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香烟烟雾提取物可减少人骨髓间充质基质细胞的成脂分化。

Cigarette smoke extract decreases human bone marrow mesenchymal stromal cell adipogenic differentiation.

机构信息

Medical Faculty, Translational Medicine Research Unit, University of Oulu, Oulu, Finland.

Medical Faculty, Translational Medicine Research Unit, University of Oulu, Oulu, Finland; Medical Research Center, University of Oulu and Oulu University Hospital, Oulu, Finland.

出版信息

Toxicol In Vitro. 2024 Dec;101:105949. doi: 10.1016/j.tiv.2024.105949. Epub 2024 Sep 27.

DOI:10.1016/j.tiv.2024.105949
PMID:39343071
Abstract

BACKGROUND

Smoking and nicotine impose detrimental health effects including adipose tissue dysfunction. Despite extensive physiological evidence, the cellular mechanisms remain poorly understood, with few studies examining the effects of cigarette smoke extract (CSE) or nicotine on adipocyte differentiation.

METHODS

Primary human bone marrow-derived mesenchymal stromal cells (MSCs) were exposed to CSE or nicotine (50-500 ng/ml) during adipogenic differentiation. Cell viability and metabolic activity were assessed via MTT assay. Lipid droplet accumulation was evaluated using Sudan III staining and quantitative image analysis. Adiponectin, IL6, and IL8 concentrations were measured after 35 days using ELISA.

RESULTS

At these doses, CSE and nicotine do not immediately affect cell viability but inhibit undifferentiated cell proliferation. Notably, both agents at 50 ng/ml significantly increased lipid accumulation during adipogenesis, while higher CSE doses nearly completely inhibited this process. Additionally, CSE dose-dependently decreased adiponectin secretion and increased IL6 and IL8, indicating a shift towards an inflammatory state. Nicotine alone primarily increased IL6 secretion with less pronounced effects.

CONCLUSION

The study highlights the complex impact of CSE and nicotine on adipocyte function during early differentiation from MSCs. Dose-dependent changes in lipid accumulation, cytokine, and adiponectin secretion induced by CSE and nicotine can partly explain smoking-related adipose tissue dysfunction.

摘要

背景

吸烟和尼古丁会对健康造成有害影响,包括脂肪组织功能障碍。尽管有大量的生理学证据,但细胞机制仍知之甚少,很少有研究检查香烟烟雾提取物(CSE)或尼古丁对脂肪细胞分化的影响。

方法

原代人骨髓间充质基质细胞(MSCs)在成脂分化过程中暴露于 CSE 或尼古丁(50-500ng/ml)。通过 MTT 测定法评估细胞活力和代谢活性。使用苏丹 III 染色和定量图像分析评估脂滴积累。用 ELISA 在 35 天后测量脂联素、IL6 和 IL8 的浓度。

结果

在这些剂量下,CSE 和尼古丁不会立即影响细胞活力,但会抑制未分化细胞的增殖。值得注意的是,两种试剂在 50ng/ml 时均显著增加了脂肪生成过程中的脂滴积累,而较高的 CSE 剂量几乎完全抑制了这一过程。此外,CSE 呈剂量依赖性降低脂联素的分泌并增加 IL6 和 IL8,表明向炎症状态转变。尼古丁单独作用主要增加 IL6 的分泌,作用不太明显。

结论

该研究强调了 CSE 和尼古丁在 MSC 早期分化为脂肪细胞过程中对脂肪细胞功能的复杂影响。CSE 和尼古丁诱导的脂质积累、细胞因子和脂联素分泌的剂量依赖性变化部分解释了与吸烟有关的脂肪组织功能障碍。

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