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吲哚-3-甲醇在高脂饮食喂养的小鼠和分离的共培养巨噬细胞和脂肪细胞中抑制炎症相关因子。

Suppression of inflammation-associated factors by indole-3-carbinol in mice fed high-fat diets and in isolated, co-cultured macrophages and adipocytes.

机构信息

School of Pharmacy, Taipei Medical University, Taipei, Taiwan.

出版信息

Int J Obes (Lond). 2011 Dec;35(12):1530-8. doi: 10.1038/ijo.2011.12. Epub 2011 Feb 22.

Abstract

AIMS

This study investigated the effects of indole-3-carbinol (I3C), a compound from cruciferous vegetables, on various parameters related to obesity, in particular, the parameters of infiltration by macrophages and of inflammatory cytokines expressed during the co-culture of adipocytes and macrophages.

METHODS

Male C57BL/6 mice were fed with a control diet (C group), high-fat diet (HF group) and HF+5 mg kg(-1) I3C (HFI group). The I3C was intraperitoneally injected (HFI group) for 12 weeks. Epididymal adipose tissue (AT) was collected and stained for F4/80, a marker of macrophages.

RESULTS

The immunohistochemical staining for F4/80 indicated a greater presence of macrophages in the HF group than in AT from the control and HFI groups. Furthermore, I3C treatment, in an in vitro cell culture system, decreased expression of inducible nitric oxide synthase (iNOS), decreased nitrite content and enhanced expression of peroxisome proliferator-activated receptor (PPAR-γ). Moreover, in vitro cell culture studies revealed that I3C inhibited intracellular lipid accumulation in hypertrophied adipocytes. In macrophage and primary adipocyte co-culture, I3C inhibited expression of interleukin-6 (IL-6).

CONCLUSIONS

In vivo treatment with I3C reduced the infiltration of macrophages in AT, and in vitro addition of I3C to co-cultured macrophages and adipocytes reduced nitrite production and IL-6 expression. With cultures of adipocytes only, I3C inhibited accumulation of intracellular lipid, either by disrupting differentiation, or by directly inhibiting triglyceride synthesis.

摘要

目的

本研究旨在探讨吲哚-3-甲醇(I3C)——一种十字花科蔬菜中的化合物——对肥胖相关的多种参数的影响,尤其是脂肪细胞与巨噬细胞共培养时,细胞浸润、巨噬细胞浸润和炎症细胞因子表达的相关参数。

方法

雄性 C57BL/6 小鼠分别用对照饮食(C 组)、高脂饮食(HF 组)和高脂饮食+5mg/kg I3C(HFI 组)喂养 12 周。通过腹腔注射给予 I3C(HFI 组)。收集附睾脂肪组织(AT)并对 F4/80 进行染色,F4/80 是巨噬细胞的标志物。

结果

免疫组织化学染色 F4/80 显示,与对照和 HFI 组的 AT 相比,HF 组的巨噬细胞更多。此外,在体外细胞培养系统中,I3C 处理降低了诱导型一氧化氮合酶(iNOS)的表达、降低了亚硝酸盐含量并增强了过氧化物酶体增殖物激活受体(PPAR-γ)的表达。此外,体外细胞培养研究表明,I3C 抑制了肥大脂肪细胞内的脂质积累。在巨噬细胞和原代脂肪细胞共培养中,I3C 抑制了白细胞介素-6(IL-6)的表达。

结论

体内给予 I3C 可减少 AT 中巨噬细胞的浸润,体外向共培养的巨噬细胞和脂肪细胞中添加 I3C 可减少亚硝酸盐的产生和 IL-6 的表达。仅培养脂肪细胞时,I3C 通过破坏分化或直接抑制甘油三酯合成来抑制细胞内脂质的积累。

https://cdn.ncbi.nlm.nih.gov/pmc/blobs/92f7/3238050/1f2fac696682/ijo201112f1.jpg

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