The objective of this study was to

The objective of this study was to explore the effect of long-term cold exposure on morphological changes of WAT and BAT, metabolic changes and inflammatory responses in vivo. We also investigated the effect of cold exposure on the osteogenic differentiation of BMMSCs and the mechanism involved was in vitro. At the end of the animal experiments, WAT and BAT were isolated and analyzed by HE staining. The results showed that both temperature and exposure time were associated with the degree of WAT browning. Then, peripheral blood samples were collected and centrifuged to obtain serum. Serum biochemical analysis was performed. After exposure to cold air for 21 d, cyclic adenosine monophosphate (cAMP) level in BAT was greatly upregulated. cAMP in WAT and glycerol levels were slightly increased. Cold exposure decreased triglyceride (TG) level and increased the levels of total cholesterol (TC) and low-density lipoprotein cholesterol (LDL-C). Whereas, high-density lipoprotein cholesterol (HDL-C) and free fatty acid (FFA) levels remains unchanged. Moreover, leptin and adiponectin (ADP) levels were remarkably downregulated. Tumor necrosis factor (TNF)-α and interleukin (IL)-6 concentrations were significantly elevated. Furthermore, the results showed that cold exposure significantly elevated runt-related transcription factor 2 (Runx2), bone sialoprotein (BSP), osteopontin (OPN) and collagenⅠ levels and promoted the phosphorylation of p38 MAPK. However, the inducing effects were greatly inhibited by p38 MAPK inhibitor SB203580. These data suggest that long-term cold exposure activate BAT, increase lipolysis rate and enhance inflammatory response in mice. Furthermore, cold
exposure promoted the osteogenic differentiation of BMMSCs partially via the p38 MAPK pathway.

結果 (中文) 1:

本研究的目的是探讨对形态学变化的扫管笏和蝙蝠、 代谢变化与炎症反应在体内长期寒冷暴露的影响。我们还考察了冷暴露对骨髓间充质干细胞向成骨细胞分化的影响和机理进行了体外。在动物实验结束后，分离和分析 HE 染色扫管笏和蝙蝠。结果表明，温度和曝光时间与扫管笏褐变度相关联。然后，外周血样本收集，离心获得血清。进行了血清生化分析。暴露于寒冷的空气为 21 d，环磷酸腺苷 (cAMP) 水平在蝙蝠后大大上调。营地扫管笏和甘油含量略有增加。冷暴露降低甘油三酯 (TG) 水平和总胆固醇 (TC) 和低密度脂蛋白胆固醇 (LDL-C) 水平升高。而高密度脂蛋白胆固醇 (HDL-C) 和游离脂肪酸 (FFA) 水平保持不变。此外，瘦素和脂联素 (ADP) 水平有明显氪。肿瘤坏死因子 (TNF)-α、 白细胞介素 (IL)-6 浓度均显著升高。此外，结果表明，冷暴露明显升高，侏儒相关转录因子 2 (Runx2) 骨涎蛋白 (BSP)，骨桥蛋白 (OPN)，ⅰ 水平和促进的 p38 MAPK 磷酸化。然而，诱导作用被大大抑制 p38 MAPK 抑制剂 SB203580。这些数据表明长期寒冷暴露激活蝙蝠，增加脂肪分解率并提高小鼠组织炎症反应。此外寒冷曝光促进骨髓间充质干细胞成骨分化部分通过 p38 MAPK 通路。

結果 (中文) 3:

本研究的目的是探讨长期冷暴露对WAT和BAT的形态学变化的影响，代谢和炎症反应在体内。我们还研究了冷暴露对骨髓间充质干细胞成骨分化及机制的体外。动物实验结束时，分离和HE染色分析WAT和BAT。结果表明，温度和曝光时间与WAT褐变程度有关。然后，抽取外周血标本，离心取血清。进行血清生化分析。21天暴露于冷空气后，环磷酸腺苷（cAMP）水平明显上调的蝙蝠。在水和甘油水平营略有增加。冷暴露降低甘油三酯（TG）水平，升高血清总胆固醇（TC）、低密度脂蛋白胆固醇（LDL-C）。然而，高密度脂蛋白胆固醇（HDL-C）和游离脂肪酸（FFA）水平保持不变。此外，瘦素和脂联素（ADP）水平均显著下调。肿瘤坏死因子-α和白细胞介素（IL）- 6浓度显著升高。此外，研究结果表明，冷暴露显著升高Runt相关转录因子2（Runx2），骨涎蛋白（BSP），骨桥蛋白（OPN）和胶原Ⅰ水平和促进p38 MAPK的磷酸化。不过诱导作用是通过p38 MAPK抑制剂SB203580可明显抑制。这些数据表明，长期暴露于寒冷的环境激活蝙蝠，增加脂肪分解率，提高小鼠的炎症反应。此外，冷
暴露促进骨髓间充质干细胞成骨分化的部分通过p38 MAPK通路。