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Protective Effects of Ligustroflavone, an Active Compound from Ligustrum lucidum, on Diabetes-Induced Osteoporosis in Mice: A Potential Candidate as Calcium-Sensing Receptor Antagonist.

Authors
  • Feng, Rui1
  • Ding, Fan1
  • Mi, Xiu-Hua2
  • Liu, Shu-Fen1, 3
  • Jiang, Ai-Ling4
  • Liu, Bi-Hui5
  • Lian, Yin5
  • Shi, Qi1, 3
  • Wang, Yong-Jun1, 3
  • Zhang, Yan1, 3
  • 1 * Spine Disease Research Institute, Longhua Hospital, Shanghai University of Traditional Chinese Medicine, Shanghai 200032, P. R. China. , (China)
  • 2 † Section of Nephrology, Yangpu Traditional Chinese Medicine Hospital, Shanghai 200090, P. R. China. , (China)
  • 3 ‡ Key Laboratory of Theory and Therapy of Muscles and Bones, Ministry of Education, Shanghai 200032, P. R. China. , (China)
  • 4 § School of Medical Instrument and Food Engineering, University of Shanghai for Science and Technology, Shanghai 200093, P. R. China. , (China)
  • 5 ¶ Department of Orthopaedic, Shenzhen Pingle Orthopaedic Hospital, Shenzhen 518000, P. R. China. , (China)
Type
Published Article
Journal
The American journal of Chinese medicine
Publication Date
Jan 01, 2019
Volume
47
Issue
2
Pages
457–476
Identifiers
DOI: 10.1142/S0192415X1950023X
PMID: 30834778
Source
Medline
Keywords
Language
English
License
Unknown

Abstract

Ligustroflavone is one major compound contained in active fraction from Fructus Ligustri Lucidi (the fruit of Ligustrum lucidum), which could regulate parathyroid hormone (PTH) levels and improve calcium balance by acting on calcium-sensing receptors (CaSR). This study aimed to explore the potency of ligustroflavone as a CaSR antagonist and its protective effects against diabetic osteoporosis in mice. LF interacted well with the allosteric site of CaSR shown by molecular docking analysis, increased PTH release of primary parathyroid gland cells and suppressed extracellular calcium influx in HEK-293 cells. The serum level of PTH attained peak value at 2 h and maintained high during the period of 1 h and 3 h than that before treatment in mice after a single dose of LF. Treatment of diabetic mice with LF inhibited the decrease in calcium level of serum and bone and the enhancement in urinary calcium excretion as well as elevated circulating PTH levels. Trabecular bone mineral density and micro-architecture were markedly improved in diabetic mice upon to LF treatment for 8 weeks. LF reduced CaSR mRNA and protein expression in the kidneys of diabetic mice. Taken together, ligustroflavone could transiently increase PTH level and regulate calcium metabolism as well as prevent osteoporosis in diabetic mice, suggesting that ligustroflavone might be an effective antagonist on CaSR.

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