Diabetes Research Center, Traditional Chinese Medicine School, Beijing University of Chinese Medicine, Beijing 100029, China.
Jean Mayer USDA Human Nutrition Research Center on Aging at Tufts University, Boston, MA 02111, USA.
Oxid Med Cell Longev. 2022 Feb 17;2022:3697067. doi: 10.1155/2022/3697067. eCollection 2022.
This study was aimed at examining the effects of lycopene on bone metabolism in high-fat diet (HFD)- induced obese mice and to identify the potential underlying mechanisms.
Mice were fed a HFD for 12 weeks and then continue with or without lycopene intervention (15 mg/kg) for additional 10 weeks. The effects of lycopene on blood glucose and lipid metabolism, as well as serum levels of total antioxidant capacity (T-AOC), superoxide dismutase (SOD), and malondialdehyde (MDA) were determined by biochemical assays. Bone histomorphological features and osteoclast activity were assessed by hematoxylin/eosin and tartrate-resistant acid phosphatase staining. Bone microstructure at the proximal tibial metaphysis and diaphysis was determined by microcomputed tomography. Tibial biomechanical strength and material profiles were measured by a three-point bending assay and Fourier transform infrared spectroscopy. Protein expressions involved in the AGE/RAGE/NF-кB signaling pathway were determined by western blot and/or immunohistochemical staining.
Lycopene consumption reduced body weight gain and improved blood glucose and lipid metabolism in HFD-induced obese mice. In addition, lycopene treatment preserved bone biomechanical strength, material profiles, and microarchitecture in obese mice. Moreover, these alterations were associated with an increase in serum levels of T-AOC and SOD, and a decline in serum levels of MDA, as well as a reduction of AGEs, RAGE, cathepsin K, and p-NF-кBp65 and NF-кBp65 expressions in the femurs and tibias of obese mice.
Lycopene may improve bone quality through its antioxidant properties, which may be linked with the regulation of the AGE/RAGE/NF-кB signaling pathway in obese mice. These results suggest that lycopene consumption may be beneficial for the management of obesity-induced osteoporosis.
本研究旨在探讨番茄红素对高脂饮食（HFD）诱导肥胖小鼠骨代谢的影响，并探讨其潜在的作用机制。
将小鼠喂食 HFD 12 周，然后继续或不继续给予番茄红素干预（15mg/kg）10 周。通过生化分析测定番茄红素对血糖和血脂代谢以及血清总抗氧化能力（T-AOC）、超氧化物歧化酶（SOD）和丙二醛（MDA）水平的影响。通过苏木精/伊红和抗酒石酸酸性磷酸酶染色评估骨组织形态学特征和破骨细胞活性。通过微计算机断层扫描评估胫骨近端干骺端和骨干的骨微结构。通过三点弯曲试验和傅里叶变换红外光谱法测量胫骨生物力学强度和材料特性。通过 Western blot 和/或免疫组织化学染色测定 AGE/RAGE/NF-кB 信号通路相关蛋白的表达。
番茄红素摄入可减少 HFD 诱导肥胖小鼠的体重增加，改善血糖和血脂代谢。此外，番茄红素治疗可维持肥胖小鼠的骨生物力学强度、材料特性和微结构。这些变化与血清 T-AOC 和 SOD 水平升高、MDA 水平降低以及肥胖小鼠股骨和胫骨中 AGEs、RAGE、组织蛋白酶 K 和 p-NF-кBp65 和 NF-кBp65 表达减少有关。
番茄红素可能通过其抗氧化特性改善骨质量，这可能与肥胖小鼠 AGE/RAGE/NF-кB 信号通路的调节有关。这些结果表明，番茄红素摄入可能有益于肥胖引起的骨质疏松症的管理。
