Li Sirui, Li Xianlong, He Feng, Jiao Rui, Zhang Song, Li Zhihua
The Second Clinical Medical College of Dalian Medical University, Dalian, China.
Clinical Medical College of Yangzhou University, Yangzhou, China.
Arch Med Sci. 2019 Nov 11;19(2):452-457. doi: 10.5114/aoms.2019.89652. eCollection 2023.
The beneficial effect of amarogentin in the management of osteoporosis was determined using and methods.
Experimental osteoporosis was induced in rats via bilateral ovariectomy. Rats were then treated for 5 weeks with amarogentin (50 and 100 mg/kg, p.o.). The levels of several biochemical markers of bone resorption and formation as well as bone mineral density (BMD) were measured in the rat serum. Isolated rat bone tissues were analysed using western blot assays. In the study, MG63 human osteoblasts were treated with amarogentin (0-100 μg/ml), after which alkaline phosphatase activity and osteoblast proliferation were evaluated. Osteoblasts treated with amarogentin and inhibitors of extracellular signal-regulated kinase (ERK) were further examined via western blotting.
In the rat model of oestrogen-deficiency-induced osteoporosis, BMD was significantly enhanced ( < 0.01) and levels of inflammatory cytokines were reduced in amarogentin-treated animals vs. the controls. Amarogentin treatment also attenuated the altered levels of osteocalcin, C-telopeptide of type 1 collagen, procollagen type I N-terminal propeptide, and bone-specific alkaline phosphatase, and the altered expression of Akt, Nrf-2, ERK, and nuclear factor-κB p65 in the serum of rats with osteoporosis. In the study, amarogentin treatment enhanced alkaline phosphatase activity and osteoblast proliferation compared to the non-treated control. Amarogentin treatment alone enhanced the expression of p-ERK compared to treatment with an amarogentin + ERK inhibitor.
Both the and the studies demonstrated the protective effect of amarogentin against oestrogen-deficiency-induced osteoporosis in rats. The mechanism seems to involve the amarogentin-mediated enhancement of osteoblast differentiation via the Nrf-2/MAPK/ERK signalling pathway.
采用[具体方法1]和[具体方法2]方法确定了苦味叶下珠素在骨质疏松症治疗中的有益作用。
通过双侧卵巢切除术在大鼠中诱导实验性骨质疏松症。然后用苦味叶下珠素（50和100mg/kg，口服）对大鼠进行5周治疗。测量大鼠血清中几种骨吸收和形成的生化标志物水平以及骨矿物质密度（BMD）。使用蛋白质印迹分析对分离的大鼠骨组织进行分析。在[细胞实验名称]研究中，用苦味叶下珠素（0 - 100μg/ml）处理MG63人成骨细胞，之后评估碱性磷酸酶活性和成骨细胞增殖。用苦味叶下珠素和细胞外信号调节激酶（ERK）抑制剂处理的成骨细胞通过蛋白质印迹进一步检测。
在雌激素缺乏诱导的骨质疏松症大鼠模型中，与对照组相比，苦味叶下珠素治疗组动物的骨矿物质密度显著提高（P < 0.01），炎症细胞因子水平降低。苦味叶下珠素治疗还减弱了骨质疏松症大鼠血清中骨钙素、I型胶原C末端肽、I型前胶原N末端前肽和骨特异性碱性磷酸酶水平的改变，以及Akt、Nrf - 2、ERK和核因子κB p65表达的改变。在[细胞实验名称]研究中，与未处理的对照组相比，苦味叶下珠素治疗增强了碱性磷酸酶活性和成骨细胞增殖。与苦味叶下珠素 + ERK抑制剂联合处理相比，单独使用苦味叶下珠素治疗增强了p - ERK的表达。
[动物实验名称]和[细胞实验名称]研究均证明了苦味叶下珠素对大鼠雌激素缺乏诱导的骨质疏松症具有保护作用。其机制似乎涉及苦味叶下珠素通过Nrf - 2/MAPK/ERK信号通路介导的成骨细胞分化增强。
