Research Article Rutin Isolated from Chrozophora tinctoria Enhances Bone Cell Proliferation and Ossification Markers Ashraf B. Abdel-Naim , 1,2 Abdullah A. Alghamdi, 3 Mardi M. Algandaby, 1,4 Fahad A. Al-Abbasi, 1,3 Ahmed M. Al-Abd, 2,5 Basma G. Eid , 2 Hossam M. Abdallah, 6,7 and Ali M. El-Halawany 7 1 Medicinal Plants Research Group, Deanship of Scientic Research, King Abdulaziz University, Jeddah, Saudi Arabia 2 Department of Pharmacology and Toxicology, Faculty of Pharmacy, King Abdulaziz University, Jeddah, Saudi Arabia 3 Department of Biochemistry, Faculty of Science, King Abdulaziz University, Jeddah, Saudi Arabia 4 Department of Biological Sciences, Faculty of Science, King Abdulaziz University, Jeddah, Saudi Arabia 5 Pharmacology Department, Medical Division, National Research Centre, Giza, Egypt 6 Department of Natural Products, Faculty of Pharmacy, King Abdulaziz University, Jeddah, Saudi Arabia 7 Department of Pharmacognosy, Faculty of Pharmacy, Cairo University, Cairo, Egypt Correspondence should be addressed to Ashraf B. Abdel-Naim; abnaim@yahoo.com Received 12 October 2017; Revised 25 November 2017; Accepted 17 December 2017; Published 13 February 2018 Academic Editor: LotAleya Copyright © 2018 Ashraf B. Abdel-Naim et al. This is an open access article distributed under the Creative Commons Attribution License, which permits unrestricted use, distribution, and reproduction in any medium, provided the original work is properly cited. Osteoporosis is a chronic disease in which the skeleton loses a weighty proportion of its mineralized mass and mechanical pliability. Currently available antiosteoporotic agents suer adverse eects that include elevated risk of thrombosis and cancer. Phytochemicals may constitute a safer and eective option. In the current work, six avonoids were obtained from Chrozophora tinctoria and identied as amentoavone (1), apigenin-7-O-β-D-glucopyranoside (2), apigenin-7-O-6′′-E-p- coumaroyl-β-D-glucopyranoside (3), acacetin-7-O-β-D-[α-L-rhamnosyl(16)]3′′-E-p-coumaroyl glucopyranoside (4), apigenin- 7-O-(6′′-Z-p-coumaroyl)-β-D-glucopyranoside (5), and rutin (6). An extensive review of the literature as well as NMR and mass spectral techniques was employed in order to elucidate the compound structures. Proliferation was enhanced in MCF7, MG-63, and SAOS-2 cells after exposure to subcytotoxic levels of the tested avonoids. Rutin was chosen for subsequent studies in SAOS-2 cells. Rutin was not found to cause any alteration in the index of proliferation of these cells, when examining the cell cycle distribution by DNA owcytometric analysis. Rutin was, however, found to increase osteocyte and osteoblast-related gene expression and lower the expression of RUNX suppressor and osteoclast genes. When examining the inuence of rutin on vitamin D levels and the activity of alkaline phosphatase enzyme, it was found to enhance both, while decreasing acid phosphatase which is a marker of osteoporosis. Thus, rutin enhances proliferation and ossication markers in bone cells. 1. Introduction Osteoporosis is a chronic disease in which the skeleton loses a weighty proportion of its mineralized mass and mechanical pliability [1]. It occurs when bone resorption surpasses bone formation, causing an imbalance [2]. As a result, the bones tend to become more fragile and more susceptible to frac- tures [3]. Studies have shown that 50% of women and 20% of men are likely to have a fracture resulting from osteoporosis during their lifetime [4]. Such fractures impose a heavy health and economic burden worldwide [5, 6]. The risk of developing osteoporosis has been shown to be directly linked to diet. Studies have reported that people eating healthy diets with a high fruit and vegetable content tend to have lower bone resorption than their counterparts eating poor diets rich in processed foods [7]. Pharmacological management of osteoporosis involves the use of bisphospho- nates and estrogen replacement therapy. However, these Hindawi Oxidative Medicine and Cellular Longevity Volume 2018, Article ID 5106469, 10 pages https://doi.org/10.1155/2018/5106469