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1.河南大学第一附属医院口腔科,河南 开封 475000
2.河南大学口腔医学院,河南 开封 475000
Published:15 December 2023,
Received:08 June 2023,
Revised:19 September 2023,
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苏娟娟,王旭,陈洪婷等.苍术素对牙周炎大鼠牙周组织炎性损伤和牙槽骨丢失的影响及机制 Δ[J].中国药房,2023,34(23):2868-2873.
SU Juanjuan,WANG Xu,CHEN Hongting,et al.Effects of atractylodin on inflammatory damage of periodontal tissue and alveolar bone loss in periodontitis rats and its mechanism[J].ZHONGGUO YAOFANG,2023,34(23):2868-2873.
苏娟娟,王旭,陈洪婷等.苍术素对牙周炎大鼠牙周组织炎性损伤和牙槽骨丢失的影响及机制 Δ[J].中国药房,2023,34(23):2868-2873. DOI: 10.6039/j.issn.1001-0408.2023.23.09.
SU Juanjuan,WANG Xu,CHEN Hongting,et al.Effects of atractylodin on inflammatory damage of periodontal tissue and alveolar bone loss in periodontitis rats and its mechanism[J].ZHONGGUO YAOFANG,2023,34(23):2868-2873. DOI: 10.6039/j.issn.1001-0408.2023.23.09.
目的
2
探讨苍术素对牙周炎大鼠牙周组织炎性损伤和牙槽骨丢失的影响及机制。
方法
2
将144只SD大鼠分为对照组(灌胃且腹腔注射生理盐水),模型组(灌胃且腹腔注射生理盐水),苍术素低、中、高剂量组(分别腹腔注射6.665、13.33、26.66 mg/kg苍术素且灌胃生理盐水),甲硝唑组(阳性对照组,灌胃0.05 g/kg甲硝唑且腹腔注射生理盐水),AMD3100[基质细胞衍生因子1(SDF-1)/CXC型趋化因子受体4(CXCR4)通路抑制剂]组(灌胃1 mg/kg AMD3100且腹腔注射生理盐水),苍术素高剂量+ AMD3100组(腹腔注射26.66 mg/kg苍术素且灌胃1 mg/kg AMD3100),每组18只。除对照组外,其余各组大鼠均采用牙龈内接种牙龈卟啉单胞菌法构建牙周炎模型。建模成功后开始给药,每天给药(或生理盐水)1次,持续4周。检测大鼠牙龈指数;检测大鼠血清中白细胞介素6(IL-6)、肿瘤坏死因子α(TNF-α)水平;采用亚甲蓝染色、HE染色、抗酒石酸磷酸酶染色法分别检测牙槽骨吸收、牙周组织病理变化、破骨细胞数;检测大鼠骨保护素(OPG)、核因子κB受体活化因子配基(RANKL)、SDF-1、CXCR4蛋白表达。
结果
2
与对照组比较,模型组大鼠牙周组织病理损伤严重,牙龈指数、IL-6和TNF-α水平、牙槽骨吸收值、破骨细胞数、RANKL蛋白表达水平显著升高(
P
<0.05),OPG 、SDF-1、CXCR4蛋白表达水平显著降低(
P
<0.05);与模型组比较,苍术素低、中、高剂量组和甲硝唑组大鼠牙周组织病理损伤减轻,牙龈指数、IL-6和TNF-α水平、牙槽骨吸收值、破骨细胞数、RANKL蛋白表达水平均显著降低(
P
<0.05),OPG、SDF-1、CXCR4蛋白表达水平均显著升高(
P
<0.05);AMD3100组大鼠对应指标的变化趋势与上述给药组相反(
P
<0.05),并且AMD3100减弱了高剂量苍术素对牙周炎大鼠炎症反应及牙槽骨丢失的抑制作用(
P
<0.05)。
结论
2
苍术素可能通过激活SDF-1/CXCR4信号通路来改善牙周炎大鼠炎症反应及牙槽骨丢失
。
OBJECTIVE
2
To investigate the effects and mechanism of atractylodin on inflammatory injury of periodontal tissue and alveolar bone loss in periodontitis rats.
METHODS
2
A total of 144 SD rats were divided into control group (intragastric and intraperitoneal injection of normal saline), model group (intragastric and intraperitoneal injection of normal saline), atractylodin low-dose, medium-dose and high-dose groups (intraperitoneal injection of 6.665, 13.33, and 26.66 mg/kg atractylodin), metronidazole group (positive control group, intragastric injection of 0.05 g/kg metronidazole, intraperitoneal injection of normal saline), AMD3100 [stromal cell-derived factor-1 (SDF-1)/CXC chemokine receptor-4 (CXCR4) pathway inhibitor] group (intragastric injection of 1 mg/kg AMD3100, intraperitoneal injection of normal saline), atractylodin high-dose+AMD 3100 group (intraperitoneal injection of 26.66 mg/kg atractylodin, intragastric injection of 1 mg/kg AMD3100), with 18 rats in each group. Except for the control group, all other groups of rats were inoculated with
Porphyromonas gingivalis
to construct a periodontitis model. After successful modeling, they were given relevant medicine or normal saline, once a day, for 4 consecutive weeks. The gingival index of rats was detected; the levels of interleukin-6 (IL-6) and tumor necrosis factor α (TNF-α) in rat serum were also determined; alveolar bone resorption, periodontal histopathologic changes and the number of osteoclasts were detected by methylene blue staining, HE staining and TRAP staining, respectively. The expressions of osteoprotegerin (OPG), receptor activator of NF-κB ligand (RANKL), SDF-1 and CXCR4 proteins were determined.
RESULTS
2
Compared with the control group, serious pathological injury of periodontal tissue was found in the model group, the gingival index, the levels of IL-6 and TNF-α, alveolar bone absorption value, the number of osteoclasts, and the expression of RANKL protein were all increased significantly (
P
<0.05), while the expressions of OPG, SDF-1 and CXCR4 proteins were decreased significantly (
P
<0.05). Compared with the model group, pathological injury of periodontal tissue in rats was reduced; the gingival index, the levels of IL-6 and TNF-α, alveolar bone resorption value, osteoclast number and RANKL protein expression were decreased significantly, while protein expressions of OPG, SDF-1 and CXCR4 were increased significantly in atractylodin low-dose, medium-dose and high-dose groups and metronidazole group (
P
<0.05). The change trend of corresponding indexes in the AMD3100 group was opposite to the above (
P
<0.05). AMD3100 attenuated the inhibitory effect of high-dose atractylodin on inflammatory response and alveolar bone loss in rats with periodontitis (
P
<0.05).
CONCLUSIONS
2
Atractylodin may improve the inflammatory response and alveolar bone loss in periodontitis rats by activating the SDF-1/CXCR4 signaling pathway.
苍术素基质细胞衍生因子1CXC型趋化因子受体4牙周炎牙周组织牙槽骨
stromal cell-derived factor-1CXC chemokine receptor-4periodontitisperiodontal tissuealveolar bone
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