Effects of Platycodin D on S100A8/A9-induced inflammatory response in murine mammary carcinoma 4T1 cells

Activation of the inflammatory signaling pathway is the most vital part of the pre-metastatic events of breast cancer. Platycodin D (PlaD) shows favorable pharmacological activities in anti-inflammatory and anti-tumor effect. The main purpose of this study was to survey the effects of PlaD on S100A8/A9-induced inflammation in mouse mammary carcinoma 4T1 cells. S100A8/A9 immunolocalization and expression in pre-metastatic lung tissue were assessed by immunofluorescence staining and ELISA. 4T1 cells were treated with 2.5 μg/mL recombinant S100A8/A9 heterodimer and 7.5, 10, or 12.5 μM of PlaD. After 24 h of incubation, cell viability, migration, and invasion were evaluated by CCK-8, wound-healing, and transwell assay, respectively. Nuclear translocation of NF-κB p65 was determined by immunostaining and western blot. The levels of pro-inflammatory cytokines including IL-1β, IL-6, and TNF-α were detected by ELISA. The results showed that S100A8/A9 was actively increased and released into the extracellular space during the pre-metastatic phase of breast cancer. PlaD treatment attenuated S100A8/A9-induced growth, migration, and invasion of 4T1 cells. Furthermore, PlaD decreased the levels of IL-1β, IL-6, and TNF-α by inhibiting nuclear translocation of NF-κB p65. In conclusion, this study demonstrated that PlaD inhibited S100A8/A9-induced inflammatory response in 4T1 cells by suppressing the expression of IL-6, IL-1β, and TNF-α via inhibition of NF-κB signaling pathways.     

Natural products: Potential therapeutic agents in multiple sclerosis

Multiple sclerosis is an autoimmune neurodegenerative disease, which usually caused by inflammation, demyelination, and axonal injury. The currently available medications for multiple sclerosis do not directly promote myelin sheath repair. Therefore, many researches have attempted to achieve better therapeutic effects through promoting remyelination. Natural products not only alleviate clinical symptoms, but also have the unique advantages of protecting and repairing effects on nervous system. We here present a systematic review on published papers about treating multiple sclerosis by natural products, aiming to provide comprehensive information on natural products in the treatment of multiple sclerosis.     

密骨胶囊对原发性骨质疏松症患者中医证候疗效的随机对照研究

目的:初步评价密骨胶囊治疗原发性骨质疏松症的中医证候疗效。方法:采用随机、阳性药物平行对照、双盲单模拟、多中心的试验设计;以符合原发性骨质疏松症和肝肾不足证诊断标准者为研究对象;试验组口服密骨胶囊,3粒/次、3次/d,对照组口服仙灵骨葆胶囊,3粒/次、2次/d,以及仙灵骨葆胶囊模拟剂,3粒/次、1次/d,疗程6个月;以肝肾不足证侯总积分和单项症状积分为疗效指标,分别评价积分值的变化和疗效。结果:密骨胶囊组中医证候总积分逐渐下降,第1个月末证候总积分与治疗前的差异具统计学意义(P<0.05)。仙灵骨葆组从第2个月末开始与治疗前比较差异具统计学意义(P<0.05)。密骨胶囊组中医证候积分总有效率为89.57%、控显率为42.61%,仙灵骨葆组分别为92.04%、40.71%,两组差异无统计学意义。治疗终点第6个月末时,两组缓解各单项症状的有效率无统计学差异。结论:密骨胶囊可明显缓解原发性骨质疏松症肝肾不足证的临床证候。     

柔肝复方及单味药提取物对体外培养人骨关节炎软骨细胞增殖及关节软骨低聚基质蛋白分泌的研究

目的:探讨柔肝单味药提取物金利胶囊及复方养血软坚胶囊对体外培养人骨关节炎(OA)软骨细胞增殖能力及关节软骨低聚基质蛋白(COMP)分泌的影响。方法:分阶段酶消化法体外培养人骨关节炎软骨细胞,以1×105/cm2密度接种3代内细胞,研究设正常对照组及金利胶囊与养血软坚胶囊2个药物干预组。药物直接添加体外培养体系,添加终浓度为10mg/ml。以MTS/PMS法观察不同药物对体外培养的软骨细胞在接种1、3、5d时增殖情况的影响,采用ELISA法检测药物对体外培养的人软骨细胞COMP分泌的影响。结果:与空白组相比,金利胶囊及养血软坚胶囊未表现出明显的促进人骨关节炎软骨细胞增殖能力(P>0.05),但在各用药组内,细胞增殖能力在1~3d时间段较3~5d时间段明显增强(P>0.05)。各药物组有上调人OA软骨细胞分泌COMP的作用,但组间未见有明显差异(P>0.05)。结论:用药干预后,柔肝单味药提取物金利胶囊及复方养血软坚胶囊可以促进人骨关节炎软骨细胞分泌COMP,细胞增殖能力在1~3d时间段较3~5d时间段明显增强,但2组药物之间未见有明显差异。