中国骨质疏松杂志
中國骨質疏鬆雜誌
중국골질소송잡지
CHINESE JOURNAL OF OSTEOPOROSIS
2014年
4期
452-456
,共5页
淫羊藿总黄酮%骨代谢%药理机制
淫羊藿總黃酮%骨代謝%藥理機製
음양곽총황동%골대사%약리궤제
Total epimedium flavonoids%Bone metabolism%Pharmacological mechanism
实验研究发现淫羊藿对不同类型骨质疏松大鼠模型均有骨代谢调节作用,临床研究亦发现采用淫羊藿治疗绝经后骨质疏松症也取得了明显的效果。其药理作用机制可能与降低破骨细胞内Ca2+浓度,影响成骨细胞增殖、分化、矿化;增加骨护骨素(OPG)mRNA的表达,提高成骨细胞Osterix基因表达水平,从而促进骨形成;通过升高人成骨细胞骨形成蛋白-2(BMP-2) mRNA的表达,增加骨形态生成蛋白2的生成刺激人类成骨细胞的增殖和分化;通过抑制TNF-αmRNA和促进TGF-β1 mRNA的表达促进转化生长因子( TGF)-β1的产生,抑制肿瘤坏死因子-α( TNF-α)表达,进而阻止骨髓基质中破骨细胞的生成,减少骨质丢失;淫羊藿总黄酮增加骨桥蛋白( OPN) mRNA和Ⅰ型胶原的表达促进骨的生成;淫羊藿苷可通过选择性上调下丘脑和海马ERα,ERβmRNA的表达,降低骨组织中IL-6的表达,从而减少骨吸收;淫羊藿总黄酮可通过抑制DKK1蛋白的表达,调控去势雌性大鼠BMSCs成骨和成脂分化平衡调节骨代谢;淫羊藿苷通过上调 Cbfal、BMP2和 BMP4mRNA 的表达而促进成骨细胞的分化,诱导大鼠骨髓间充质干细胞向成骨细胞分化;淫羊藿总黄酮可显著改善雄性生殖系统和生殖内分泌功能,促进性腺的分泌,产生类雄激素样作用而促进成骨细胞的增殖与分化。笔者从多个层面对淫羊藿黄酮类成分抗骨质疏松作用机制进行阐述,提出今后在此研究基础上尚需进一步深入全面、系统的研究和阐述。
實驗研究髮現淫羊藿對不同類型骨質疏鬆大鼠模型均有骨代謝調節作用,臨床研究亦髮現採用淫羊藿治療絕經後骨質疏鬆癥也取得瞭明顯的效果。其藥理作用機製可能與降低破骨細胞內Ca2+濃度,影響成骨細胞增殖、分化、礦化;增加骨護骨素(OPG)mRNA的錶達,提高成骨細胞Osterix基因錶達水平,從而促進骨形成;通過升高人成骨細胞骨形成蛋白-2(BMP-2) mRNA的錶達,增加骨形態生成蛋白2的生成刺激人類成骨細胞的增殖和分化;通過抑製TNF-αmRNA和促進TGF-β1 mRNA的錶達促進轉化生長因子( TGF)-β1的產生,抑製腫瘤壞死因子-α( TNF-α)錶達,進而阻止骨髓基質中破骨細胞的生成,減少骨質丟失;淫羊藿總黃酮增加骨橋蛋白( OPN) mRNA和Ⅰ型膠原的錶達促進骨的生成;淫羊藿苷可通過選擇性上調下丘腦和海馬ERα,ERβmRNA的錶達,降低骨組織中IL-6的錶達,從而減少骨吸收;淫羊藿總黃酮可通過抑製DKK1蛋白的錶達,調控去勢雌性大鼠BMSCs成骨和成脂分化平衡調節骨代謝;淫羊藿苷通過上調 Cbfal、BMP2和 BMP4mRNA 的錶達而促進成骨細胞的分化,誘導大鼠骨髓間充質榦細胞嚮成骨細胞分化;淫羊藿總黃酮可顯著改善雄性生殖繫統和生殖內分泌功能,促進性腺的分泌,產生類雄激素樣作用而促進成骨細胞的增殖與分化。筆者從多箇層麵對淫羊藿黃酮類成分抗骨質疏鬆作用機製進行闡述,提齣今後在此研究基礎上尚需進一步深入全麵、繫統的研究和闡述。
실험연구발현음양곽대불동류형골질소송대서모형균유골대사조절작용,림상연구역발현채용음양곽치료절경후골질소송증야취득료명현적효과。기약리작용궤제가능여강저파골세포내Ca2+농도,영향성골세포증식、분화、광화;증가골호골소(OPG)mRNA적표체,제고성골세포Osterix기인표체수평,종이촉진골형성;통과승고인성골세포골형성단백-2(BMP-2) mRNA적표체,증가골형태생성단백2적생성자격인류성골세포적증식화분화;통과억제TNF-αmRNA화촉진TGF-β1 mRNA적표체촉진전화생장인자( TGF)-β1적산생,억제종류배사인자-α( TNF-α)표체,진이조지골수기질중파골세포적생성,감소골질주실;음양곽총황동증가골교단백( OPN) mRNA화Ⅰ형효원적표체촉진골적생성;음양곽감가통과선택성상조하구뇌화해마ERα,ERβmRNA적표체,강저골조직중IL-6적표체,종이감소골흡수;음양곽총황동가통과억제DKK1단백적표체,조공거세자성대서BMSCs성골화성지분화평형조절골대사;음양곽감통과상조 Cbfal、BMP2화 BMP4mRNA 적표체이촉진성골세포적분화,유도대서골수간충질간세포향성골세포분화;음양곽총황동가현저개선웅성생식계통화생식내분비공능,촉진성선적분비,산생류웅격소양작용이촉진성골세포적증식여분화。필자종다개층면대음양곽황동류성분항골질소송작용궤제진행천술,제출금후재차연구기출상상수진일보심입전면、계통적연구화천술。
Researches have found that the regulating effect of epimedium on bone metabolism exists in different osteoporotic rat models.The clinical studies also indicate an obvious efficacy of epimedium in the treatment of postmenopausal osteoporosis.Its possible mechanism may rely on reducing Ca2+level in osteoclasts, influencing the proliferation, differentiation, and mineralization of osteoblasts.It may also increase the expression of OPG mRNA and promote the expression of Osterix gene in osteoblasts, thus promoting bone formation.Epimedium can also promote the expression of BMP-2 mRNA, increase the expression of BMP-2, in order to stimulate the proliferation and differentiation of osteoblasts.Meanwhile, by inhibiting the expression of TNF-αmRNA and promoting the expression of TGF-β1 mRNA, epimedium promotes the production of TGF-β1 , thus preventing the generation of osteoclasts in bone marrow and reducing bone loss.Total epimedium flavonoids ( TFP) can promote bone formation by increasing the expression of OPN mRNA and type-I collagen.By selectively up-regulating the expression of ERαand ERβmRNA in the hypothalamus and the hippocampus, epimedium can down-regulate the expression of IL-6, thus reducing the bone resorption.TFP can regulate bone metabolism by inhibiting the expression of DKK1 protein, thus controlling the balance of osteogeic and adipogenic differentiation of BMSCs in OVX rats.Epimedium can promote the expression of Cbfal, BMP2, and BMP4 mRNA, thus promoting the differentiation of osteoblasts and inducing the osteogenic differentiation of rat BMSCs.TFP can remarkably improve the function of male genital system and reproductive endocrine, stimulate the secretion of gonad, and exert androgen-like function to accelerate the proliferation and differentiation of osteoblasts.This article elaborates the mechanism of epimedium flavonoids in anti-osteoporosis treatment from several aspects, proposing a deeper and systemic research and description in the future.