肥胖加速了衰老过程,导致衰老引起的骨质疏松症加重。我们通过测量细胞衰老来研究高压氧治疗(HBOT)对肥胖和瘦年龄大鼠的抗骨质疏松作用。缺氧,炎症,抗氧化剂,和骨骼微结构。肥胖和瘦雄性Wistar大鼠注射150mg/kg/天的D-半乳糖8周以诱导衰老。然后,所有大鼠随机给予假手术或HBOT14天。测定代谢参数。骨mRNA在细胞衰老中的表达,缺氧,炎症,抗氧化能力,和骨重建进行了检查。进行显微计算机断层扫描和原子吸收光谱以评估骨骼微结构和骨矿物质轮廓。分别。我们发现HBOT恢复了p16,p21,HIF-1α的mRNA表达水平的改变,TNF-α,IL-6,RANKL,RANK,NFATc1,DC-STAMP,Osx,ALP,和Col1a1在肥胖和瘦衰老大鼠的骨骼中。在肥胖衰老的大鼠中,HBOT增加了Sirt1和CuZnSODmRNA的表达水平,并将HIF-2α和ctskmRNA的表达水平降低至与对照组相同的水平。然而,HBOT未能改变肥胖老年大鼠过氧化氢酶和OCNmRNA的表达。HBOT部分改善了肥胖老年大鼠的骨微结构,但在瘦龄老鼠身上完全恢复了。有趣的是,HBOT保护肥胖老年大鼠免受肥胖诱导的脱矿质。总之,HBOT在瘦老年大鼠中发挥抗骨质疏松作用,但并不是肥胖老年疾病对骨骼健康的所有负面影响。因此,HBOT被认为是一种潜在的治疗衰老引起的骨质疏松症,无论肥胖状况如何。
Obesity accelerates the aging processes, resulting in an aggravation of aging-induced osteoporosis. We investigated the anti-osteoporotic effect of hyperbaric oxygen therapy (
HBOT) in obese- and lean-aged rats through measurement of cellular senescence, hypoxia, inflammation, antioxidants, and bone microarchitecture. Obese and lean male Wistar rats were injected with 150 mg/kg/day of D-galactose for 8 weeks to induce aging. Then, all rats were randomly given either sham or
HBOT for 14 days. Metabolic parameters were determined. Expression by bone mRNA for cellular senescence, hypoxia, inflammation, antioxidative capacity, and bone remodeling were examined. Micro-computed tomography and atomic absorption spectroscopy were performed to evaluate bone microarchitecture and bone mineral profiles, respectively. We found that
HBOT restored the alterations in the mRNA expression level of p16, p21, HIF-1α, TNF-α, IL-6, RANKL, RANK, NFATc1, DC-STAMP, Osx, ALP, and Col1a1 in the bone in obese-and lean- aging rats. In obese-aging rats, HBOT increased the level of expression of Sirt1 and CuZnSOD mRNA and diminished the expression level of HIF-2α and ctsk mRNA to the same levels as the control group. However,
HBOT failed to alter catalase and OCN mRNA expression in obese-aged rats. HBOT partially improved the bone microarchitecture in obese-aged rats, but completely restored it in lean-aged rats. Interestingly,
HBOT protected against obesity-induced demineralization in obese-aged rats. In summary, HBOT exerts an anti-osteoporotic effect in lean-aged rats and prevents some, but not all the negative effects of obese-aged conditions on bone health. Therefore, HBOT is considered as a potential therapy for aging-induced osteoporosis, regardless of obese status.