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茶多糖抑制 RAW264.7 细胞中 RANKL 诱导的破骨细胞生成,并改善去卵巢大鼠骨质疏松症。

Tea polysaccharide inhibits RANKL-induced osteoclastogenesis in RAW264.7 cells and ameliorates ovariectomy-induced osteoporosis in rats.

机构信息

Key Laboratory of Pu-er Tea Science, Ministry of Education, Yunnan Agricultural University, Kunming 650201, China; College of Food Science and Technology, Yunnan Agricultural University, Kunming 650201, China.

Jilin Academy of Traditional Chinese Medicine, Changchun 130021, China.

出版信息

Biomed Pharmacother. 2018 Jun;102:539-548. doi: 10.1016/j.biopha.2018.03.125. Epub 2018 Apr 5.

Abstract

BACKGROUND AND PURPOSE

Tea drinking has positive effects on bone health and may prevent and treat osteoporosis, especially in older and postmenopausal women. Tea polysaccharide (TPS) is a major bioactive constituent in tea. Despite its profound effects on human health, whether TPS has anti-osteoporotic effects remains largely unknown. As such, we investigated the anti-osteoporotic effects of TPS.

METHODS

In vitro, TPS effects on osteoclastogenesis were examined using osteoclast precursor RAW264.7 cells. TPS effects on osteoclastogenesis-related expression of marker genes and proteins were determined by gene expression and immunoblotting analyses, respectively. For in vivo studies, 12-week-old female Wistar rats were divided randomly into a sham-operated group (sham) and four ovariectomized (OVX) subgroups: OVX with vehicle (model) and OVX with low-, medium-, and high-dose TPS (0.32, 0.64 and 1.28 g/kg body weight/day, respectively). TPS was administered intragastrically to rats for 13 weeks. Body weight, blood biochemical parameters, organ weight, organ coefficients, femoral length, bone mineral density (BMD), biomechanical properties, and bone microarchitecture were documented.

RESULTS

TPS inhibited osteoclast differentiation significantly and dose-dependently, and its inhibitory effect was not due to toxicity to RAW264.7 cells. TPS suppressed expression of osteoclastogenesis-related marker genes and proteins significantly. In in vivo studies, medium-dose TPS treatment ameliorated OVX-induced calcium loss significantly. Low-dose TPS treatment decreased the activity of acid phosphatase (ACP) in OVX rats significantly. In addition, TPS treatment improved other blood biochemical parameters and femoral biomechanical properties to a certain extent. More importantly, TPS treatment ameliorated bone microarchitecture in OVX rats strikingly because of increased cortical bone thickness and trabecular bone area in the femur.

CONCLUSION

TPS can inhibit receptor activator nuclear factor-kappa B ligand (RANKL)-induced osteoclastogenesis in RAW264.7 cells and ameliorate ovariectomy-induced osteoporosis in rats.

摘要

背景与目的

饮茶对骨骼健康有积极影响,可预防和治疗骨质疏松症,尤其是对老年和绝经后妇女。茶多糖(TPS)是茶叶中的主要生物活性成分。尽管它对人类健康有深远影响,但 TPS 是否具有抗骨质疏松作用仍知之甚少。因此,我们研究了 TPS 的抗骨质疏松作用。

方法

在体外,使用破骨细胞前体细胞 RAW264.7 细胞研究 TPS 对破骨细胞生成的影响。通过基因表达和免疫印迹分析分别测定 TPS 对破骨细胞生成相关标记基因和蛋白的影响。对于体内研究,将 12 周龄雌性 Wistar 大鼠随机分为假手术组(sham)和 4 组卵巢切除(OVX)亚组:OVX 加载体(模型)和 OVX 加低、中、高剂量 TPS(0.32、0.64 和 1.28g/kg 体重/天,分别)。TPS 通过灌胃给予大鼠 13 周。记录体重、血液生化参数、器官重量、器官系数、股骨长度、骨密度(BMD)、生物力学性能和骨微结构。

结果

TPS 显著抑制破骨细胞分化,呈剂量依赖性,其抑制作用不是由于对 RAW264.7 细胞的毒性。TPS 显著抑制破骨细胞生成相关标记基因和蛋白的表达。在体内研究中,中剂量 TPS 治疗显著改善 OVX 引起的钙丢失。低剂量 TPS 治疗显著降低 OVX 大鼠酸性磷酸酶(ACP)活性。此外,TPS 治疗在一定程度上改善了其他血液生化参数和股骨生物力学性能。更重要的是,TPS 治疗显著改善了 OVX 大鼠的骨微结构,因为股骨皮质骨厚度和小梁骨面积增加。

结论

TPS 可抑制核因子-κB 受体激活剂配体(RANKL)诱导的 RAW264.7 细胞破骨细胞生成,并改善去卵巢大鼠骨质疏松症。

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