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      Antiosteoporotic Activity of Anthraquinones from Morinda officinalis on Osteoblasts and Osteoclasts

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          Abstract

          Bioactivity-guided fractionation led to the successful isolation of antiosteoporotic components, i.e. physicion ( 1), rubiadin-1-methyl ether ( 2), 2-hydroxy-1-methoxy- anthraquinone ( 3), 1,2-dihydroxy-3-methylanthraquinone ( 4), 1,3,8-trihydroxy-2-methoxy- anthraquinone ( 5), 2-hydroxymethyl-3-hydroxyanthraquinone ( 6), 2-methoxyanthraquinone ( 7) and scopoletin ( 8) from an ethanolic extract of the roots of Morinda officinalis. Compounds 4-8 are isolated for the first time from M. officinalis. Among them, compounds 2 and 3 promoted osteoblast proliferation, while compounds 4, 5 increased osteoblast ALP activity. All of the isolated compounds inhibited osteoclast TRAP activity and bone resorption, and the inhibitory effects on osteoclastic bone resorption of compounds 1 and 5 were stronger than that of other compounds. Taken together, antiosteoporotic activity of M. officinalis and its anthraquinones suggest therapeutic potential against osteoporosis.

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          Progressive development of the rat osteoblast phenotype in vitro: reciprocal relationships in expression of genes associated with osteoblast proliferation and differentiation during formation of the bone extracellular matrix.

          Xian J. Lian, Elizabeth Kennedy, T. Owen … (1990)
          The relationship of cell proliferation to the temporal expression of genes characterizing a developmental sequence associated with bone cell differentiation was examined in primary diploid cultures of fetal calvarial derived osteoblasts by the combined use of autoradiography, histochemistry, biochemistry, and mRNA assays of osteoblast cell growth and phenotypic genes. Modifications in gene expression define a developmental sequence that has 1) three principle periods--proliferation, extracellular matrix maturation, and mineralization--and 2) two restriction points to which the cells can progress but cannot pass without further signals--the first when proliferation is down-regulated and gene expression associated with extracellular matrix maturation is induced, and the second when mineralization occurs. Initially, actively proliferating cells, expressing cell cycle- and cell growth-regulated genes, produce a fibronectin/type I collagen extracellular matrix. A reciprocal and functionally coupled relationship between the decline in proliferative activity and the subsequent induction of genes associated with matrix maturation and mineralization is supported by 1) a temporal sequence of events in which there is an enhanced expression of alkaline phosphatase immediately following the proliferative period, and later, an increased expression of osteocalcin and osteopontin at the onset of mineralization; 2) increased expression of a specific subset of osteoblast phenotype markers, alkaline phosphatase and osteopontin, when proliferation is inhibited by hydroxyurea; and 3) enhanced levels of expression of the osteoblast markers as a function of ascorbic acid-induced collagen deposition, suggesting that the extracellular matrix contributes to both the shutdown of proliferation and the development of the osteoblast phenotype.
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            Interleukin-1β and tumor necrosis factor-α, but not interleukin-6, stimulate osteoprotegerin ligand gene expression in human osteoblastic cells

            T.C Spelsberg, B.L. Riggs, S Khosla … (1999)
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              Antioxidant intake and risk of osteoporotic hip fracture in Utah: an effect modified by smoking status.

              Jianjun Zhang, Ronald Munger, Nancy West … (2006)
              The role of antioxidant intake in osteoporotic hip fracture risk is uncertain and may be modified by smoking. In the Utah Study of Nutrition and Bone Health, a statewide, population-based case-control study, the authors investigated whether antioxidant intake was associated with risk of osteoporotic hip fracture and whether this association was modified by smoking status. The analyses included data on 1,215 male and female cases aged > or = 50 years who incurred a hip fracture during 1997-2001 and 1,349 age- and sex-matched controls. Diet was assessed by food frequency questionnaire. Among ever smokers, participants in the highest quintile of vitamin E intake (vs. the lowest) had a lower risk of hip fracture after adjustment for confounders (odds ratio = 0.29, 95% confidence interval (CI): 0.16, 0.52; p-trend < 0.0001). The corresponding odds ratio for beta-carotene intake was 0.39 (95% CI: 0.23, 0.68; p-trend = 0.0004), and for selenium intake it was 0.27 (95% CI: 0.12, 0.58; p-trend = 0.0003). Vitamin C intake did not have a significant graded association with hip fracture risk among ever smokers. Similar findings were obtained when an overall antioxidant intake score was used (odds ratio = 0.19, 95% CI: 0.10, 0.37; p-trend < 0.0001). No similar associations were found in never smokers. Antioxidant intake was associated with reduced risk of osteoporotic hip fracture in these elderly subjects, and the effect was strongly modified by smoking status.
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                Author and article information

                Journal
                Journal ID (nlm-ta): Molecules
                Journal ID (iso-abbrev): Molecules
                Journal ID (publisher-id): molecules
                Title: Molecules
                Publisher: Molecular Diversity Preservation International
                ISSN (Electronic): 1420-3049
                Publication date (Electronic): 23 January 2009
                Publication date Collection: January 2009
                Volume: 14
                Issue: 1
                Pages: 573-583
                Affiliations
                [1 ]Department of Pharmacy, Fujian University of Traditional Chinese Medicine, Fuzhou, Fujian 350108, P.R. China; E-mail: wxsq1@ 123456163.com (Y-B. W.)
                [2 ]Department of Pharmacognosy, School of Pharmacy, Second Military Medical University, Shanghai 200433, P.R. China
                [3 ]Academy of Integrative Medicine, Fujian University of Traditional Chinese Medicine, Fuzhou, Fujian 350108, P.R. China
                Author notes
                [* ] Authors to whom correspondence should be addressed; E-Mails: zqy1965@ 123456163.com or qyzhang@ 123456smmu.edu.cn (Q-Y. Z.), jinzhongfj@ 123456126.com (J-Z. W.); Tel. +86-21-25074579 (Q-Y. Z.), +86-591-22861611 (J-Z. W.); Fax: +86-21-25074574 (Q-Y. Z.), +86-591-22861611 (J-Z. W.).
                Article
                Publisher ID: molecules-14-00573
                DOI: 10.3390/molecules14010573
                PMC ID: 6253840
                PubMed ID: 19169204
                SO-VID: 24d62aa1-9f7c-4a19-b93a-0927a78ff604
                Copyright © © 2009 by the authors;
                License:

                licensee Molecular Diversity Preservation International, Basel, Switzerland. This article is an open-access article distributed under the terms and conditions of the Creative Commons Attribution license ( http://creativecommons.org/licenses/by/3.0/).

                History
                Date received : 16 December 2008
                Date revision received : 17 January 2009
                Date accepted : 22 January 2009
                Categories
                Subject: Article

                Keywords: morinda officinalis,anthraquinones,osteoblast,osteoclast,osteoporosis.
                Data availability:
                Keywords: morinda officinalis, anthraquinones, osteoblast, osteoclast, osteoporosis.

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