[1]姚璐莎,罗常春,张超.盐酸青藤碱对佐剂性关节炎大鼠NLRP3炎性小体的影响及分子机制的研究[J].西部中医药,2022,35(02):11-16.[doi:10.12174/j.issn.2096-9600.2022.02.03]
YAO Lusha,LUO Changchun,ZHANG Chao.Influence of Sinomenine Hydrochloride on NLRP3 Inflammasome in Adjuvant Arthritis Rats and the Study on Molecular Mechanism[J].Western Journal of Traditional Chinese Medicine,2022,35(02):11-16.[doi:10.12174/j.issn.2096-9600.2022.02.03]
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盐酸青藤碱对佐剂性关节炎大鼠NLRP3炎性小体的影响及分子机制的研究
《西部中医药》[ISSN:2096-9600/CN:62-1204/R]
- 卷:
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35
- 期数:
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2022年02期
- 页码:
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11-16
- 栏目:
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- 出版日期:
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2022-02-15
文章信息/Info
- Title:
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Influence of Sinomenine Hydrochloride on NLRP3 Inflammasome in Adjuvant Arthritis Rats and the Study on Molecular Mechanism
- 作者:
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姚璐莎, 罗常春, 张超
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湖南中医药大学第一附属医院,湖南 长沙 410007
- Author(s):
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YAO Lusha, LUO Changchun, ZHANG Chao
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The First Hospital of Hunan University of Chinese Medicine, Changsha 410007, China
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- 关键词:
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盐酸青藤碱; 佐剂性关节炎; NLRP3炎症小体; NF-B/NLRP3炎性小体信号通路; 动物实验
- Keywords:
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sinomenine; adjuvant arthritis rat; NLRP3 inflammasome; NF-B/NLRP3 inflammasome signaling pathway; zoopery
- 分类号:
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R285
- DOI:
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10.12174/j.issn.2096-9600.2022.02.03
- 文献标志码:
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A
- 摘要:
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目的探讨盐酸青藤碱(sinomenine,SN)对佐剂性关节炎(adjuvant arthritis,AA)大鼠核苷酸结合寡聚化结构域受体(NOD-like receptor protein 3,NLRP3)炎性小体的影响及其分子机制。 方法选用Wistar大鼠50只,采用随机数字表法分为正常对照组,模型组,阳性对照组,青藤碱高、低剂量组,每组10只。除正常对照组外,其余各组制备AA模型大鼠,各组给予对应药物灌胃。采用HE染色法观察大鼠踝关节组织病理改变。测定大鼠关节炎指数。采用ELISA法检测大鼠血清炎性因子[白细胞介素18(Interleukin 18,IL-18)、白细胞介素1β(Interleukin 1β,IL-1β)、肿瘤坏死因子α(tumor necrosis factor-α,TNF-α)、8-羟基脱氧鸟苷(8-hydroxy-2 deoxyguanosine,8-OHdG)、丙二醛(Malondialdehyde,MDA)]的表达。采用Western Blot检测大鼠滑膜组织内核转录因子κB(nuclear factor kappa-B,NF-κB)/核苷酸结合寡聚化结构域样受体蛋白3(NOD-like receptor protein 3,NLRP3)炎症小体信号通路相关蛋白的表达水平。 结果与正常对照组比较,模型组大鼠关节组织病理损伤明显加重(P<0.05);与模型组比较,阳性对照组及青藤碱各剂量组滑膜炎症明显减轻,炎细胞浸润减少,血管翳形成减轻,病理表现评分明显降低(P<0.05)。与模型组比较,阳性对照组及青藤碱各剂量组大鼠关节炎指数,IL-18、IL-1β、TNF-α、8-OHdG、MDA表达水平,NF-κB/NLRP3信号通路相关蛋白表达水平均降低(P<0.05),且青藤碱高剂量组改善程度优于低剂量组(P>0.05)。 结论SN能够通过抑制大鼠体内NF-κB/NLRP3炎性信号通路的活化,发挥较强的抗炎作用,对AA大鼠具有保护作用。
- Abstract:
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ObjectiveTo discuss the influence of SN on NLRP3 inflammasome in adjuvant arthritis (AA) rats and its molecular mechanism. MethodsFifty Wistar rats were chosen, and allocated into normal control group, the model group, positive control group, high and low dosages groups of SN according to random number table method, ten rats in each group. Except normal control group, the rats in the other groups were prepared into the models with AA, different groups were drenched with the corresponding medicines. HE staining was used to observe histopathological changes of ankle joint in rats, and measure arthritis index (AI), ELISA method was applied to detect the expressions of serum inflammatory factors [IL-18, IL-1β, TNF-α, 8-OHdG and MDA], Western Blot was adopted to measure the expressions of NF-κB/NLRP3 inflammasome signaling pathway related protein in synovial tissue of the rats. ResultsCompared with normal control group, the pathological injury of joint tissue was significantly aggravated in the model group (P<0.05); compared with the model group, synovial inflammation relieved notably, the infiltration of inflammatory cells decreased, pannus formation alleviated, and the score of pathological manifesta-tions significantly reduced in positive control group and different dosages groups of SN (P<0.05). Compared with the model group, AI, the levels of IL-18, IL-1β, TNF-α, 8-OHdG and MDA, the expressions of NF-κB/NLRP3 inflammasome signaling pathway related protein decreased in positive control group and different dosages groups of SN (P<0.05), and the improvements of high dosage group of SN were better than these of low dosage group (P>0.05). ConclusionSN could protect AA rats through inhibiting the activation of NF-κB/NLRP3 inflammasome signaling pathway in rat body and developing stronger anti-inflammatory effects.
备注/Memo
- 备注/Memo:
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姚璐莎(1984—),女,硕士学位,主治医师。研究方向:风湿病的中医诊治。湖南省自然科学基金(2018JJ3405)。
更新日期/Last Update:
2022-06-22