Mao Songbo, Xu Chuntao, Zou Lin
Orthepadic Department, The 960th Hospital of the PLA Joint Logistics Support Force, Jinan, Shandong, China.
J Biochem Mol Toxicol. 2025 Aug;39(8):e70432. doi: 10.1002/jbt.70432.
Osteoporosis is a condition in where bones gradually become thin and weak, making them more susceptible to fractures. Columbianadin has showed potential anti-inflammatory and antioxidant effect. In this experimental study, anti-osteoporosis effect of Columbianadin against glucocorticoid induced osteoporosis in rats.
In this study, Sprague Dawley (SD) rats were used and osteoporosis was induced by administering dexamethasone (DEX) at a dosage of 2.5 mg/kg/day. Following induction, the rats were treated orally with different doses of columbianadin. The body weight, organ (femoral, vagina and uterus) weights were measured. The bone parameters, antioxidant, cytokines, hormones were evaluated.
Columbianadin improved body weight and altered the organ weight such as femoral, vagina and uterus. It also modulated the various bone related parameters including bone mineral density (BMD), tissue mineral density (TMD), bone mineral content (BMC), tissue mineral content (TMC); bone parameters like tartrate-resistant acid phosphatase (TRAP), β -C-terminal telopeptide of type I collagen (β-CTX), osteocalcin (OC), bone gla protein (BGP), acid phosphatase (ACP), alkaline phosphatase (ALP). Additionally, Columbianadin influence hormone level such as estradiol (E) and parathyroid hormone (PTH) and enhanced antioxidant defense via modulating glutathione peroxidase (GPx), thiobarbituric acid reactive substances (TBARS), catalase (CAT), superoxide dismutase (SOD), glutathione (GSH). It also regulated the cytokines parameters like tumor necrosis factor- α (TNF-α), interleukin-1β (IL-1β), interleukin-6 (IL-6), insulin-like growth factor (IGF), transforming growth factor-β (TGF-β). Furthermore, columbianadin modulated the levels of receptor activator of nuclear factor-κB ligand (RANKL), osteoprotegerin (OPG) and OPG/RANKL ratio. Columbianadin also altered mRNA expression of ALP, OPN, runt-related transcription factor 2 (RunX2), OCN, bone morphogenetic proteins (BMP)-2, 4, 6, 7, 9, B-cell lymphoma 2 (BcL-2), B-cell lymphoma-extra-large (BcLxL), Inhibitor of Apoptosis Protein (IAP) 1, 2, X-linked Inhibitor of apoptosis Protein (XIAP), caspase-3,6,7,9, respectively.
The finding of the study clearly demonstrates that columbianadin exerts a significant antiosteoporosis effect against glucocorticoid-induced osteoporosis in rats.
骨质疏松症是一种骨骼逐渐变薄和变弱的病症，使其更容易发生骨折。哥伦比亚苷元已显示出潜在的抗炎和抗氧化作用。在本实验研究中，观察哥伦比亚苷元对大鼠糖皮质激素诱导的骨质疏松症的抗骨质疏松作用。
在本研究中，使用Sprague Dawley（SD）大鼠，通过以2.5mg/kg/天的剂量给予地塞米松（DEX）诱导骨质疏松症。诱导后，大鼠口服不同剂量的哥伦比亚苷元。测量体重、器官（股骨、阴道和子宫）重量。评估骨参数、抗氧化剂、细胞因子、激素。
哥伦比亚苷元改善了体重，并改变了器官重量，如股骨、阴道和子宫。它还调节了各种与骨相关的参数，包括骨矿物质密度（BMD）、组织矿物质密度（TMD）、骨矿物质含量（BMC）、组织矿物质含量（TMC）；骨参数如抗酒石酸酸性磷酸酶（TRAP）、I型胶原β-羧基末端肽（β-CTX）、骨钙素（OC）、骨钙蛋白（BGP）、酸性磷酸酶（ACP）、碱性磷酸酶（ALP）。此外，哥伦比亚苷元影响激素水平，如雌二醇（E）和甲状旁腺激素（PTH），并通过调节谷胱甘肽过氧化物酶（GPx）、硫代巴比妥酸反应性物质（TBARS）、过氧化氢酶（CAT）、超氧化物歧化酶（SOD）、谷胱甘肽（GSH）增强抗氧化防御。它还调节细胞因子参数，如肿瘤坏死因子-α（TNF-α）、白细胞介素-1β（IL-1β）、白细胞介素-6（IL-6）、胰岛素样生长因子（IGF）、转化生长因子-β（TGF-β）。此外，哥伦比亚苷元调节核因子-κB配体受体激活剂（RANKL）、骨保护素（OPG）和OPG/RANKL比值的水平。哥伦比亚苷元还分别改变了ALP、骨桥蛋白（OPN）、 runt相关转录因子2（RunX2）、骨钙蛋白（OCN）、骨形态发生蛋白（BMP）-2、4、6、7、9、B细胞淋巴瘤2（BcL-2）、B细胞淋巴瘤-超大（BcLxL）、凋亡抑制蛋白（IAP）1、2、X连锁凋亡抑制蛋白（XIAP）、半胱天冬酶-3、6、7、9的mRNA表达。
该研究结果清楚地表明，哥伦比亚苷元对大鼠糖皮质激素诱导的骨质疏松症具有显著的抗骨质疏松作用。
