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抑制甲羟戊酸的膳食异戊烯醇类化合物对骨骼健康的作用。

Mevalonate-suppressive dietary isoprenoids for bone health.

机构信息

Department of Nutrition and Food Sciences, Texas Woman's University, Denton, TX 76204, USA.

出版信息

J Nutr Biochem. 2012 Dec;23(12):1543-51. doi: 10.1016/j.jnutbio.2012.07.007. Epub 2012 Sep 13.

Abstract

Osteoclastogenesis and osteoblastogenesis, the balancing acts for optimal bone health, are under the regulation of small guanosine triphosphate-binding proteins (GTPases) including Ras, Rac, Rho and Rab. The activities of GTPases require post-translational modification with mevalonate-derived prenyl pyrophosphates. Mevalonate deprivation induced by competitive inhibitors of 3-hydroxy-3-methylglutaryl coenzyme A (HMG CoA) reductase (e.g., statins) prevents the activation of GTPases, suppresses the expression of the receptor for activation of nuclear factor kappa B (NFκB) ligand (RANKL) and activation of NFκB and, consequently, inhibits osteoclast differentiation and induces osteoclast apoptosis. In contrast, statin-mediated inactivation of GTPases enhances alkaline phosphatase activity and the expression of bone morphogenetic protein-2, vascular epithelial growth factor, and osteocalcin in osteoblasts and induces osteoblast proliferation and differentiation. Animal studies show that statins inhibit bone resorption and increase bone formation. The anabolic effect of statins and other mevalonate pathway-suppressive pharmaceuticals resembles the anti-osteoclastogenic and bone-protective activities conferred by dietary isoprenoids, secondary products of plant mevalonate metabolism. The tocotrienols, vitamin E molecules with HMG CoA reductase-suppressive activity, induce mevalonate deprivation and concomitantly suppress the expression of RANKL and cyclooxygenase-2, the production of prostaglandin E2 and the activation of NFκB. Accordingly, tocotrienols inhibit osteoclast differentiation and induce osteoclast apoptosis, impacts reminiscent of those of statins. In vivo studies confirm the bone protective activity of tocotrienols at nontoxic doses. Blends of tocotrienols, statins and isoprenoids widely found in fruits, vegetables, grains, herbs, spices, and essential oils may synergistically suppress osteoclastogenesis while promoting osteoblastogenesis, offering a novel approach to bone health that warrants clinical studies.

摘要

破骨细胞生成和成骨细胞生成是维持骨骼健康的平衡过程,受小 G 三磷酸结合蛋白(GTPases)的调节,包括 Ras、Rac、Rho 和 Rab。GTPases 的活性需要经过异戊烯焦磷酸的翻译后修饰。3-羟基-3-甲基戊二酰辅酶 A(HMG CoA)还原酶的竞争性抑制剂(如他汀类药物)剥夺了异戊烯焦磷酸,从而阻止了 GTPases 的激活,抑制了核因子κB(NFκB)配体(RANKL)受体的表达和 NFκB 的激活,进而抑制了破骨细胞分化并诱导了破骨细胞凋亡。相反,他汀类药物介导的 GTPases 失活增强了碱性磷酸酶活性和成骨细胞中骨形态发生蛋白-2、血管内皮生长因子和骨钙素的表达,并诱导了成骨细胞的增殖和分化。动物研究表明,他汀类药物抑制骨吸收并增加骨形成。他汀类药物和其他异戊烯焦磷酸途径抑制性药物的合成代谢作用类似于饮食异戊烯类化合物、植物异戊烯代谢的次级产物所赋予的抗破骨细胞生成和骨保护作用。生育三烯酚是具有 HMG CoA 还原酶抑制活性的维生素 E 分子,它会引起异戊烯焦磷酸的剥夺,同时抑制 RANKL 和环氧化酶-2 的表达、前列腺素 E2 的产生和 NFκB 的激活。因此,生育三烯酚抑制破骨细胞分化并诱导破骨细胞凋亡,其作用类似于他汀类药物。体内研究证实了生育三烯酚在非毒性剂量下的骨骼保护活性。广泛存在于水果、蔬菜、谷物、草药、香料和精油中的生育三烯酚、他汀类药物和异戊烯类化合物的混合物可能会协同抑制破骨细胞生成,同时促进成骨细胞生成,为骨骼健康提供了一种值得临床研究的新方法。

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