N-actylcysteine inhibits diethyl phthalate-induced inflammation via JNK and STAT pathway in RAW264.7 macrophages.

IF 2.4 3区 生物学 Q4 CELL BIOLOGY
Jin Hee Kim, Jae Hoon Lee, Yoon Jung Koo, Jong Wook Song
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Abstract

Background: Phthalates are plasticizers that cause inflammation in several cell types and adversely affect the health of humans and animals. Nacetylcysteine (NAC) has been shown to exert antioxidant effects in various diseases. However, the effect of NAC on diethyl phthalate (DEP)-induced toxicity in macrophages has not yet been elucidated. In this study, we investigated the effect and underlying mechanisms of NAC on DEP-induced inflammation in RAW264.7 macrophages. RAW264.7 macrophages were pretreated with NAC for 2 h followed by exposure to DEP. We investigated the effect of NAC on NO, reactive oxygen species (ROS), prostaglandin E2 (PGE2), and glutathione (GSH) levels following DEP exposure. In addition, pathway-related genes including cyclooxygenase-2 (COX-2), inducible nitric oxide synthase (iNOS), mitogen-activated protein kinase (MAPK), and signal transducer and activator of transcription (STAT) were evaluated using western blot.

Results: Treatment with 100 and 300 µM DEHP, DBP, and DEP significantly increased the protein levels of cyclooxygenase-2 (COX-2) and inducible nitric oxide synthase (iNOS) compared with those in the control group. However, NAC pretreatment downregulated the levels of NO, PGE2, and ROS, elevated GSH levels, and suppressed the mRNA levels of inflammatory cytokines such as interleukin (IL)-1β, IL-6, COX-2, and iNOS compared with those in the DEP-treated group. In addition, NAC significantly reduced the levels of p-JNK and p-STAT1/3 in RAW264.7 macrophages treated with DEP.

Conclusions: NAC pretreatment inhibits DEP-induced inflammation via the MAPK/JNK and STAT1/3 pathways in macrophages.

n -乙酰半胱氨酸通过JNK和STAT途径抑制RAW264.7巨噬细胞中邻苯二甲酸二乙酯诱导的炎症。
背景:邻苯二甲酸酯是一种增塑剂,可引起几种细胞类型的炎症,并对人类和动物的健康产生不利影响。乙酰半胱氨酸(NAC)已被证明在多种疾病中发挥抗氧化作用。然而,NAC对邻苯二甲酸二乙酯(DEP)诱导的巨噬细胞毒性的影响尚未阐明。在本研究中,我们研究了NAC对deep诱导的RAW264.7巨噬细胞炎症的影响及其机制。我们用NAC预处理RAW264.7巨噬细胞2小时,然后暴露于DEP,研究NAC对DEP暴露后NO、活性氧(ROS)、前列腺素E2 (PGE2)和谷胱甘肽(GSH)水平的影响。此外,采用western blot方法对途径相关基因包括环氧化酶-2 (COX-2)、诱导型一氧化氮合酶(iNOS)、丝裂原活化蛋白激酶(MAPK)和转录信号转导和激活因子(STAT)进行检测。结果:与对照组相比,100和300µM DEHP、DBP和DEP处理可显著提高环氧化酶-2 (COX-2)和诱导型一氧化氮合酶(iNOS)的蛋白水平。然而,与深度治疗组相比,NAC预处理可下调NO、PGE2和ROS水平,升高GSH水平,抑制炎症细胞因子如白细胞介素(IL)-1β、IL-6、COX-2和iNOS的mRNA水平。此外,NAC显著降低了depa处理RAW264.7巨噬细胞中p-JNK和p-STAT1/3的水平。结论:NAC预处理通过MAPK/JNK和STAT1/3通路抑制depa诱导的巨噬细胞炎症。
本文章由计算机程序翻译,如有差异,请以英文原文为准。
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来源期刊
BMC Molecular and Cell Biology
BMC Molecular and Cell Biology Biochemistry, Genetics and Molecular Biology-Cell Biology
CiteScore
5.50
自引率
0.00%
发文量
46
审稿时长
27 weeks
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