关键词: Bone disease Bone mineral density Molecular docking Osteocalcin Postmenopausal osteoporosis Toxicity study

Mesh : Female Humans Rats Animals Osteoporosis, Postmenopausal / drug therapy Molecular Docking Simulation Rats, Sprague-Dawley Bone Remodeling Estrogens Biomarkers

来  源:   DOI:10.1002/cbdv.202400172

Abstract:
Kariavattom Campus Postmenopausal osteoporosis (PMO) is an old age disorder associated with estrogen deficiency, which reduces bone mass and makes bones more prone to fracture. The present study was proposed to evaluate the invivo osteogenic efficiency of Pterospermum rubiginosum methanolic bark extract (PRME) in the PMO model. Molecular docking studies on transcription factor NFATC1 showed excellent interactions with phytochemical ligands with the lowest binding energies. Female Sprague Dawley (SD) rats (n=24) were divided into four groups, (n=6 each) sham control (Group I) and osteoporotic control (Group II) groups treated with saline, PRME (50 mg/kg/day) and alendronate (10 mg/kg/day) treated with Group III and Group IV (n=6) respectively. The serum tartrate-resistant acid phosphatase 5b and cathepsin-K also exhibited a significant rise after PRME treatment 12.33±2.30 mU/ml and 427.68±46.97 pg/ml, respectively. DEXA results exhibited a remarkable increase in total bone mineral content and density values in PRME-treated animals (0.175±0.002 g/cm2) and (7.95±0.23 g) when compared to osteoporotic control (0.163±0.004 g/cm2) and (6.83±0.34 g). Long-term toxicity study revealed that PRME is non-toxic, up to 100 mg/kg bodyweight for 6 months. Our findings suggest PRME protects osteoporotic SD rats from PMO damage resulting from estrogen deficiency by regulating bone remodelling markers and upregulating BMD indices.
摘要:
绝经后骨质疏松症(PMO)是一种与雌激素缺乏相关的老年疾病,这减少了骨量,使骨骼更容易骨折。本研究旨在评估Pterospermumrubiginosum甲醇树皮提取物(PRME)在PMO模型中的体内成骨效率。对转录因子NFATC1的分子对接研究显示与具有最低结合能的植物化学配体的优异相互作用。雌性SD大鼠(n=24)分为4组,(n=6各)假对照(组I)和骨质疏松对照组(组II)用盐水处理,PRME(50mg/kg/天)和阿仑膦酸盐(10mg/kg/天)分别用III组和IV组(n=6)处理。PRME处理后,血清抗酒石酸酸性磷酸酶5b和组织蛋白酶-K也显示出显着升高12.33±2.30mU/ml和427.68±46.97pg/ml,分别。与骨质疏松对照(0.163±0.004g/cm2)和(6.83±0.34g)相比,DEXA结果显示,PRME治疗的动物的总骨矿物质含量和密度值显着增加(0.175±0.002g/cm2)和(7.95±0.23g)。长期毒性研究表明,PRME是无毒的,高达100毫克/公斤体重6个月。我们的发现表明,PRME通过调节骨骼重塑标志物和上调BMD指数来保护骨质疏松SD大鼠免受雌激素缺乏引起的PMO损伤。
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