摘要
目的 探究三七总皂苷对牙髓炎大鼠炎症反应及下游p38丝裂原活化蛋白激酶(p38MAPK)/核因子-κB(NF-κB)通路的影响。方法 取SD大鼠,用脂多糖诱导建立牙髓炎模型,并随机分为模型组、三七总皂苷组、p38MAPK激活剂组、三七总皂苷+激活剂组、p38MAPK抑制剂组,每组15只,另取15只正常对照组大鼠。各组给予相应药物7 d后,取牙髓组织,HE染色观察组织炎症病变,并进行评分;免疫荧光共定位法检测M1型巨噬细胞(标记抗体CD86)与磷酸化p38MAPK(p-p38MAPK)阳性共表达水平;免疫组化法检测磷酸化NF-κB(p-NF-κB)阳性表达;Western blot法检测牙髓组织Toll样受体4(TLR4)/p38MAPK/NF-κB通路蛋白、M1型巨噬细胞极化相关蛋白以及白细胞介素-10(IL-10)蛋白表达。结果 给予三七总皂苷或阻断p38MAPK通路,均能同等程度的缓解牙髓组织病理损伤,抑制TLR4/p38MAPK/NF-κB通路活化,降低M1型巨噬细胞极化介导的促炎反应(P<0.05)。反之激活p38MAPK,可加重牙髓炎大鼠牙髓组织炎症损伤,且激活p38MAPK可减弱三七总皂对TLR4/p38MAPK/NF-κB通路活化及M1型巨噬细胞极化介导的促炎反应的抑制作用(P<0.05)。结论 三七总皂苷可能通过抑制p38MAPK/NF-κB通路活化,抑制M1型巨噬细胞介导的促炎反应,改善牙髓炎大鼠牙髓组织炎症反应。
Objective To explore the effects of Panax notoginseng saponins on inflammatory response and p38 mitogen-activated protein kinase(p38MAPK)/nuclear factor-kB(NF-κB)pathway in pulpitis rats.Methods SD rats were induced with lipopolysaccharide to establish a pulpitis model,and then randomly divided into model group,Panax notoginseng saponins group,p38MAPK activator group,Panax notoginseng saponins+activator group,and p38MAPK inhibitor group,with 15 rats in the group.Another 15 normal rats were introduced as normal control group.Seven days after rats of different group were given the corresponding drugs,the pulp tissue was gathered and subjected to HE staining for evaluating tissue inflammatory lesions and scoring;immunofluorescence co-localization method was used to detect the positive co-expression level of M1 type macrophages(labeled antibody CD86)and phosphorylated p38MAPK(p-p38MAPK);immunohistochemical method was used to detect the positive expression of phosphorylated NF-κB(p-NF-κB);Western blot method was used to detect the expression of Toll-like receptor 4(TLR4)/p38MAPK/NF-κB pathway proteins,M1 type macrophage polarization-related proteins,and interleukin-10(IL-10)protein in dental pulp tissue.Results Administration of Panax notoginseng saponins and blocking the p38MAPK pathway could alleviate the pathological damage of dental pulp tissue to the same extent,inhibit the activation of TLR4/p38MAPK/NF-κB pathway,and reduce the pro-inflammatory response mediated by M1 macrophage polarization(P<0.05).On the contrary,activation of p38MAPK could aggravate the inflammatory injury of pulp tissue in rats with pulpitis,and the activation of p38MAPK could weaken the inhibitory effects of Panax notoginseng saponins on the activation of TLR4/p38MAPK/NF-κB pathway and the pro-inflammatory responses mediated by M1 macrophage polarization(P<0.05).Conclusion Panax notoginseng saponins may inhibit the activation of p38MAPK/NF-κB pathway,inhibit the pro-inflammatory response mediated by M1 type macrophages,and alleviate the inflammatory response of dental pulp tissue in rats with pulpitis.
作者
蒋斯
周彪
李晔
匙莹
JIANG Si;ZHOU Biao;LI Ye;CHI Ying(Department of Stomatology,Baoding First Central Hospital,Baoding 071000,China;Department of Stomatology,Baoding Second Hospital,Baoding 071000,China)
出处
《免疫学杂志》
CSCD
2024年第9期716-721,共6页
Immunological Journal
