Melatonin Attenuates Intervertebral Disk Degeneration via Maintaining Cartilaginous Endplate Integrity in Rats

التفاصيل البيبلوغرافية
العنوان: Melatonin Attenuates Intervertebral Disk Degeneration via Maintaining Cartilaginous Endplate Integrity in Rats
المؤلفون: Huilin Yang, Jiacheng Du, Dechun Geng, Yijie Liu, Li Ni, Hong Zhou, Pengfei Zhu, Jiayi Lin, Fanchen Kong, Xiexing Wu, Haiqing Mao, Xiaoping Li
المصدر: Frontiers in Physiology, Vol 12 (2021)
Frontiers in Physiology
بيانات النشر: Frontiers Media S.A., 2021.
سنة النشر: 2021
مصطلحات موضوعية: medicine.medical_specialty, Lipopolysaccharide, Physiology, Inflammation, melatonin, NF-κB, Melatonin, 03 medical and health sciences, chemistry.chemical_compound, 0302 clinical medicine, Physiology (medical), Internal medicine, hemic and lymphatic diseases, matrix degradation, medicine, QP1-981, Receptor, neoplasms, osteoclastogenesis, Original Research, biology, intervertebral disk degeneration, Intervertebral disk, Endocrinology, chemistry, RANKL, inflammation, 030220 oncology & carcinogenesis, biology.protein, medicine.symptom, Luzindole, 030217 neurology & neurosurgery, medicine.drug, cartilaginous endplates
الوصف: ObjectiveThe aim of this study is to verify whether melatonin (Mel) could mitigate intervertebral disk degeneration (IVDD) in rats and to investigate the potential mechanism of it.MethodA rat acupuncture model of IVDD was established with intraperitoneal injection of Mel. The effect of Mel on IVDD was analyzed via radiologic and histological evaluations. The specific Mel receptors were investigated in both the nucleus pulposus (NP) and cartilaginous endplates (EPs). In vitro, EP cartilaginous cells (EPCs) were treated by different concentrations of Mel under lipopolysaccharide (LPS) and Luzindole conditions. In addition, LPS-induced inflammatory response and matrix degradation following nuclear factor kappa-B (NF-κB) pathway activation were investigated to confirm the potential mechanism of Mel on EPCs.ResultsThe percent disk height index (%DHI) and MRI signal decreased after initial puncture in the degeneration group compared with the control group, while Mel treatment protected disk height from decline and prevented the loss of water during the degeneration process. In the meantime, the histological staining of the Mel groups showed more integrity and well-ordered construction of the NP and EPs in both low and high concentration than that of the degeneration group. In addition, more deep-brown staining of type II collagen (Coll-II) was shown in the Mel groups compared with the degeneration group. Furthermore, in rat samples, immunohistochemical staining showed more positive cells of Mel receptors 1a and 1b in the EPs, instead of in the NP. Moreover, evident osteochondral lacuna formation was observed in rat EPs in the degeneration group; after Mel treatment, the osteochondral destruction alleviated accompanying fewer receptor activator for nuclear factor-κB ligand (RANKL) and tartrate-resistant acid phosphatase (TRAP)-stained positive cells expressed in the EPs. In vitro, Mel could promote the proliferation of EPCs, which protected EPCs from degeneration under LPS treatment. What is more, Mel downregulated the inflammatory response and matrix degradation of EPCs activated by NF-κB pathway through binding to its specific receptors.ConclusionThese results indicate that Mel protects the integrity of the EPs and attenuates IVDD by binding to the Mel receptors in the EPs. It may alleviate the inflammatory response and matrix degradation of EPCs activated by NF-κB pathway.
اللغة: English
URL الوصول: https://explore.openaire.eu/search/publication?articleId=doi_dedup___::1a1d1085d26c15dbb62c3111bf19f0b7
https://www.frontiersin.org/articles/10.3389/fphys.2021.672572/full
حقوق: OPEN
رقم الأكسشن: edsair.doi.dedup.....1a1d1085d26c15dbb62c3111bf19f0b7
قاعدة البيانات: OpenAIRE