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栀子对结扎诱导大鼠牙周炎模型的影响。

The Effects of Gardenia Jasminoides on Periodontitis in Ligature-Induced Rat Model.

作者信息

Lee Dae Hoon, Lee Haesu, Kim Mi Hye, Yang Woong Mo

出版信息

Oral Health Prev Dent. 2020 Sep 4;18(4):799-806. doi: 10.3290/j.ohpd.a45084.

DOI:10.3290/j.ohpd.a45084
PMID:32895664
原文链接:https://pmc.ncbi.nlm.nih.gov/articles/PMC11654503/
Abstract

PURPOSE

Periodontitis is characterised by inflammation of periodontium and alveolar bone loss. Gardenia jasminoides is reported to have anti-inflammatory effects. In this study, we investigated the effects of aqueous extract of G. jasminoides (GJ) on periodontitis.

MATERIALS AND METHODS

Male Sprague-Dawley rats aged 7 weeks were randomly placed in three groups (n = 7); non-ligatured and non-treated (NL group), ligatured and distilled water-treated (L group) and ligatured and 100 mg/kg GJ-treated (GJ group). After oral administration of GJ for 14 days, the mandibles were removed for histology. In addition, RAW 264.7 cells were treated with 100 ng/ml receptor activator of nuclear factor-κΒ ligand (RANKL) and 1, 10 and 100 μg/ml GJ for 7 days to analyse the expression of periodontitis-related factors.

RESULTS

In GJ-treated mice, the score of alveolar bone loss was statistically significantly attenuated compared with the L group. GJ treatment showed inhibition effect in the progress of cementum demineralisation. The expressions of proinflammatory cytokines in gingival tissue were statistically significantly regulated by GJ treatment. Additionally, GJ treatment showed the dose-dependent inhibition of RANKL-induced osteoclast formation. Furthermore, GJ treatment downregulated the RANKL-induced cytokine production in RAW 264.7 cells.

CONCLUSION

In summary, GJ ameliorated periodontitis-induced alveolar bone loss via inhibiting transcription factors including nuclear factor-κB, c-fos and extracellular signal-regulated kinase signalling. Therefore, GJ might be a therapeutic option for treating periodontitis.

摘要

目的

牙周炎的特征是牙周组织炎症和牙槽骨丧失。据报道,栀子具有抗炎作用。在本研究中,我们调查了栀子水提取物(GJ)对牙周炎的影响。

材料与方法

将7周龄的雄性Sprague-Dawley大鼠随机分为三组(n = 7);非结扎未处理组(NL组)、结扎蒸馏水处理组(L组)和结扎100 mg/kg GJ处理组(GJ组)。口服GJ 14天后,取出下颌骨进行组织学检查。此外,用100 ng/ml核因子κB受体激活剂配体(RANKL)和1、10和100 μg/ml GJ处理RAW 264.7细胞7天,以分析牙周炎相关因子的表达。

结果

与L组相比,GJ处理的小鼠牙槽骨丧失评分在统计学上显著降低。GJ处理对牙骨质脱矿进程有抑制作用。GJ处理在统计学上显著调节了牙龈组织中促炎细胞因子的表达。此外,GJ处理对RANKL诱导的破骨细胞形成具有剂量依赖性抑制作用。此外,GJ处理下调了RAW 264.7细胞中RANKL诱导的细胞因子产生。

结论

总之,GJ通过抑制包括核因子κB、c-fos和细胞外信号调节激酶信号在内的转录因子,改善了牙周炎诱导的牙槽骨丧失。因此,GJ可能是治疗牙周炎的一种治疗选择。

https://cdn.ncbi.nlm.nih.gov/pmc/blobs/0d7d/11654503/fca0c8e422c5/ohpd-18-4-793-g006.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/0d7d/11654503/e228f81f16a0/ohpd-18-4-793-g001.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/0d7d/11654503/d6777756e1e6/ohpd-18-4-793-g002.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/0d7d/11654503/a66e535cc05d/ohpd-18-4-793-g003.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/0d7d/11654503/cb1815f67dc9/ohpd-18-4-793-g004.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/0d7d/11654503/ca95bc1f9e16/ohpd-18-4-793-g005.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/0d7d/11654503/fca0c8e422c5/ohpd-18-4-793-g006.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/0d7d/11654503/e228f81f16a0/ohpd-18-4-793-g001.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/0d7d/11654503/d6777756e1e6/ohpd-18-4-793-g002.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/0d7d/11654503/a66e535cc05d/ohpd-18-4-793-g003.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/0d7d/11654503/cb1815f67dc9/ohpd-18-4-793-g004.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/0d7d/11654503/ca95bc1f9e16/ohpd-18-4-793-g005.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/0d7d/11654503/fca0c8e422c5/ohpd-18-4-793-g006.jpg

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