| 王 芹,李立恒,冯建梅,胥爱文,安 峰.紫草素调节IL-6/STAT3信号通路对牙髓炎大鼠牙髓组织损伤的影响[J].,2024,(9):1639-1644 |
| 紫草素调节IL-6/STAT3信号通路对牙髓炎大鼠牙髓组织损伤的影响 |
| Effect of Shikonin Regulating IL-6/STAT3 Signaling Pathway on Pulp Tissue Injury in Pulpitis Rats |
| 投稿时间：2023-10-07 修订日期：2023-10-29 |
| DOI：10.13241/j.cnki.pmb.2024.09.007 |
| 中文关键词: 紫草素 IL-6/STAT3信号通路 牙髓炎 大鼠 牙髓组织损伤 |
| 英文关键词: Shikonin IL-6/STAT3 signaling pathway Pulpitis Rat Pulp tissue injury |
| 基金项目:河北省医学科学研究计划项目（20210456） |
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| 中文摘要: |
| 摘要 目的：探究紫草素（SHI）调节白细胞介素（IL）-6/信号转导子和转录激活子3（STAT3）信号通路对牙髓炎大鼠牙髓组织损伤的影响及机制。方法：建立牙髓炎大鼠模型。实验分为对照组（Control组）、模型组（Model组）、SHI低、中、高剂量组（SHI-L、SHI-M、SHI-H组，0.125 mg/kg/d、0.25 mg/kg/d、0.5 mg/kg/d SHI）、SHI高剂量+STAT3激动剂Colivelin组（SHI-H+Colivelin组，0.5 mg/kg/d SHI+1 mg/kg/d Colivelin），每组18只。观察大鼠一般行为变化；酶联免疫吸附法（ELISA）检测血清IL-6、IL-1β、肿瘤坏死因子α（TNF-α）、CXC趋化因子配体10（CXCL10）、血管内皮生长因子（VEGF）水平。苏木精-伊红（HE）染色观察牙髓组织病理变化；免疫组化法检测牙髓组织IL-6表达；免疫印迹法检测IL-6/STAT3信号通路相关蛋白表达。结果：与Control组相比，Model组大鼠饮食减少，不敢咬食物，精神萎靡；牙髓组织出现坏死，牙本质细胞排列紊乱，炎性细胞浸润及纤维组织增加，根髓充血扩张；血清IL-6、IL-1β、TNF-α、CXCL10和VEGF水平，IL-6平均光密度及IL-6和JAK2蛋白水平、p-STAT3/STAT3水平显著增加（P<0.05）。与Model组相比，SHI-L、SHI-M和SHI-H组大鼠饮食较正常，精神状态较佳，牙髓组织病理变化减轻；血清IL-6、IL-1β、TNF-α、CXCL10和VEGF水平，IL-6平均光密度及IL-6和JAK2蛋白水平、p-STAT3/STAT3水平逐渐降低（P<0.05）。与SHI-H组相比，SHI-H+Colivelin组大鼠饮食较差，精神不佳，牙髓组织病变加重；血清IL-6、IL-1β、TNF-α、CXCL10和VEGF水平，IL-6平均光密度及IL-6和JAK2蛋白水平、p-STAT3/STAT3水平显著增加（P<0.05）。结论：SHI能抑制牙髓炎大鼠炎症水平，减轻牙髓组织损伤，其机制可能与抑制IL-6/STAT3信号通路有关。 |
| 英文摘要: |
| ABSTRACT Objective: To investigate the effect and mechanism of shikonin (SHI) on pulp tissue injury in pulpitis rats by regulating interleukin (IL)-6/signal transducer and activator of transcription 3 (STAT3) signaling pathway. Methods: The pulpitis rat model was established. The experiment was divided into control group (Control group), model group (Model group), SHI low, medium and high dose group (SHI-L, SHI-M, SHI-H group, 0.125 mg/kg/d, 0.25 mg/kg/d, 0.5 mg/kg/d SHI), SHI high dose+STAT3 agonist Colivelin group (SHI-H+Colivelin group, 0.5 mg/kg/d SHI+1mg/kg/d Colivelin), 18 rats in each group. The general behavior changes of rats were observed. The levels of serum IL-6, IL-1β, tumor necrosis factor-α (TNF-α), CXC chemokine ligand 10 (CXCL10) and vascular endothelial growth factor (VEGF) were detected by enzyme-linked immunosorbent assay (ELISA). The pathological changes of dental pulp tissue were observed by hematoxylin-eosin (HE) staining; the expression of IL-6 in dental pulp tissue was detected by immunohistochemistry; the expression of IL-6/STAT3 signaling pathway-related proteins was detected by western blotting. Results: Compared with Control group, rats in Model group had a reduced diet, not dare to bite food, and were depressed. Necrosis of dental pulp tissue, disordered arrangement of dentin cells, infiltration of inflammatory cells and increase of fibrous tissue, congestion and dilation of root pulp; the levels of serum IL-6, IL-1β, TNF-α, CXCL10 and VEGF, the average optical density of IL-6, the protein levels of IL-6 and JAK2, and the level of p-STAT3/STAT3 were significantly increased(P<0.05). Compared with Model group, rats in SHI-L, SHI-M and SHI-H groups had a normal diet, a better mental state, and reduced pathological changes in dental pulp tissue. The levels of serum IL-6, IL-1β, TNF-α, CXCL10 and VEGF, IL-6 average optical density, IL-6 and JAK2 protein levels, and p-STAT3/STAT3 levels gradually decreased (P<0.05). Compared with SHI-H group, rats in SHI-H+Colivelin group had poor diet and poor spirit, pulp tissue lesions aggravated. The levels of serum IL-6, IL-1β, TNF-α, CXCL10 and VEGF, the average optical density of IL-6, the protein levels of IL-6 and JAK2, and the level of p-STAT3/STAT3 were significantly increased(P<0.05). Conclusion: SHI can inhibit the level of inflammation in pulpitis rats and reduce the damage of pulp tissue, the mechanism may be relate to the inhibition of IL-6/STAT3 signaling pathway. |
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