این سایت در حال حاضر پشتیبانی نمی شود و امکان دارد داده های نشریات بروز نباشند
Iranian Journal of Basic Medical Sciences، جلد ۲۵، شماره ۵، صفحات ۶۳۵-۶۴۲
عنوان فارسی
چکیده فارسی مقاله
کلیدواژه‌های فارسی مقاله
عنوان انگلیسی Transient receptor potential vanilloid type-1 regulates periodontal disease damage via the PI3K/AKT signaling pathway
چکیده انگلیسی مقاله Objective(s): This study aimed to investigate the function of transient receptor potential vanilloid 1 (TRPV1) in regulating periodontal lesions. In addition, we explored the underlying mechanism of the phosphatidylinositol 3-kinase/protein kinase B (PI3K/AKT) pathway.Materials and Methods: Lipopolysaccharide (LPS) stimulation of human periodontal ligament cells (HPDLCs) was used to construct a periodontitis cell model, and experimental periodontitis (EP) rats were established by ligation. The mechanism by which TRPV1 regulates periodontitis was further verified by injecting the TRPV1 agonist capsaicin (CPS) and antagonist capsazepine (CPZ) into the gingiva of rats; the alveolar bone losses in each group were measured by stereomicroscopy. Real-time quantitative polymerase chain reaction (qRT-PCR) and Western blotting (WB) were used to research the expression of TRPV1 and proinflammatory cytokines, and WB was performed to test the phosphorylation of PI3K and AKT.Results: In vitro experiments showed that LPS induced the upregulation of TRPV1 and proinflammatory cytokines and promoted the phosphorylation of PI3K and AKT proteins in HPDLCs, which was consistent with their expression in the rat periodontitis model. Moreover, in vivo studies indicated that CPZ had anti-inflammatory effects through the PI3K/AKT pathway and inhibited bone loss induced by periodontal ligation in rats, while CPS had the opposite effect.Conclusion: TRPV1 was involved in the process of alveolar bone defects and the inflammatory response in rats with periodontitis induced by ligation. Its mechanism might be related to the phosphorylation of related proteins in the PI3K/AKT signaling pathway.
کلیدواژه‌های انگلیسی مقاله alveolar bone loss, Cytokines, Periodontitis, PI3K/Akt, TRPV1
نویسندگان مقاله | xiaolu xu
Stomatological Hospital of Chongqing Medical University, Chongqing, China|Chongqing Key Laboratory of Oral Diseases and Biomedical Sciences, Chongqing, China|Chongqing Municipal Key Laboratory of Oral Biomedical Engineering of Higher Education, Chongqing, China


| Yue-heng Li
Stomatological Hospital of Chongqing Medical University, Chongqing, China|Chongqing Key Laboratory of Oral Diseases and Biomedical Sciences, Chongqing, China|Chongqing Municipal Key Laboratory of Oral Biomedical Engineering of Higher Education, Chongqing, China


| Zhengyan Yang
Stomatological Hospital of Chongqing Medical University, Chongqing, China|Chongqing Key Laboratory of Oral Diseases and Biomedical Sciences, Chongqing, China|Chongqing Municipal Key Laboratory of Oral Biomedical Engineering of Higher Education, Chongqing, China


| Zhi Zhou
Stomatological Hospital of Chongqing Medical University, Chongqing, China|Chongqing Key Laboratory of Oral Diseases and Biomedical Sciences, Chongqing, China|Chongqing Municipal Key Laboratory of Oral Biomedical Engineering of Higher Education, Chongqing, China
نشانی اینترنتی https://ijbms.mums.ac.ir/article_20269.html
فایل مقاله فایلی برای مقاله ذخیره نشده است
کد مقاله (doi)
زبان مقاله منتشر شده en
موضوعات مقاله منتشر شده
نوع مقاله منتشر شده Original Article
برگشت به: صفحه اول پایگاه   |   نسخه مرتبط   |   نشریه مرتبط   |   فهرست نشریات