Huo Jiang, Ding Yu, Wei Xinyuan, Chen Qi, Zhao Bin
Department of Orthopedics, The Second Hospital of Shanxi Medical University of Taiyuan, Taiyuan, China.
Department of Neurology, Shanxi Provincial Hospital of Integrated Traditional Chinese and Western Medicine, Taiyuan, China.
J Biochem Mol Toxicol. 2022 Dec;36(12):e23209. doi: 10.1002/jbt.23209. Epub 2022 Sep 9.
Osteoporosis is a metabolic, hereditary, progressive disease characterized by unusual bone production across the skeleton and a loss the bone tissue microstructure and mass. In this experimental study, we scrutinized the antiosteoporosis effect of nimbolide against glucocorticoid (GCs) induced osteoporosis in rats.
Swiss albino female rats were employed for the current experiment study and the rats were divided into different groups. Dexamethasone (0.1 mg/kg/day) was used for induction the osteoporosis and the rats were received the different doses of nimbolide (2.5, 5, and 7.5 mg/kg) for the estimation of bone protective effects. The body weight was estimated (initially and finally). Hormones, bone metabolic markers, bone turnover markers, bone structure, biomechanical, histomorphometric dynamic, biochemical markers, and histomorphometric static parameters were analyzed.
The body weight of GCs group rats considerably suppressed and nimbolide treatment remarkably improved the body weight. Nimbolide treated group exhibited the enhancement of bone metabolic, bone structure markers, and histomophometric dynamic markers, which was suppressed during the GCs-induced osteoporosis. GCs-induced osteoporosis rats exhibited the enhancement of procollagen type 1 C-terminal propeptide (P1CP), carboxy-terminal crosslinked telopeptide of type 1 collagen (CTX-1), Dickkopf-1 (DKK1), tartrate-resistant acid phosphatase 5b (TRACP 5b), and suppressed the level of bone alkaline phosphatase (BAP), which was reversed by the nimbolide treatment. Nimbolide treatment remarkably improved the level of estradiol and suppressed the level of parathyroid hormone (PTH), which was altered during the osteoporosis. Nimbolide treatment significantly (p < 0.001) improved the level of calcium, magnesium, and phosphorus in the serum and bone tissue. Nimbolide treatment also altered the level of bone metabolic markers and suppressed the level of inflammatory cytokines.
Based on the findings, we may conclude that nimbolide has antiosteoporosis properties via balancing the bone mass and improving vitamin and hormone levels.
骨质疏松症是一种代谢性、遗传性、进行性疾病，其特征是全身骨骼异常骨质生成以及骨组织微结构和骨量丢失。在本实验研究中，我们仔细观察了印楝素对糖皮质激素（GCs）诱导的大鼠骨质疏松症的抗骨质疏松作用。
选用瑞士白化雌性大鼠进行本实验研究，将大鼠分为不同组。地塞米松（0.1mg/kg/天）用于诱导骨质疏松症，给予大鼠不同剂量的印楝素（2.5、5和7.5mg/kg）以评估其对骨骼的保护作用。测量大鼠体重（初始和最终）。分析激素、骨代谢标志物、骨转换标志物、骨结构、生物力学、组织形态计量学动态、生化标志物和组织形态计量学静态参数。
GCs组大鼠体重明显受到抑制，印楝素治疗显著改善了体重。印楝素治疗组的骨代谢、骨结构标志物和组织形态计量学动态标志物有所增强，而这些在GCs诱导的骨质疏松症期间受到抑制。GCs诱导的骨质疏松症大鼠的I型前胶原C末端前肽（P1CP）、I型胶原羧基末端交联端肽（CTX-1）、Dickkopf-1（DKK1）、抗酒石酸酸性磷酸酶5b（TRACP 5b）水平升高，骨碱性磷酸酶（BAP）水平降低，印楝素治疗可使其逆转。印楝素治疗显著提高了雌二醇水平，降低了骨质疏松症期间发生改变的甲状旁腺激素（PTH）水平。印楝素治疗显著（p<0.001）提高了血清和骨组织中钙、镁和磷的水平。印楝素治疗还改变了骨代谢标志物水平，降低了炎性细胞因子水平。
基于这些发现，我们可以得出结论，印楝素具有抗骨质疏松特性，可通过平衡骨量以及改善维生素和激素水平来实现。
