桑黄素调控SIRT1/PGC-1α/Nrf2通路对牙周炎小鼠牙槽骨吸收的影响 点击下载
论文标题: 桑黄素调控SIRT1/PGC-1α/Nrf2通路对牙周炎小鼠牙槽骨吸收的影响
英文标题:
中文摘要: 目的 基于沉默信息调节因子1/过氧化物酶体增殖物激活受体γ共激活因子1α/核转录因子红系2相关因子2(SIRT1/PGC-1α/Nrf2)通路,研究桑黄素对牙周炎小鼠牙槽骨吸收的影响及机制。方法将小鼠随机分为对照组、模型组、桑黄素组(40mg/kg)、SRT1720(SIRT1激活剂)组(5mg/kg)、桑黄素+EX527(SIRT1抑制剂)组(40mg/kg桑黄素+7.5mg/kgEX527),每组18只。除对照组外,其余各组小鼠均通过丝线结扎法建立牙周炎模型。建模成功后,各组小鼠灌胃或腹腔注射相应药液/生理盐水,每天给药1次,连续2周。末次给药后,检测小鼠血清中肿瘤坏死因子α(TNF-α)、白细胞介素(IL)-1β、IL-6、IL-10水平;测量小鼠釉牙骨质界与牙槽骨嵴顶的距离,并计算骨体积分数和骨矿物质密度;观察小鼠牙周组织病理学形态;检测小鼠牙周组织中破骨细胞数;检测小鼠牙周组织中核因子κB受体激活蛋白配体(RANKL)、骨保护素(OPG)mRNA表达水平和丙二醛(MDA)、超氧化物歧化酶(SOD)水平以及SIRT1、PGC-1α、Nrf2蛋白表达水平。结果与模型组比较,桑黄素组、SRT1720组小鼠牙槽骨吸收和牙周组织炎症细胞浸润现象有所改善;血清中TNF-α、IL-1β、IL-6水平,釉牙骨质界与牙槽骨嵴顶的距离,牙周组织中破骨细胞数、RANKLmRNA表达水平、MDA水平均显著降低/缩短/减少(P<0.05);血清中IL-10水平,骨体积分数和骨矿物质密度,牙周组织中OPGmRNA表达水平、SOD水平和SIRT1、PGC-1α、Nrf2蛋白表达水平均显著升高(P<0.05)。与桑黄素组比较,桑黄素+EX527组小鼠上述病理改变明显加重,定量指标水平均显著逆转(P<0.05)。结论桑黄素可能通过激活SIRT1/PGC-1α/Nrf2通路,减轻炎症反应和氧化应激反应,从而抑制牙周炎小鼠牙槽骨吸收。
英文摘要: OBJECTIVE To investigate the effect and mechanism of morin on alveolar bone resorption in periodontitis mice based on the silent information regulator 1 (SIRT1)/peroxisome proliferator-activated receptor γ coactivator-1α (PGC-1α)/nuclear factor-erythroid 2-related factor 2 (Nrf2) pathway. METHODS The mice were randomly divided into control group, model group, morin group (40 mg/kg), SRT1720 (SIRT1 activator) group (5 mg/kg), and morin+EX527 (SIRT1 inhibitor) group (40 mg/kg morin+7.5 mg/kg EX527), with 18 mice in each group. Except for control group, mice in other groups were subjected to silk ligation to establish periodontitis model. After successful modeling, mice in each group were treated with corresponding medicinal solutions or normal saline intragastrically or intraperitoneally, once a day, for two consecutive weeks. After the last medication, serum levels of tumor necrosis factor-α (TNF-α), interleukin (IL)-1β, IL-6 and IL-10 were measured. The distance between the cementoenamel junction and alveolar bone crest was determined, and bone volume fraction and bone mineral density were calculated. Pathological changes of periodontal tissue were observed, and the number of osteoclasts was measured. mRNA expressions of receptor activator of nuclear factor-κB ligand (RANKL) and osteoprotegerin (OPG) in periodontal tissue, the levels of malondialdehyde (MDA) and superoxide dismutase (SOD) as well as protein expressions of SIRT1, PGC-1α, and Nrf2 were determined. RESULTS Compared with model group, the alveolar bone resorption and inflammatory cell infiltration in the periodontal tissues of mice were improved in morin group and SRT1720 group. The serum levels of TNF-α, IL-1β and IL-6, the distance between cementoenamel junction and alveolar bone crest, the number of osteoclasts in periodontal tissue, RANKL mRNA expression and the MDA level were decreased, shortened and reduced significantly ( P <0.05); however, serum level of IL-10, bone volume fraction and bone mineral density, OPG mRNA expression in periodontal tissue, SOD level and protein expressions of SIRT1, PGC-1α and Nrf2 were increased significantly ( P <0.05). Compared with morin group, the above pathological changes were significantly aggravated in the morin+EX527 group; and the levels of quantitative indicators were markedly reversed ( P <0.05). CONCLUSIONS Morin may inhibit alveolar bone resorption in periodontitis mice by activating the SIRT1/PGC-1α/Nrf2 pathway to reduce inflammatory reaction and oxidative stress.
期刊: 2026年第37卷第07期
作者: 丁春燕;汪瑞娟;王毅军;孟丽颖;房广林
英文作者: DING Chunyan,WANG Ruijuan,WANG Yijun,MENG Liying,FANG Guanglin
关键字: 牙周炎;桑黄素;SIRT1/PGC-1α/Nrf2通路;牙槽骨吸收;氧化应激
KEYWORDS: periodontitis; morin; SIRT1/PGC-1α/Nrf2 pathway; alveolar bone resorption; oxidative stress
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