PDF(Pubmed)
Abstract：
Background and Objectives: This study evaluated the in vitro anti-adipogenic and anti-inflammatory properties of black cumin (Nigella sativa L.) seed extract (BCS extract) as a potential candidate for developing herbal formulations targeting metabolic disorders. Materials and Methods: We evaluated the BCS extract by assessing its 2,2-diphenyl-1-picrohydrazyl (DPPH) radical scavenging activity, levels of prostaglandin E2 (PGE2) and nitric oxide (NO), and mRNA expression levels of key pro-inflammatory mediators. We also quantified the phosphorylation of nuclear factor kappa light chain enhancer of activated B cells (NF-κB) and mitogen-activated protein kinases (MAPK) signaling molecules. To assess anti-adipogenic effects, we used differentiated 3T3-L1 cells and BCS extract in doses from 10 to 100 μg/mL. We also determined mRNA levels of key adipogenic genes, including peroxisome proliferator-activated receptor γ (PPARγ), CCAAT/enhancer binding protein α (C/BEPα), adipocyte protein 2 (aP2), lipoprotein lipase (LPL), fatty acid synthase (FAS), and sterol-regulated element-binding protein 1c (SREBP-1c) using real-time quantitative polymerase chain reaction (qPCR). Results: This study showed a concentration-dependent DPPH radical scavenging activity and no toxicity at concentrations up to 30 μg/mL in Raw264.7 cells. BCS extract showed an IC50 of 328.77 ± 20.52 μg/mL. Notably, pre-treatment with BCS extract (30 μg/mL) significantly enhanced cell viability in lipopolysaccharide (LPS)-treated Raw264.7 cells. BCS extract treatment effectively inhibited LPS-induced production of PGE2 and NO, as well as the expression of monocyte chemoattractant protein-1 (MCP-1), tumor necrosis factor-α (TNF-α), cyclooxygenase-2 (COX-2), inducible NO synthase (iNOS), interleukin (IL)-1β and IL-6, possibly by limiting the phosphorylation of p38, p65, inhibitory κBα (I-κBα), and c-Jun N-terminal kinase (JNK). It also significantly attenuated lipid accumulation and key adipogenic genes in 3T3-L1 cells. Conclusions: This study highlights the in vitro anti-adipogenic and anti-inflammatory potential of BCS extract, underscoring its potential as a promising candidate for managing metabolic disorders.
摘要：
背景和目的：这项研究评估了黑孜然（NigellasativaL.）种子提取物（BCS提取物）作为开发针对代谢紊乱的草药制剂的潜在候选物的体外抗脂肪生成和抗炎特性。材料和方法：我们通过评估其2,2-二苯基-1-吡啶基（DPPH）自由基清除活性来评估BCS提取物，前列腺素E2（PGE2）和一氧化氮（NO）的水平，和关键促炎介质的mRNA表达水平。我们还定量了活化B细胞（NF-κB）和丝裂原活化蛋白激酶（MAPK）信号分子的核因子κ轻链增强剂的磷酸化。为了评估抗脂肪生成作用，我们使用分化的3T3-L1细胞和BCS提取物,剂量为10-100μg/mL.我们还确定了关键成脂基因的mRNA水平，包括过氧化物酶体增殖物激活受体γ（PPARγ），CCAAT/增强子结合蛋白α（C/BEPα），脂肪细胞蛋白2（aP2），脂蛋白脂酶（LPL），脂肪酸合成酶（FAS），和固醇调节元件结合蛋白1c（SREBP-1c）使用实时定量聚合酶链反应（qPCR）。结果：本研究显示了浓度依赖性的DPPH自由基清除活性，在Raw264.7细胞中浓度高达30μg/mL时没有毒性。BCS提取物的IC50为328.77±20.52μg/mL。值得注意的是,在脂多糖(LPS)处理的Raw264.7细胞中,用BCS提取物(30μg/mL)预处理显著增强细胞活力。BCS提取物处理有效抑制LPS诱导的PGE2和NO的产生，以及单核细胞趋化蛋白-1（MCP-1）的表达，肿瘤坏死因子-α(TNF-α),环氧合酶-2（COX-2），诱导型NO合酶（iNOS），白细胞介素（IL）-1β和IL-6，可能通过限制p38，p65，抑制性κBα（I-κBα）的磷酸化，和c-Jun氨基末端激酶(JNK)。它还显著减弱3T3-L1细胞中的脂质积累和关键脂肪生成基因。结论：本研究强调了BCS提取物的体外抗脂肪生成和抗炎潜力，强调其作为一个有希望的候选人管理代谢紊乱的潜力。
