摘要
目的:研究p38MAPK信号通路在慢性牙髓炎疼痛大鼠中的表达及作用机制。方法:选取SPF级Wistar雄性大鼠25只,将大鼠分成3组,正常组5只,模型组15只,MAPK抑制剂组5只。MAPK抑制剂组、模型组大鼠制备牙髓炎模型,成功造模后MAPK抑制剂组由颈静脉注入剂量为5mg/kg的SB203580,连续注射14d;造模后14d选取MAPK抑制剂组和正常组大鼠及造模3、7、14d模型组分别选取5只大鼠处死,观察其牙髓组织病理、血清白细胞介素-6(IL-6)、IL-8含量、牙髓组织内p-p38MAPK、ERK、p-ERK、p38MAPK蛋白表达及p38MAPK、ERKmRNA表达。结果:和正常组相比,造模后3、7、14d大鼠根尖破损水平长度、根尖周牙周膜宽度及第一磨牙根髓坏死比率显著升高;和造模后3、7、14d相比,MAPK抑制剂组大鼠根尖破损水平长度、根尖周牙周膜宽度及第一磨牙根髓坏死比率显著降低,差异有统计学意义(P<0.05);和正常组相比,造模后3、7、14d大鼠血清IL-6、IL-8含量显著升高;和造模后3、7、14d相比,MAPK抑制剂组大鼠血清IL-6、IL-8含量显著降低,差异有统计学意义(P<0.05);和正常组相比,模型组大鼠牙髓组织内p-p38MAPK、p-ERK蛋白表达升高;和模型组相比,MAPK抑制剂组大鼠牙髓组织内p-p38MAPK、p-ERK蛋白表达降低,差异有统计学意义(P<0.05)。结论:慢性牙髓炎大鼠牙髓组织内p38MAPK信号通路激活增大了炎症反应程度,促进病情进展,抑制p38MAPK信号通路可有效降低炎症因子表达。
AIM : To investigate the expression of p38MAPK signaling pathway in chronic pulpitis pain rats and its mechanism of action. METHODS : Twenty-five Wistar male rats of SPF grade were selected and divided into 3 groups, 5 in normal group, 15 in model group and 5 in MAPK inhibitor group. In the MAPK inhibitor group and the model group, the model of pulpitis was prepared. After successful modeling, the MAPK inhibitor group was injected with SB203580 at a dose of 5 mg/kg from the jugular vein for 14 days. The MAPK inhibitor group was selected 14 days after modeling. Five rats in the model group were sacrificed at 3, 7 and 14 d after modeling, respectively. Their pulp tissue pathology, serum interleukin-6 (IL-6), IL-8 content, p-p38MAPK, ERK, p-ERK, p38MAPK protein expression and p38MAPK, ERK mRNA expression were observed. RESULTS :Compared with the normal group, the length of apical damage, the width of the periapical periodontal membrane and the root necrosis rate of the first molar were significantly increased at 3, 7 and 14 days after modeling;while those in the MAPK inhibitor group were significantly lower ( P < 0.05 ). The levels of serum IL-6 and IL-8 in rats at 3, 7 and 14 days after modeling were significantly increased. Compared with 3, 7 and 14 days after modeling, serum IL-6 and IL-8 levels in rats with MAPK inhibitor group were significantly lower ( P < 0.05 ). Compared with the normal group, the expression of p-p38MAPK and p-ERK protein in the pulp tissue of the model group was increased. Compared with the model group, the MAPK inhibitor group The expression of p-p38MAPK and p-ERK protein in rat dental pulp tissue decreased ( P < 0.05 ). CONCLUSION : Activation of p38MAPK signaling pathway in dental pulp tissue of rats with chronic pulpitis increases the degree of inflammatory response, promotes disease progression, and inhibits p38MAPK signaling pathway, which can effectively reduce the expression of inflammatory factors.
作者
李敏
王珊珊
刘中和
姜德国
LI Min;WANG Shanshan;LIU Zhonghe;JIANG Deguo(Shaoxing People's Hospital,Shaoxing 312000,Zhejiang,China;The Seventh People's Hospital,Wenzhou 325005,Zhejiang,China)
出处
《中国临床药理学与治疗学》
CAS
CSCD
2019年第6期644-649,共6页
Chinese Journal of Clinical Pharmacology and Therapeutics
基金
浙江省基础公益研究计划(LGF18H090002)
