Lertsinthai Parinya, Charoenphandhu Jantarima, Suntornsaratoon Panan, Krishnamra Nateetip, Charoenphandhu Narattaphol
Department of Physiology, Faculty of Science, Mahidol University, Bangkok, 10400, Thailand.
J Bone Miner Metab. 2015 May;33(3):261-9. doi: 10.1007/s00774-014-0597-3. Epub 2014 Jul 11.
In estrogen-deficient rodents with osteopenia, repetitive exposure to mild-to-moderate stress, which mimics the chronic aversive stimuli (CAS) of the modern urban lifestyle in postmenopausal women, has been hypothesized to cause the bone microstructure to further deteriorate. Recently, we have provided evidence in rats that voluntary impact exercise, e.g., wheel running, is as effective as pharmacological treatments for stress-induced anxiety and depression. The present study, therefore, aims to investigate whether a 4-week CAS exposure aggravates trabecular bone loss in ovariectomized (Ovx) rats, and whether CAS-induced bone loss can be rescued by voluntary wheel running. CAS was found to elevate the serum levels of corticosterone, a stress hormone from the adrenal gland. Dual energy X-ray absorptiometry revealed a decrease in bone mineral content (BMC) in the tibiae of CAS-exposed Ovx rats as compared to the CAS-free Ovx rats (control), while having no detectable effect on bone mineral density (BMD). Bone histomorphometric analysis of the proximal tibial metaphysis showed that CAS decreased trabecular bone volume and increased trabecular separation, which were completely restored to the baseline values of Ovx rats by voluntary wheel running. This CAS-induced trabecular bone loss in Ovx rats was probably due to an enhancement of osteoclast-mediated bone resorption, as indicated by increases in osteoclast surface and active erosion surface. Moreover, wheel running as well as non-impact exercise (endurance swimming) effectively increased the tibial BMD and BMC of CAS-exposed Ovx rats. It can be concluded that exercise is an effective intervention in mitigating CAS-induced bone loss in estrogen-deficient rats.
在雌激素缺乏且患有骨质减少症的啮齿动物中，反复暴露于轻度至中度应激下，这种应激模拟了绝经后女性现代城市生活方式中的慢性厌恶刺激（CAS），据推测会导致骨微结构进一步恶化。最近，我们在大鼠中发现，自愿冲击运动，例如跑步，对于应激诱导的焦虑和抑郁与药物治疗一样有效。因此，本研究旨在调查4周的CAS暴露是否会加重去卵巢（Ovx）大鼠的小梁骨丢失，以及CAS诱导的骨丢失是否可以通过自愿跑步来挽救。发现CAS会升高血清皮质酮水平，皮质酮是一种来自肾上腺的应激激素。双能X线吸收法显示，与未暴露于CAS的Ovx大鼠（对照组）相比，暴露于CAS的Ovx大鼠胫骨的骨矿物质含量（BMC）降低，而对骨矿物质密度（BMD）没有可检测到的影响。胫骨近端干骺端的骨组织形态计量学分析表明，CAS降低了小梁骨体积并增加了小梁间距，而自愿跑步将这些指标完全恢复到了Ovx大鼠的基线值。Ovx大鼠中这种由CAS诱导的小梁骨丢失可能是由于破骨细胞介导的骨吸收增强，这表现为破骨细胞表面和活跃侵蚀表面增加。此外，跑步以及非冲击运动（耐力游泳）有效地增加了暴露于CAS的Ovx大鼠的胫骨BMD和BMC。可以得出结论，运动是减轻雌激素缺乏大鼠中CAS诱导的骨丢失的有效干预措施。
