Xin Meng, Huijuan Qu, Xueying Zhang, Honghai Ji, Minmin Sun
{"title":"人参皂苷Rb3抑制氧化应激，减轻实验性牙周炎。","authors":"Xin Meng, Huijuan Qu, Xueying Zhang, Honghai Ji, Minmin Sun","doi":"10.1111/odi.15318","DOIUrl":null,"url":null,"abstract":"<p><strong>Objective: </strong>This study investigated the anti-inflammatory and antioxidative effects of ginsenoside Rb3 on experimental periodontitis.</p><p><strong>Methods: </strong>Experimental periodontitis was established by ligating the maxillary first molars. After 21 days of Rb3 treatment, rats were sacrificed for micro-CT and H&E staining analysis and serum assay. qPCR detected the expression of inflammatory genes. IF detected MAPKs pathway activation in periodontal tissues. The effects were determined using LPS-induced RAW264.7 cells. Gene expression levels were determined by qPCR. Intracellular ROS generation was detected by DCFH-DA staining and flow cytometry. WB detected the activation of signaling pathways.</p><p><strong>Results: </strong>Rb3 inhibited oxidative stress in experimental periodontitis, showing reduced gingivitis and alveolar bone resorption on H&E staining and micro-CT, and reduced iNOS mRNA in rats. Colorimetric results showed that Rb3 increased serum SOD and GSH-Px activities and decreased MDA levels in rats. IF analysis showed that Rb3 inhibited P38, ERK, and JNK activation. Rb3 pretreatment significantly decreased iNOS and IL-6 mRNA expression and ROS in Raw264.7 cells. WB analysis demonstrated that Rb3 blocked the activation of P38 and ERK.</p><p><strong>Conclusion: </strong>Rb3 inhibits the level of oxidative stress and attenuates gingivitis and alveolar bone resorption in rats via the MAPKs signaling pathway.</p>","PeriodicalId":19615,"journal":{"name":"Oral diseases","volume":" ","pages":""},"PeriodicalIF":2.9000,"publicationDate":"2025-03-24","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":"0","resultStr":"{\"title\":\"Ginsenoside Rb3 Inhibits Oxidative Stress and Alleviates Experimental Periodontitis in Rats.\",\"authors\":\"Xin Meng, Huijuan Qu, Xueying Zhang, Honghai Ji, Minmin Sun\",\"doi\":\"10.1111/odi.15318\",\"DOIUrl\":null,\"url\":null,\"abstract\":\"<p><strong>Objective: </strong>This study investigated the anti-inflammatory and antioxidative effects of ginsenoside Rb3 on experimental periodontitis.</p><p><strong>Methods: </strong>Experimental periodontitis was established by ligating the maxillary first molars. After 21 days of Rb3 treatment, rats were sacrificed for micro-CT and H&E staining analysis and serum assay. qPCR detected the expression of inflammatory genes. IF detected MAPKs pathway activation in periodontal tissues. The effects were determined using LPS-induced RAW264.7 cells. Gene expression levels were determined by qPCR. Intracellular ROS generation was detected by DCFH-DA staining and flow cytometry. WB detected the activation of signaling pathways.</p><p><strong>Results: </strong>Rb3 inhibited oxidative stress in experimental periodontitis, showing reduced gingivitis and alveolar bone resorption on H&E staining and micro-CT, and reduced iNOS mRNA in rats. Colorimetric results showed that Rb3 increased serum SOD and GSH-Px activities and decreased MDA levels in rats. IF analysis showed that Rb3 inhibited P38, ERK, and JNK activation. Rb3 pretreatment significantly decreased iNOS and IL-6 mRNA expression and ROS in Raw264.7 cells. WB analysis demonstrated that Rb3 blocked the activation of P38 and ERK.</p><p><strong>Conclusion: </strong>Rb3 inhibits the level of oxidative stress and attenuates gingivitis and alveolar bone resorption in rats via the MAPKs signaling pathway.</p>\",\"PeriodicalId\":19615,\"journal\":{\"name\":\"Oral diseases\",\"volume\":\" \",\"pages\":\"\"},\"PeriodicalIF\":2.9000,\"publicationDate\":\"2025-03-24\",\"publicationTypes\":\"Journal Article\",\"fieldsOfStudy\":null,\"isOpenAccess\":false,\"openAccessPdf\":\"\",\"citationCount\":\"0\",\"resultStr\":null,\"platform\":\"Semanticscholar\",\"paperid\":null,\"PeriodicalName\":\"Oral diseases\",\"FirstCategoryId\":\"3\",\"ListUrlMain\":\"https://doi.org/10.1111/odi.15318\",\"RegionNum\":3,\"RegionCategory\":\"医学\",\"ArticlePicture\":[],\"TitleCN\":null,\"AbstractTextCN\":null,\"PMCID\":null,\"EPubDate\":\"\",\"PubModel\":\"\",\"JCR\":\"Q1\",\"JCRName\":\"DENTISTRY, ORAL SURGERY & MEDICINE\",\"Score\":null,\"Total\":0}","platform":"Semanticscholar","paperid":null,"PeriodicalName":"Oral diseases","FirstCategoryId":"3","ListUrlMain":"https://doi.org/10.1111/odi.15318","RegionNum":3,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":null,"EPubDate":"","PubModel":"","JCR":"Q1","JCRName":"DENTISTRY, ORAL SURGERY & MEDICINE","Score":null,"Total":0}
Ginsenoside Rb3 Inhibits Oxidative Stress and Alleviates Experimental Periodontitis in Rats.
Objective: This study investigated the anti-inflammatory and antioxidative effects of ginsenoside Rb3 on experimental periodontitis.
Methods: Experimental periodontitis was established by ligating the maxillary first molars. After 21 days of Rb3 treatment, rats were sacrificed for micro-CT and H&E staining analysis and serum assay. qPCR detected the expression of inflammatory genes. IF detected MAPKs pathway activation in periodontal tissues. The effects were determined using LPS-induced RAW264.7 cells. Gene expression levels were determined by qPCR. Intracellular ROS generation was detected by DCFH-DA staining and flow cytometry. WB detected the activation of signaling pathways.
Results: Rb3 inhibited oxidative stress in experimental periodontitis, showing reduced gingivitis and alveolar bone resorption on H&E staining and micro-CT, and reduced iNOS mRNA in rats. Colorimetric results showed that Rb3 increased serum SOD and GSH-Px activities and decreased MDA levels in rats. IF analysis showed that Rb3 inhibited P38, ERK, and JNK activation. Rb3 pretreatment significantly decreased iNOS and IL-6 mRNA expression and ROS in Raw264.7 cells. WB analysis demonstrated that Rb3 blocked the activation of P38 and ERK.
Conclusion: Rb3 inhibits the level of oxidative stress and attenuates gingivitis and alveolar bone resorption in rats via the MAPKs signaling pathway.
期刊介绍：
Oral Diseases is a multidisciplinary and international journal with a focus on head and neck disorders, edited by leaders in the field, Professor Giovanni Lodi (Editor-in-Chief, Milan, Italy), Professor Stefano Petti (Deputy Editor, Rome, Italy) and Associate Professor Gulshan Sunavala-Dossabhoy (Deputy Editor, Shreveport, LA, USA). The journal is pre-eminent in oral medicine. Oral Diseases specifically strives to link often-isolated areas of dentistry and medicine through broad-based scholarship that includes well-designed and controlled clinical research, analytical epidemiology, and the translation of basic science in pre-clinical studies. The journal typically publishes articles relevant to many related medical specialties including especially dermatology, gastroenterology, hematology, immunology, infectious diseases, neuropsychiatry, oncology and otolaryngology. The essential requirement is that all submitted research is hypothesis-driven, with significant positive and negative results both welcomed. Equal publication emphasis is placed on etiology, pathogenesis, diagnosis, prevention and treatment.
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