口腔医学研究

口腔医学研究 ›› 2020, Vol. 36 ›› Issue (11): 1045-1049.DOI: 10.13701/j.cnki.kqyxyj.2020.11.014

• 口腔颌面外科学研究 • 上一篇    下一篇

复方甘菊利多卡因对兔口腔溃疡愈合的影响及相关药理机制研究

程英杰1,2,3, 高昕1,2,3, 汪苑苑1,2, 徐礼鲜1,4, 顾宜1,5, 王新文1,2*   

  1. 1.军事口腔医学国家重点实验室,口腔疾病国家临床医学研究中心,陕西省口腔疾病临床医学研究中心;
    2.空军军医大学第三附属医院黏膜科;
    3.空军军医大学基础医学院;
    4.空军军医大学第三附属医院麻醉科;
    5.空军军医大学第三附属医院药剂科
  • 收稿日期:2020-03-06 出版日期:2020-11-28 发布日期:2020-11-27
  • 通讯作者: *王新文,E-mail:landw211@163.com
  • 作者简介:程英杰(1996~ ),男,陕西西安人,本科,研究方向:口腔黏膜病。
  • 基金资助:
    国家口腔疾病临床医学研究中心专项课题(编号:LCA202008)军事口腔医学国家重点实验室室自主课题(编号:2018ZB01)

Efficacy of Compound Chamomile and Lidocaine in the Treatment of Oral Ulcer and Associated Pharmacological Mechanisms

CHENG Yingjie1,2,3, GAO Xin1,2,3, WANG Yuanyuan1,2, XU Lixian1,4, GU Yi1,5, WANG Xinwen1,2*   

  1. 1. State Key Laboratory of Millitary Stomatology, National Clinical Research Center for Oral Diseases, Shaanxi Clinical Research Center for Oral Diseases, Xi'an 710032, China;
    2. Department of Oral Medicine, School of Stomatology, Fourth Military Medical University, Xi'an 710032, China;
    3. School of Basic Medicine, Fourth Military Medical University, Xi'an 710032, China;
    4. Department of Anesthesiology, Fourth Military Medical University, Xi'an 710032, China;
    5. Department of Pharmacy, Fourth Military Medical University, Xi'an 710032, China
  • Received:2020-03-06 Online:2020-11-28 Published:2020-11-27

PDF (PC)

256

摘要： 目的:研究复方甘菊利多卡因(Compound Chamomile and Lidocaine,CCL)对口腔溃疡的促愈合作用及发挥临床治疗作用的可能药理机制。方法:化学灼烧法建立新西兰兔口腔溃疡动物模型,每日各组分别涂抹CCL、成纤维生长因子(basic fibroblast growth factor,bFGF)3次,记录口腔溃疡面积;3、5、7d取溃疡组织固定,HE染色进行组织病理学观察;免疫组化检测各组IL-8、TNF-α和SOD的表达差异。抑菌环实验评价CCL对金黄色葡萄球菌、大肠埃希菌的抑菌能力。结果:CCL对兔口腔溃疡的促愈合作用不明显,7d CCL组溃疡区虽可见增生的移行上皮层,结缔组织内仍见大量炎症细胞;但免疫组化显示,CCL组中IL-8,SOD表达水平接近bFGF组,均显著低于空白对照组(P＜0.05);抑菌环实验显示,CCL对金黄色葡萄球菌和大肠埃希菌的抑菌作用与金霉素相当,与bFGF凝胶相比具有绝对的抑菌优势(P＜0.001)。结论:除了具有明确的止痛作用外,降低某些炎症因子的表达及加强局部的抗感染能力可能是CCL发挥临床治疗作用的主要机制。

关键词: 口腔溃疡, 溃疡愈合, 复方甘菊利多卡因, 抑菌

Abstract: Objective: To evaluate the efficacy of Compound Chamomile and Lidocaine (CCL) in the treatment of oral ulcer, and to investigate the potential mechanisms. Methods: Oral ulcers were induced in New Zealand rabbits by chemical cauterization. CCL and bFGF were applied respectively on ulcers three times per day. The ulcer area was measured at baseline, day 1, day 3, day 5, and day 7. The expressing levels of IL-8, TNF-α, and SOD were determined by immunohistochemistry. The antibacterial activities of CCL were assessed in vitro by bacteria inhibition ring test. Results: CCL could not promote the healing of oral ulcer compared with the control. Histological staining demonstrated that a large number of inflammatory cells still existed in the connective tissue of CCL group at day 7, however, the expressions of IL-8 and SOD were obviously down-regulated (P＜0.05), which was similar to that in the bFGF group. As to TNF-α expression, there was no significantly difference between the CCL group and other groups. CCL showed a strong activity in bacteria inhibition ring test, which was comparable to aureomycin. Conclusion: Besides the definite analgesic effect, reducing the expression of inflammatory cytokines and inhibiting the local infection may be the main mechanisms for CCL to play its clinical therapeutic role.

Key words: oral ulcer, oral ulcer healing, compound chamomile and lidocaine, antibacterial activity