Peng Xiaohui, Nie Yao, Wu Jianjun, Huang Qiang, Cheng Yuqiang
College of Aerospace Science and Engineering, National Univ. of Defense Technology, Changsha, Hunan 430000, China.
College of Aerospace Science and Engineering, National Univ. of Defense Technology, Changsha, Hunan 430000, China.
Biochem Biophys Res Commun. 2015 Jul 3;462(3):245-50. doi: 10.1016/j.bbrc.2015.04.124. Epub 2015 May 9.
Juglone as a natural production mainly extracted from green walnut husks of Juglans mandshurica has been defined as the functional composition among a series of compounds. It showed powerful protective effect in various diseases by inhibiting inflammation and tumor cells growth. However, studies on its anti-inflammatory effect based on high-fat diet-induced hepatitis and neuroinflammation are still not available. In this regard, we first investigated whether juglone suppresses high-fat diet-stimulated liver injury, hypothalamus inflammation and underlying mechanisms by which they may recover them. SD rats were orally treated with or without high-fat diet, 0.25 mg/kg or 1 mg/kg juglone for 70 days. Subsequently, blood, hypothalamus and liver tissue were collected for different analysis. Also, the primary astrocytes were isolated and used to analyze the inhibitory effect of juglone in vitro. Analysis of inflammatory cytokines declared that the inhibition of TNF-α, IL-1β and IL-6 could be carried by juglone in response to high-fat diet rats. Meanwhile, TLR4 expression and NF-kappa activity also have been confirmed to be the key link in the development of hepatitis and nerve inflammation. The activation was significantly suppressed in treatment group as compared with model. These results indicated that juglone prevents high-fat diet-induced liver injury and nerve inflammation in mice through inhibition of inflammatory cytokine secretion, NF-kappa B activation and endotoxin production.
胡桃醌作为一种主要从胡桃楸青核桃壳中提取的天然产物,在一系列化合物中被定义为功能成分。它通过抑制炎症和肿瘤细胞生长,在多种疾病中显示出强大的保护作用。然而,关于其基于高脂饮食诱导的肝炎和神经炎症的抗炎作用的研究仍然缺乏。在这方面,我们首先研究了胡桃醌是否能抑制高脂饮食刺激的肝损伤、下丘脑炎症以及它们可能恢复的潜在机制。将SD大鼠分为高脂饮食组和非高脂饮食组,分别给予0.25mg/kg或1mg/kg胡桃醌口服给药70天。随后,收集血液、下丘脑和肝脏组织进行不同分析。此外,分离原代星形胶质细胞用于分析胡桃醌在体外的抑制作用。炎症细胞因子分析表明,胡桃醌可抑制高脂饮食大鼠体内肿瘤坏死因子-α(TNF-α)、白细胞介素-1β(IL-1β)和白细胞介素-6(IL-6)。同时,Toll样受体4(TLR4)表达和核因子κB(NF-κB)活性也被证实是肝炎和神经炎症发展的关键环节。与模型组相比,治疗组的激活明显受到抑制。这些结果表明,胡桃醌通过抑制炎症细胞因子分泌、NF-κB激活和内毒素产生,预防小鼠高脂饮食诱导的肝损伤和神经炎症。