Lu Rongrong, Zheng Zicong, Yin Yimin, Jiang Zhuoqin
Department of Nutrition, School of Public Health, Sun Yat-Sen University, Guangzhou, People's Republic of China.
Food Nutr Res. 2020 Dec 9;64. doi: 10.29219/fnr.v64.3666. eCollection 2020.
Diabetic osteoporosis has become a severe public health problem in the aging societies. Genistein has been reported to play an important role in preventing and treating metabolic diseases via its anti-inflammatory, antioxidant, anti-estrogenic, and estrogen-like functions.
We aimed to investigate whether genistein exerts bone-protective effect on diabetic rats induced by 35 mg/kg streptozotocin (STZ) plus a 4-week high-fat diet.
Sprague-Dawley rats were randomly divided into four groups: (1) control group, (2) type 2 diabetes mellitus (T2DM) model group, (3) T2DM with 10 mg/kg genistein, and (4) T2DM with 30 mg/kg genistein. After an 8-week treatment with genistein, the femurs, tibias, and blood were collected from all rats for further analysis.
Genistein at 10 mg/kg showed little effect on diabetic osteoporosis, whereas genistein at 30 mg/kg significantly improved glucose and bone metabolisms compared with diabetic rats. Our results showed that 30 mg/kg genistein significantly increased bone mineral density, serum osteocalcin, and bone alkaline phosphatase. Genistein also effectively lowered fasting blood glucose, tartrate-resistant acid phosphatase 5b, tumor necrosis factor-α, interleukin-6, and numbers of adipocytes and osteoclasts. Compared with the T2DM group, protein levels of receptor activator of nuclear factor κB ligand (RANKL) and peroxisome proliferator-activated receptor-γ (PPAR-γ) were decreased, while protein levels of osteoprotegerin (OPG), β-catenin, and runt-related transcription factor 2 (Runx-2) were increased after genistein intervention.
Genistein could effectively improve abnormal bone metabolism in STZ-induced diabetic rats; the underlying molecular mechanisms might be related to OPG/RANKL, PPAR-γ, and β-catenin/Runx-2 pathways.
在老龄化社会中，糖尿病性骨质疏松已成为一个严重的公共卫生问题。据报道，染料木黄酮通过其抗炎、抗氧化、抗雌激素和雌激素样功能，在预防和治疗代谢性疾病中发挥重要作用。
我们旨在研究染料木黄酮对由35mg/kg链脲佐菌素（STZ）加4周高脂饮食诱导的糖尿病大鼠是否具有骨保护作用。
将Sprague-Dawley大鼠随机分为四组：（1）对照组，（2）2型糖尿病（T2DM）模型组，（3）10mg/kg染料木黄酮治疗的T2DM组，（4）30mg/kg染料木黄酮治疗的T2DM组。用染料木黄酮治疗8周后，收集所有大鼠的股骨、胫骨和血液进行进一步分析。
10mg/kg的染料木黄酮对糖尿病性骨质疏松几乎没有影响，而30mg/kg的染料木黄酮与糖尿病大鼠相比，显著改善了血糖和骨代谢。我们的结果表明，30mg/kg的染料木黄酮显著提高了骨密度、血清骨钙素和骨碱性磷酸酶。染料木黄酮还有效降低了空腹血糖、抗酒石酸酸性磷酸酶5b、肿瘤坏死因子-α、白细胞介素-6以及脂肪细胞和破骨细胞的数量。与T2DM组相比，染料木黄酮干预后，核因子κB受体激活剂配体（RANKL）和过氧化物酶体增殖物激活受体-γ（PPAR-γ）的蛋白水平降低，而骨保护素（OPG）、β-连环蛋白和 runt相关转录因子2（Runx-2）的蛋白水平升高。
染料木黄酮可有效改善STZ诱导的糖尿病大鼠的异常骨代谢；潜在的分子机制可能与OPG/RANKL、PPAR-γ和β-连环蛋白/Runx-2途径有关。
