmcfigs5.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/77ac/11336819/3ecb190b061f/mmcfigs6.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/77ac/11336819/c51505d996e1/mmcfigs7.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/77ac/11336819/9935727a4c8a/mmcfigs8.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/77ac/11336819/ea9609c73fb9/mmcfigs9.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/77ac/11336819/410e7451922b/mmcfigs10.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/77ac/11336819/fec075368e50/mmcfigs11.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/77ac/11336819/24f2956daf15/mmcfigs12.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/77ac/11336819/becea2998319/mmcfigs13.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/77ac/11336819/d1406feef5bf/mmcfigs14.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/77ac/11336819/09a06fb2fc7b/mmcfigs15.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/77ac/11336819/2ec3f353cfba/mmcfigs16.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/77ac/11336819/d3e7962b214c/mmcfigs17.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/77ac/11336819/354d92bfc597/mmcfigs18.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/77ac/11336819/47d2caeb77a4/mmcfigs19.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/77ac/11336819/ccf6b2346259/gr1.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/77ac/11336819/2ff1e084d26c/gr2.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/77ac/11336819/e07e3106069d/gr3.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/77ac/11336819/c86a8c22ec1c/gr4.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/77ac/11336819/c51e0a238443/gr5.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/77ac/11336819/0b020111d54b/gr6.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/77ac/11336819/b28f6403c4f1/gr7.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/77ac/11336819/3e1e79419d07/mmcfigs1.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/77ac/11336819/39590282c6bb/mmcfigs2.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/77ac/11336819/9d819508d6f6/mmcfigs3.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/77ac/11336819/b70d5b8c1b72/mmcfigs4.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/77ac/11336819/e7ef941c7558/mmcfigs5.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/77ac/11336819/3ecb190b061f/mmcfigs6.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/77ac/11336819/c51505d996e1/mmcfigs7.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/77ac/11336819/9935727a4c8a/mmcfigs8.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/77ac/11336819/ea9609c73fb9/mmcfigs9.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/77ac/11336819/410e7451922b/mmcfigs10.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/77ac/11336819/fec075368e50/mmcfigs11.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/77ac/11336819/24f2956daf15/mmcfigs12.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/77ac/11336819/becea2998319/mmcfigs13.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/77ac/11336819/d1406feef5bf/mmcfigs14.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/77ac/11336819/09a06fb2fc7b/mmcfigs15.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/77ac/11336819/2ec3f353cfba/mmcfigs16.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/77ac/11336819/d3e7962b214c/mmcfigs17.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/77ac/11336819/354d92bfc597/mmcfigs18.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/77ac/11336819/47d2caeb77a4/mmcfigs19.jpg

相似文献

1
Leptin protects chondrocytes by inhibiting autophagy via phosphoinositide 3 kinase/protein kinase B/mammalian target of rapamycin signaling pathway.瘦素通过磷酸肌醇3激酶/蛋白激酶B/雷帕霉素哺乳动物靶标信号通路抑制自噬来保护软骨细胞。
Heliyon. 2024 Aug 6;10(15):e35665. doi: 10.1016/j.heliyon.2024.e35665. eCollection 2024 Aug 15.
2
Intra-articular Injection of Chloramphenicol Reduces Articular Cartilage Degeneration in a Rabbit Model of Osteoarthritis.关节内注射氯霉素可减少兔骨关节炎模型中关节软骨的退变。
Clin Orthop Relat Res. 2019 Dec;477(12):2785-2797. doi: 10.1097/CORR.0000000000001016.
3
microRNA-206 is required for osteoarthritis development through its effect on apoptosis and autophagy of articular chondrocytes via modulating the phosphoinositide 3-kinase/protein kinase B-mTOR pathway by targeting insulin-like growth factor-1.miR-206 通过靶向胰岛素样生长因子-1 调控磷酸肌醇 3-激酶/蛋白激酶 B-雷帕霉素靶蛋白通路对关节软骨细胞凋亡和自噬的影响，从而促进骨关节炎的发生发展。
J Cell Biochem. 2019 Apr;120(4):5287-5303. doi: 10.1002/jcb.27803. Epub 2018 Oct 18.
4
ADSCs increase the autophagy of chondrocytes through decreasing miR-7-5p in Osteoarthritis rats by targeting ATG4A.脂肪间充质干细胞通过靶向 ATG4A 降低 miR-7-5p 增加骨关节炎大鼠软骨细胞自噬。
Int Immunopharmacol. 2023 Jul;120:110390. doi: 10.1016/j.intimp.2023.110390. Epub 2023 May 30.
5
Microbial Metabolite Sodium Butyrate Attenuates Cartilage Degradation by Restoring Impaired Autophagy and Autophagic Flux in Osteoarthritis Development.微生物代谢产物丁酸钠通过恢复骨关节炎发展过程中受损的自噬和自噬通量来减轻软骨降解。
Front Pharmacol. 2021 Apr 9;12:659597. doi: 10.3389/fphar.2021.659597. eCollection 2021.
6
Icariin alleviates osteoarthritis by regulating autophagy of chondrocytes by mediating PI3K/AKT/mTOR signaling.淫羊藿苷通过调节 PI3K/AKT/mTOR 信号通路介导的软骨细胞自噬来缓解骨关节炎。
Bioengineered. 2021 Dec;12(1):2984-2999. doi: 10.1080/21655979.2021.1943602.
7
Vitamin D plays a protective role in osteoarthritis by regulating AMPK/mTOR signalling pathway to activate chondrocyte autophagy.维生素 D 通过调节 AMPK/mTOR 信号通路激活软骨细胞自噬，在骨关节炎中发挥保护作用。
Clin Exp Rheumatol. 2024 Mar;42(3):736-745. doi: 10.55563/clinexprheumatol/chmuts. Epub 2023 Oct 19.
8
LncRNA SNHG1 overexpression alleviates osteoarthritis via activating PI3K/Akt signal pathway and suppressing autophagy.长链非编码 RNA SNHG1 通过激活 PI3K/Akt 信号通路和抑制自噬来减轻骨关节炎。
Immunobiology. 2024 May;229(3):152799. doi: 10.1016/j.imbio.2024.152799. Epub 2024 Apr 6.
9
Exosomal miR-429 derived from adipose-derived stem cells ameliorated chondral injury in osteoarthritis via autophagy by targeting FEZ2.脂肪间充质干细胞来源的外泌体 miR-429 通过靶向 FEZ2 促进自噬改善骨关节炎软骨损伤。
Int Immunopharmacol. 2023 Jul;120:110315. doi: 10.1016/j.intimp.2023.110315. Epub 2023 May 27.
10
Inhibition of PI3K/AKT/mTOR signaling pathway promotes autophagy of articular chondrocytes and attenuates inflammatory response in rats with osteoarthritis.抑制 PI3K/AKT/mTOR 信号通路可促进骨关节炎大鼠关节软骨细胞自噬并减轻炎症反应。
Biomed Pharmacother. 2017 May;89:1252-1261. doi: 10.1016/j.biopha.2017.01.130. Epub 2017 Mar 17.

本文引用的文献

1
Leptin Promotes the Proliferation and Neuronal Differentiation of Neural Stem Cells through the Cooperative Action of MAPK/ERK1/2, JAK2/STAT3 and PI3K/AKT Signaling Pathways.瘦素通过 MAPK/ERK1/2、JAK2/STAT3 和 PI3K/AKT 信号通路的协同作用促进神经干细胞的增殖和神经元分化。
Int J Mol Sci. 2023 Oct 13;24(20):15151. doi: 10.3390/ijms242015151.
2
Resistin targets TAZ to promote osteogenic differentiation through PI3K/AKT/mTOR pathway.抵抗素通过PI3K/AKT/mTOR信号通路作用于TAZ以促进成骨分化。
iScience. 2023 Jun 7;26(7):107025. doi: 10.1016/j.isci.2023.107025. eCollection 2023 Jul 21.
3
Beyond mechanical loading: The metabolic contribution of obesity in osteoarthritis unveils novel therapeutic targets.
超越机械负荷：肥胖在骨关节炎中的代谢作用揭示了新的治疗靶点。
Heliyon. 2023 Apr 25;9(5):e15700. doi: 10.1016/j.heliyon.2023.e15700. eCollection 2023 May.
4
Artemisinin relieves osteoarthritis by activating mitochondrial autophagy through reducing TNFSF11 expression and inhibiting PI3K/AKT/mTOR signaling in cartilage.青蒿素通过降低 TNFSF11 表达和抑制软骨中 PI3K/AKT/mTOR 信号通路激活线粒体自噬缓解骨关节炎。
Cell Mol Biol Lett. 2022 Jul 28;27(1):62. doi: 10.1186/s11658-022-00365-1.
5
mTOR substrate phosphorylation in growth control.mTOR 底物磷酸化在生长调控中的作用。
Cell. 2022 May 26;185(11):1814-1836. doi: 10.1016/j.cell.2022.04.013. Epub 2022 May 16.
6
Leptin in Osteoarthritis and Rheumatoid Arthritis: Player or Bystander?瘦素在骨关节炎和类风湿关节炎中的作用：是主角还是旁观者？
Int J Mol Sci. 2022 Mar 5;23(5):2859. doi: 10.3390/ijms23052859.
7
Fluoride regulates chondrocyte proliferation and autophagy via PI3K/AKT/mTOR signaling pathway.氟化物通过 PI3K/AKT/mTOR 信号通路调节软骨细胞增殖和自噬。
Chem Biol Interact. 2021 Nov 1;349:109659. doi: 10.1016/j.cbi.2021.109659. Epub 2021 Sep 16.
8
Leptin Induced TLR4 Expression via the JAK2-STAT3 Pathway in Obesity-Related Osteoarthritis.瘦素通过JAK2-STAT3信号通路诱导肥胖相关性骨关节炎中TLR4的表达。
Oxid Med Cell Longev. 2021 Aug 17;2021:7385160. doi: 10.1155/2021/7385160. eCollection 2021.
9
Level of Adiponectin, Leptin and Selected Matrix Metalloproteinases in Female Overweight Patients with Primary Gonarthrosis.原发性膝关节炎女性超重患者脂联素、瘦素及特定基质金属蛋白酶水平
J Clin Med. 2021 Mar 18;10(6):1263. doi: 10.3390/jcm10061263.
10
Control of the Autophagy Pathway in Osteoarthritis: Key Regulators, Therapeutic Targets and Therapeutic Strategies.控制骨关节炎自噬途径：关键调控因子、治疗靶点和治疗策略。
Int J Mol Sci. 2021 Mar 7;22(5):2700. doi: 10.3390/ijms22052700.