从桔梗中提取的皂苷基于 NLRP3/ASC/caspase-1 通路缓解痛风性关节炎

Ping Sun, Yang Liu, Tingting Zhang, Shanshan Wang, Yanhong Huang, Ze-Wang Li, Yupeng Nie, Hui Xu, Jianjun Liu
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引用次数: 0

摘要

桔梗是一种传统食品,具有促进肺部健康、祛痰和止咳等出色的药用功效。多项研究发现,桔梗的主要化学成分皂甙对乳腺炎、皮炎和咽喉炎等多种炎症非常有效。然而,用桔梗皂苷治疗痛风性关节炎尚未见报道,其作用机制也未进行系统研究。本研究建立了痛风性关节炎小鼠模型,对空白组、模型组、秋水仙碱(1 毫克/千克)组和桔梗皂苷(12.5 毫克/千克、25 毫克/千克、50 毫克/千克)组小鼠进行为期 7 天的灌胃治疗。MSU 消毒后于第五天注射到关节中。通过测定关节肿胀程度、血清炎症因子(IL-6、IL-1β、TNF-α)、过氧化物(SOD、MDA、GSH-PX)、关节组织病理学和相关蛋白质的特征,说明了 PGS 在痛风性关节炎治疗中的抗炎作用。结果显示,PGS 能有效减轻肿胀,降低 IL-1β (181.49 vs. 161.01)、IL-6 (273.10 vs. 241.69)、TNG-α (637.89 vs. 455.80) 和过氧化物水平,其机制可能与 NLRP3/ASC/caspase-1 通路上的蛋白质减少有关。
本文章由计算机程序翻译,如有差异,请以英文原文为准。
Alleviation of Gouty Arthritis Based on NLRP3/ASC/caspase-1 Pathway by Saponins Extracted from Platycodon grandiflorus
Platycodon grandiflorus is a traditional food with excellent medicinal properties, such as promotion of lung health, expectorants, and cough suppression. Various studies have found that saponins, the main chemical component of Platycodon grandiflorus, are very effective against many inflammatory conditions, including mastitis, dermatitis, and laryngitis. However, the treatment of gouty arthritis with Platycodon grandiflorus saponins has not yet been reported and their mechanism of action have not been systematically investigated. In this study, a mouse model of gouty arthritis was established, and mice were treated with gavage for seven days in the blank, model, colchicine (1 mg/kg), and Platycodon grandiflorus saponin (12.5 mg/kg, 25 mg/kg, 50 mg/kg) groups. MSU was sterilized and injected into the joints on the fifth day. The anti-inflammatory effect of PGS in the treatment of gouty arthritis was illustrated by measuring the degree of joint swelling, serum inflammatory factors (IL-6, IL-1β, TNF-α), peroxides (SOD, MDA, GSH-PX), joint histopathology, and characterization of related proteins. The results show that PGS was effective in reducing swelling and lowering IL-1β (181.49 vs. 161.01), IL-6 (273.10 vs. 241.69), TNG-α (637.89 vs. 455.80), and peroxide levels, presumably by a mechanism related to the reduction of proteins on the NLRP3/ASC/caspase-1 pathway.
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