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Anti-Inflammatory and Antioxidant Effects of Carpesium cernuum L. Methanolic Extract in LPS-Stimulated RAW 264.7 Macrophages.
Mediators of Inflammation ( IF 4.6 ) Pub Date : 2020-08-08 , DOI: 10.1155/2020/3164239
Yea-Jin Park 1 , Se-Yun Cheon 1, 2 , Dong-Sung Lee 3 , Divina C Cominguez 1 , Zhiyun Zhang 4 , Sangwoo Lee 5 , Hyo-Jin An 1
Affiliation  

A hypernomic reaction or an abnormal inflammatory process could cause a series of diseases, such as cardiovascular disease, neurodegeneration, and cancer. Additionally, oxidative stress has been identified to induce severe tissue injury and inflammation. Carpesium cernuum L. (C. cernuum) is a Chinese folk medicine used for its anti-inflammatory, analgesic, and detoxifying properties. However, the underlying molecular mechanism of C. cernuum in inflammatory and oxidative stress conditions remains largely unknown. The aim of this study was to examine the effects of a methanolic extract of C. cernuum (CLME) on lipopolysaccharide- (LPS-) induced RAW 264.7 mouse macrophages and a sepsis mouse model. The data presented in this study indicated that CLME inhibited LPS-induced production of proinflammatory mediators such as nitric oxide (NO) and prostaglandin E2 (PGE2) in RAW 264.7 cells. CLME treatment also reduced reactive oxygen species (ROS) generation and enhanced the expression of heme oxygenase-1 (HO-1) protein in a dose-dependent manner in the LPS-stimulated RAW 264.7 cells. Moreover, CLME treatment abolished the nuclear translocation of nuclear factor-κB (NF-κB), enhanced the activation of nuclear factor-erythroid 2 p45-related factor 2 (Nrf2), and reduced the expression of extracellular signal-related kinase (ERK) and ERK kinase (MEK) phosphorylation in LPS-stimulated RAW 264.7 cells. These outcomes implied that CLME could be a potential antioxidant and anti-inflammatory agent.

中文翻译:

Carpesium cernuum L. 甲醇提取物在 LPS 刺激的 RAW 264.7 巨噬细胞中的抗炎和抗氧化作用。

过度神经反应或异常炎症过程可能导致一系列疾病,如心血管疾病、神经变性和癌症。此外,已发现氧化应激会导致严重的组织损伤和炎症。Carpesium cernuum L. (C. cernuum ) 是一种中草药,具有抗炎、镇痛和解毒特性。然而,C. cernuum在炎症和氧化应激条件下的潜在分子机制在很大程度上仍然未知。本研究的目的是检查 C. cernuum甲醇提取物的影响(CLME) 对脂多糖-(LPS-) 诱导的 RAW 264.7 小鼠巨噬细胞和败血症小鼠模型。本研究中提供的数据表明,CLME 抑制了 LPS 诱导的RAW 264.7 细胞中促炎介质的产生,例如一氧化氮 (NO) 和前列腺素 E 2 (PGE 2 )。在 LPS 刺激的 RAW 264.7 细胞中,CLME 处理还减少了活性氧 (ROS) 的产生并以剂量依赖性方式增强了血红素加氧酶-1 (HO-1) 蛋白的表达。此外,治疗CLME废除核因子的核转位κ B(NF- κB),增强了核因子-红细胞 2 p45 相关因子 2 (Nrf2) 的激活,并降低了 LPS 刺激的 RAW 264.7 细胞中细胞外信号相关激酶 (ERK) 和 ERK 激酶 (MEK) 磷酸化的表达。这些结果暗示 CLME 可能是一种潜在的抗氧化剂和抗炎剂。
更新日期:2020-08-09
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