黄芩素调控 NLRP3 / Caspase-1 通路对牙周炎大鼠牙槽骨吸收的影响

目的 探索黄芩素调控核苷酸结合寡聚化结构域样受体蛋白 3 ( nucleotide-binding oligomerization domain-like receptor protein 3, NLRP3) / 半胱氨酸天冬氨酸蛋白酶 1 ( cysteine aspartate protease 1, Caspase1) 通路对牙周炎大鼠牙槽骨吸收的影响。 方法 将 40 只牙周炎大鼠随机分为模型组、 黄芩素组、 激活剂 组、 黄芩素 + 激活剂组, 另取 10 只正常作为对照组。 检测大鼠釉牙骨质界到牙槽嵴顶 (CEJ-AC) 的距离、 血清中白细胞介素-6 (IL-6)、 转化生长因子-β (TGF-β) 含量以及牙周组织病理变化、 IL-6、 TGF-β 阳性 表达和 NLRP3、 Caspase-1 蛋白表达。 结果 模型组大鼠 CEJ-AC、 NLRP3、 Caspase-1、 IL-6、 TGF-β 水平及 阳性表达水平以及蛋白表达水平均升高 (P< 0. 05); 经黄芩素干预后, 各项指标均降低 (P< 0. 05); 引入 激活剂明显削弱了黄芩素对牙周炎大鼠的抗炎作用。 结论 黄芩素通过抑制 NLRP3 / Caspase-1 通路减轻炎性反应, 控制牙槽骨吸收。

Baicalein Regulates NLRP3 / Caspase-1 Pathway and Its Effect on Alveolar Bone Resorption in Rats with Periodontitis

Objective To explore the effect of baicalein on alveolar bone resorption in rats with periodontitis and its regulation of nucleotide-binding oligomerization domain-like receptor protein 3 / cysteine aspartate protease 1 (NLRP3 / Caspase-1) pathway. Methods A total of 40 rats with periodontitis were randomly divided into model group, baicalein group, activator group and baicalein + activator group, another 10 rats without any treatment were taken as the control group. The distance from the cemento-enamel junction to aleolar crest (CEJ-AC) of the rats were measured. The expressions of interleukin-6 ( IL-6) and transforming growth factor-β ( TGF-β) in the serum and the periodontal tissues were detected. The pathological changes in periodontal tissues were observed. The expression levels of NLRP3 and Caspase-1 proteins were detected. Results The CEJ-AC distance, the expression levels of IL-6 and TGF-β in the serum, the positive rates of IL-6 and TGF-β expression in the periodontal tissues, and the expression levels of NLRP3 and Caspase-1 proteins were all increased in the model group (P< 0. 05). After the intervention with baicalein, all those indexes above were decreased (P< 0. 05). The treatment of activator significantly attenuated the effect of baicalein on above indexes. Conclusion Baicalein reduces the inflammation response, and controls alveolar bone resorption by inhibition of NLRP3 / Caspase-1 pathway.