Abstract：【Objective】To study the effects of poly ADP-ribose polymerase (PARP) inhibitor Benzamide on the levels of inflammatory cells and inflammatory cytokines in experimental periodontitis of rats. 【Methods】 Fourty male Wistar rats ( SPF grade,3-month-old) of periodontitis model were randomly divided into periodontitis group, periodontitis intervention group, drug control group and blank group, with 10 mice in each group. The rat model of periodontitis was established by ligature of the first maxillary molar with stainless steel wire. At the fifth week after modeling, the periodontitis intervention group and the drug control group were intraperitoneally injected with 0.3 mg / kg PARP inhibitor Benzamide, while the periodontitis group and the blank group were intraperitoneally injected with equal doses of normal saline. Three rats in each group were randomly sacrificed at the end of 4,5 and 6 weeks. The histopathological changes of periodontal tissue were observed with H＆E staining.The levels of serum hs-CRP、IL-1β、IL-6 and TNF-α were measured by ELISA.Results were analyzed by using SPSS 17.0, and P<0.05 was considered statistically significant. 【Results】Periodontitis intervention group showed that, at the 5th and 6th weeks, there were slightly migration of cells from the gingival epithelium toward the root, a shallow periodontal pocket, and a small amount of inflammatory cell infiltration in the gingival epithelium, the groove epithelium and the lamina propria. In the same time period, the periodontitis group showed periodontal vascular dilatation and hyperemia, migration of gingival epithelium cells to the root, a deep periodontal pocket, and a large number of inflammatory cell infiltration in the gingival epithelium, under the groove epithelium and underlying lamina propria. The drug control group and the blank group showed that the epithelial cells were located at the border of glazed cementum and that the periodontal membrane fibers were arranged in an orderly manner without inflammatory cell infiltration. Serum levels of hs-CRP, IL-1β, IL-6 and TNF-α in the drug control group and the blank group at week 5 and 6 were significantly lower than those in periodontitis intervention group and periodontitis group (P<0.05). The periodontitis intervention group was significantly lower than the periodontitis group, but there was no significant difference between the drug control group and the blank group (P>0.05).【Conclusion】 Activation of PARP aggravates the symptoms of periodontitis in the pathogenesis of periodontitis. Benzoamide relieves periodontal lesions by inhibiting PARP, which reduces the inflammatory cells and inflammatory cytokines in the periodontium in experimental rats.
李小红, 许应宏, 邢孔才. 苯甲酰胺对实验大鼠牙周炎炎症细胞和炎症因子水平的影响[J]. 医学临床研究, 2018, 35(6): 1066-1068.
LI Xiao-hong, XU Ying-hong, XING Kong-cai. Effect of Benzamide on Inflammatory Cells and Inflammatory Factors in Periodontitis in Experimental Rats. JOURNAL OF CLINICAL RESEARCH, 2018, 35(6): 1066-1068.
[1] 李毅本. 牙周病病因与治疗研究进展[J].中国基层医药, 2003, 10(12):1325-1326. [2] 王勤涛,吴亚菲,章锦才.牙周病学[M].北京:人民卫生出版社,2011. [3] Adachi K, Miyajima S, Nakamura N,et al. Role of poly(ADP-ribose) polymerase activation in the pathogenesis of periodontitis in diabetes [J].J Clin Periodontol,2017,44(10):971-980. [4] Drel VR, Pacher P, Stavniichuk R, et al. Poly(ADP-ribose)polymerase inhibition counteracts renal hypertrophy and multiple manifestations of peripheral neuropathy in diabetic Akita mice[J].Int J Mol Med,2011 ,28(4):629-635. [5] Drel VR, Xu W, Zhang J, et al. Poly(Adenosine 5'-diphosphate-ribose) polymerase inhibition counteracts multiple manifestations of experimental type 1 diabetic nephropathy[J].Endocrinology,2009, 150(12):5273. [6] Virág L, Szabó C. The therapeutic potential of poly(ADP-ribose) polymerase inhibitors[J].Pharmacol Rev,2002 ,54(3):375-429. [7] Lohinai Z, Mabley J G, Fehér E, et al. Role of the activation of the nuclear enzyme poly(ADP-ribose) polymerase in the pathogenesis of periodontitis [J].J Dent Res,2003, 82(12):987-992. [8] Jog NR, Dinnall JA, Gallucci S, et al. Poly(ADP-ribose) polymerase-1 regulates the progression of autoimmune nephritis in males by inducing necrotic cell death and modulating inflammation [J].J Immunol,2009, 182(11):7297-7306. [9] Mattuella LG, Campagnaro MB, Vargas AE, et al. Plasma cytokines levels in aggressive and chronic periodontitis [J].Acta Odontol Scand,2013, 71(3-4):683-688. [10] Bickel M, Axtelius B, Solioz C, et al. Cytokine gene expression in chronic periodontitis[J].J Clin Periodontol,2010, 28(9):840-847. [11] Yang H, Aprecio RM, Zhou X, et al. Therapeutic effect of TSG-6 engineered iPSC-derived MSCs on experimental periodontitis in rats: a pilot study [J].PLoS One,2014, 9(6):e100285. [12] Yoneda K, Yamamoto T, Ueta E, et al. Suppression by azelastine hydrochloride of NF-kappa B activation involved in generation of cytokines and nitric oxide [J].Jpn J Pharmacol,1997, 73(2):145-153. [13] Lohinai Z, Mabley J G, Fehér E, et al. Role of the activation of the nuclear enzyme poly(ADP-ribose) polymerase in the pathogenesis of periodontitis [J].J Dent Res,2003, 82(12):987-892. [14] Richards D, Rutherford RB. Interleukin-1 regulation of procollagenase mRNA and protein in periodontal fibroblasts in vitro[J].J Periodontal Res,2010, 25(4):222-229. [15] Miyajima S, Naruse K, Kobayashi Y, et al. Periodontitis-activated monocytes/macrophages cause aortic inflammation [J].Sci Rep,2014, 4(6):5171. [16] Di PR, Mazzon E, Muià C, et al. 5-Aminoisoquinolin-1(2H)-one, a water-soluble poly (ADP-ribose) polymerase (PARP) inhibitor reduces the evolution of experimental periodontitis in rats[J].J Clin Periodontol,2010, 34(2):95-102.
2018, Vol. 35 
