p38丝裂原活化蛋白激酶
一氧化氮合酶
激酶
肿瘤坏死因子α
超氧化物歧化酶
炎症
脂多糖
一氧化氮
αBκ
氧化应激
化学
蛋白激酶A
活性氧
信号转导
谷胱甘肽过氧化物酶
分子生物学
药理学
生物化学
NF-κB
生物
免疫学
内分泌学
作者
Jiha Byun,Su Kang Kim,Ju Yeon Ban
标识
DOI:10.1142/s0192415x21500336
摘要
Inflammatory macrophages stimulated by LPS disrupt homeostasis in the production of inflammatory cytokines and nitric oxide (NO). These are the causes of inflammation-related diseases and various cancers. The present study aimed to evaluate the protective effects of Korean ginseng berry extract (KGB) on lipopolysaccharide (LPS)-induced inflammation in RAW264.7 macrophage cells. NO and prostaglandin E2 (PGE[Formula: see text] production was elevated in response to LPS stimulation and was dose-dependently reduced by pretreatment with KGB. The expression levels of inducible NO synthase (iNOS) and cyclooxygenase-2 (COX-2) mRNA and protein were also reduced by KGB treatment. KGB treatment significantly suppressed the LPS-induced gene expression and production of cytokines, including interleukin (IL)-1[Formula: see text], IL-6, and tumor necrosis factor-[Formula: see text] (TNF-[Formula: see text]. Furthermore, KGB inhibited the translocation of nuclear expression of nuclear factor-kappa B (NF-[Formula: see text]B) by preventing inhibitory factor-kappa B (I[Formula: see text]B[Formula: see text] phosphorylation and suppressing the phosphorylation of extracellular signal-related kinase (ERK1/2), c-Jun N-terminal kinase (JNK), and p38. Additionally, decreased reactive oxygen species (ROS) generation and increased glutathione peroxidase (GSH-Px), superoxide dismutase (SOD), and catalase (CAT) activities were observed following KGB treatment. Taken together, these results indicated that KGB possesses anti-inflammatory and anti-oxidant effects, mediated by the inhibition of the mitogen-activated protein kinases (MAPKs) signaling pathway in LPS-induced RAW264.7 macrophages. KGB may represent a potential therapeutic agent for inflammatory and oxidative stress-related diseases.
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