【摘要】 目的:研究脂多糖(LPS)诱导人牙髓细胞(HDPCs)炎症信号受体——Toll样受体4(TLR4)表达、肿瘤坏死因子-α(TNF-α)分泌情况以及黄芩苷对其的影响,并探讨黄芩苷可能的细胞保护作用机理。方法:采用组织块法原代培养人牙髓细胞,免疫组化技术鉴定细胞来源,流式细胞术(FC)与酶联免疫法(ELISA)分别检测TLR4与TNF-α的表达。结果:正常HDPCs微量表达TLR4与TNF-α;100μg/mLLPS诱导HDPCs表达TLR4与TNF-α显著增加(P<0.01);与对照组比较,10μg/mL黄芩苷诱导HDPCs表达TLR4与TNF-α,差异无统计学意义(P>0.05);0.001～20μg/mL黄芩苷均可抑制LPS诱导HDPCs表达TLR4与TNF-α,随着黄芩苷浓度升高,TLR4与TNF-α表达逐渐降低,且不同浓度组间比较,抑制作用有显著性差异(P<0.01)。结论:LPS可能通过TLR4信号受体参与牙髓组织炎症过程。黄芩苷可抑制由LPS诱导的TLR4表达及TNF-α分泌,对LPS引起的牙髓炎可能具有潜在的治疗作用。更多还原

【Abstract】 AIM:To study the effects of baicalin on the expression of Toll-like receptor 4(TLR4)and the secretion of tumor necrosis factor alpha(TNF-α)in human dental pulp cells(HDPCs)induced by lipopolysaccharide(LPS),and the mechanism of the effects.METHODS:HDPCs were primarily cultured in vitro and their phenotype was identified by immunohistochemcial staining.Flow Cytometry(FC)was used to analyse the expression of TLR4,and enzyme-labeled immunosorbent assay(ELISA)was used to measure the secretion of TNF-α.RESULTS:TLR4 and TNF-α were detected weakly in normal HDPCs,but their expessions significantly increased after being stimulated with LPS at 100μg/mL(P< 0.01).The expressions of TLR4 and TNF-α had no statistical differences between the control group and the group of 10μg/mL baicalin(P>0.05).Baicalin at the concentrations from 0.001 μg/mL to 20μg/mL could significantly inhibit the activity of TLR4 and TNF-α induced by LPS in a dose-dependent manner.Among the different baicalin concentration groups,the differences of expression were statistically significant(P<0.01).CONCLUSION:LPS may participate in the inflammation of pulp tissue by TLR4.Baicalin may play a role in the treatment of pulpitis induced by LPS with the help of inhibiting the expression of TLR4 and secretion of TNF-α.更多还原