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一种生物活性组分通过调节PPAR-γ/SREBP-1c和TNF-α/IL-6抑制3T3-L1细胞的脂肪生成和炎症。

A bioactive fraction of inhibits adipogenesis and inflammation in 3T3-L1 cells via modulation of PPAR-γ/SREBP-1c and TNF-α/IL-6.

作者信息

Reddy Sankaran Karunakaran, Ganjayi Muni Swamy, Oruganti Lokanatha, Chippada Appa Rao, Meriga Balaji

机构信息

Division of Cell Culture and Molecular Biology, Department of Biochemistry, Sri Venkateswara University, Tirupati, Andhra Pradesh 517502 India.

出版信息

3 Biotech. 2021 May;11(5):233. doi: 10.1007/s13205-021-02771-2. Epub 2021 Apr 23.

Abstract

has huge demand owing to its commercial and medicinal value. However, there are limited research studies on its therapeutic activity against obesity and obesity-induced inflammation and underlying mechanism of action. Therefore, in the present study, chloroform bioactive fraction of (CFP) was isolated and evaluated for its activity against adipogenesis and adipogenesis-induced inflammation in 3T3-L1 cell culture model. LC-MS/MS analysis of CFP was performed to identify the compounds present. CFP-treated 3T3-L1 cells (50, 100 and 200 μg/ml) have significantly ( < 0.01 or < 0.05) enhanced glycerol release and adiponectin level, but reduced lipid accumulation and leptin, and MTT assay demonstrated CFP was non-toxic till a dose of 300 µg/ml at 24 and 48 h. A considerable reduction in tumor necrosis factor-α (TNF-α) and interleukin-6 (IL-6) levels was witnessed in lipopolysaccharide (LPS)-induced 3T3-L1 cells with CFP treatment in dose-dependent manner. Gene expression studies demonstrated down-regulation of mRNA expression of peroxisome proliferator-activated receptor-γ (PPAR-γ), sterol regulatory element-binding protein-1c (SREBP-1c), leptin, TNF-α and IL-6 but up-regulation of adiponectin and uncoupling protein-1 (UCP-1) and the same trend was observed in protein expression also. In conclusion, it is suggested that CFP could be beneficial to treat obesity and associated inflammation.

摘要

由于其商业和药用价值,对其需求巨大。然而,关于其抗肥胖和肥胖诱导炎症的治疗活性及其潜在作用机制的研究有限。因此,在本研究中,分离了[具体物质]的氯仿生物活性组分(CFP),并在3T3-L1细胞培养模型中评估其对脂肪生成和脂肪生成诱导炎症的活性。对CFP进行了LC-MS/MS分析以鉴定其中存在的化合物。用CFP处理的3T3-L1细胞(50、100和200μg/ml)显著(<0.01或<0.05)提高了甘油释放和脂联素水平,但减少了脂质积累以及瘦素水平,MTT试验表明在24小时和48小时时,CFP在剂量达300μg/ml时无毒。在用CFP处理的脂多糖(LPS)诱导的3T3-L1细胞中,观察到肿瘤坏死因子-α(TNF-α)和白细胞介素-6(IL-6)水平以剂量依赖性方式显著降低。基因表达研究表明,过氧化物酶体增殖物激活受体-γ(PPAR-γ)、固醇调节元件结合蛋白-1c(SREBP-1c)、瘦素、TNF-α和IL-6的mRNA表达下调,但脂联素和解偶联蛋白-1(UCP-1)的表达上调,并且在蛋白质表达中也观察到相同趋势。总之,提示CFP可能有益于治疗肥胖及相关炎症。

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