豨莶草水提取物对痛风性关节炎大鼠JNK信号通路影响

背景:现代药理研究表明豨签草主要含有豨签甙、生物碱、皂甙等有效成分,有明确的抗炎、镇痛、改善微循环作用,能有效控制急性痛风的炎症改变。目的:研究豨莶草水提取物对痛风性关节炎大鼠JNK信号通路影响。方法:将24只SD大鼠随机分为对照组、模型组和豨莶草组。对照组和模型组灌胃给予生理盐水,连续7 d,豨莶草组灌胃给予2 g/kg的豨莶草水提取物,连续7 d,第7天给药1 h后向模型组和豨莶草组大鼠膝关节腔注射尿酸钠建立痛风性关节炎模型,对照组给予同体积的生理盐水。采用苏木精-伊红染色观察大鼠膝关节滑膜组织病理情况,ELISA检测大鼠血清中白细胞介素β、白细胞介素8和肿瘤坏死因子α水平,Western bloting测定大鼠膝关节滑膜组织中JNK和p-JNK蛋白表达,RT-PCR测定大鼠膝关节滑膜组织中c-jun和AP-1 mRNA表达。结果与结论:(1)与对照组比较,模型组膝关节滑膜组织中炎性细胞浸润,滑膜细胞增生,成纤维细胞及小血管增生,豨莶草组膝关节滑膜组织中炎性细胞浸润明显减少,滑膜细胞增生和成纤维细胞增生明显减轻;(2)模型组大鼠血清中白细胞介素1β、白细胞介素8和肿瘤坏死因子α质量浓度明显增高,豨莶草组血清中白细胞介素1β、白细胞介素8和肿瘤坏死因子α质量浓度明显降低;(3)模型组滑膜组织中JNK和p-JNK蛋白表达明显增加,AP-1和c-jun mRNA表达明显增加,豨莶草组能够明显降低痛风性关节炎大鼠JNK和p-JNK蛋白及c-jun和AP-1mR NA表达;(4)结果表明,痛风性关节炎能够诱导JNK信号通路异常激活,豨莶草水提物能够明显改善痛风性关节炎症状,并且明显改善JNK信号通路异常激活。

雌激素受体抑制下氯化锂对成骨细胞AKT-mTOR通路的影响

背景:氯化锂可以通过Wnt通路激活来治疗骨质疏松,并能激活诱导骨细胞自噬,推测提高氯化锂在Akt,mTOR磷酸化表达可以作为提高成骨细胞分化的作用机制之一。目的:分析雌激素受体抑制下氯化锂对大鼠成骨细胞AKT-mTOR通路作用机制。方法:SPF级出生3 d的SD乳鼠,购买于黑龙江中医药大学动物实验中心。麻醉下分离乳鼠颅骨成骨细胞,采用酶消化法和茜素红染色法获得和鉴定成骨细胞。将成骨细胞随机分为空白组(正常培养细胞)、抑制剂组(ICI182780)、治疗组(氯化锂+ICI182780)。倒置显微镜下观察细胞形态;加入不同浓度的氯化锂(0,1,2,5 nmol/L)处理细胞24 h,采用CCK-8检测各组细胞增殖情况;采用茜素红染色及碱性磷酸酶活性检测成骨细胞分化情况;Western blot法测定成骨细胞中p-AKT,p-mTOR的表达。结果与结论:①倒置显微镜下观察细胞多为单核、多边形及梭形,局部有细胞密集的细胞团;②不同浓度的氯化锂都能对成骨细胞增殖产生促进作用,在一定范围内随着氯化锂浓度的增加促进作用逐渐增强;③与空白组比较,抑制剂组成骨细胞矿化能力明显降低,与抑制剂组比较,治疗组成骨细胞矿化结节能力明显增加;④与空白组比较,抑制剂组中碱性磷酸酶活性明显降低,与抑制剂组比较,治疗组中碱性磷酸酶活性明显增加;⑤与空白组比较,抑制剂组中细胞p-AKT,p-mTOR蛋白表达明显降低,与抑制剂组比较,治疗组中p-AKT,p-mTOR蛋白表达显著增加;⑥结果说明,雌激素受体抑制下氯化锂可以通过激活AKT-mTOR通路促进成骨细胞增殖分化。

基于知识图谱的大数据治理研究热点与趋势分析

【目的/意义】大数据技术的发展与应用使大数据治理成为学术界的研究热点。可视化图谱能够直观地揭示该领域的研究概况与趋势。【方法/过程】运用文献计量信息可视化软件CiteSpace,以CNKI数据库中CSSCI期刊收录的大数据治理研究相关文献为数据来源,对该领域研究成果的总体概况、研究机构、期刊来源等进行特征分析,并绘制关键词共现图谱、聚类图谱和突变词信息表,分析了关键词的特点与发展趋势。【结果/结论】结果表明该领域的研究热点主题包括大数据治理的基本概念、大数据的管理和大数据治理的应用等方面,研究内容丰富且不断演变创新,未来有较大的发展空间。【创新/局限】借助可视化文献计量工具系统梳理了大数据治理的研究现状和发展趋势,提出了未来的发展建议。

Efficacy of Xixiancao (Herba Siegesbeckiae Orientalis) on interactions between nuclear factor kappa-B and inflammatory cytokines in inflammatory reactions of rat synovial cells induced by sodium urate

OBJECTIVE:To investigate the interaction between nuclear factor kappa-B(NF-κB)and inflammatory cytokines in synovial cell inflammatory responses induced by sodium urate,and to evaluate the efficacy of Xixiancao(Herba Siegesbeckiae Orientalis)on these interactions.METHODS:The interactions between NF-κB and inflammatory cytokines/mediators in synovial cells in acute gouty arthritis were investigated.We observed the expressions of NF-κB,interleukin(IL)-1β,IL-8,and tumor necrosis factor alpha(TNF-α)in synovial cells at different timepoints in an in vitro model of synovial cell inflammatory responses induced by sodium urate and in an in vivo model of gouty arthritis.Changes in the expressions of NF-κB,IL-1β,IL-8,and TNF-αin synovial cells of all experimental groups were compared and observed after treatment with different doses of Xixiancao(Herba Siegesbeckiae Orientalis)and colchicine.The interactions between NF-κB and IL-1β,IL-8,and TNF-αwere analyzed.Pathological changes in synovial tissues were observed in rats with acute gouty arthritis.RESULTS:Compared with the blank group,the expression levels of NF-κB,IL-1β,IL-8,and TNF-αwere increased significantly at different timepoints in the in vitro model of synovial cell inflammatory responses induced by sodium urate,and in the in vivo model of gouty arthritis.Compared with the model group,the expressions of NF-κB,IL-1β,IL-8,and TNF-αin synovial cells induced by sodium urate were decreased in the different Xixiancao(Herba Siegesbeckiae Orientalis)dose groups and the colchicine group.The effect was more obvious in the high dose Xixiancao(Herba Siegesbeckiae Orientalis)group.The expression of NF-κB in synovial cells was positively correlated with the expressions of IL-1β,IL-8,and TNF-α.Histopathological examination of synovial tissues in the high dose Xixiancao(Herba Siegesbeckiae Orientalis)group and Colchicine group showed that the characteristics of acute gouty arthritis were reduced,and there was a trend towards a positive correlation between NF-κB and inflammatory cytokine expressions.CONCLUSION:The activation of NF-κB is associated with the activation of IL-1β,IL-8,and TNF-αduring the pathogenesis of acute gouty arthritis,leading to the continuation and enhancement of the inflammatory response.Expressions of IL-1β,IL-8,and TNF-αin synoviocytes during acute gouty arthritis effectively inhibit local inflammation.