Royal jelly prevents the progression of sarcopenia in aged mice in vivo and in vitro

Kaijun Niu, Hui Guo, Yinting Guo, Satoru Ebihara, Masanori Asada, Takashi Ohrui, Katsutoshi Furukawa, Masakazu Ichinose, Kazuhiko Yanai, Yukitsuka Kudo, Hiroyuki Arai, Tatsuma Okazaki, Ryoichi Nagatomi

Research output: Contribution to journalArticlepeer-review

23 Citations (Scopus)

Abstract

Sarcopenia is characterized by the age-related loss of muscle mass and strength. One of the mechanisms of sarcopenia is the loss in the function and number of muscle satellite cells. Royal jelly (RJ) is a health food used worldwide. To obtain better digestion and absorption than RJ, protease-treated RJ (pRJ) has been developed. RJ and pRJ have been suggested to have potential pharmacological benefits such as prolonging the life span and reducing fatigue. Because these effects may improve sarcopenia and the functions of satellite cells, we examined the effects of RJ or pRJ treatment on the skeletal muscles in an animal model using aged mice. In vivo, RJ/pRJ treatment attenuated the decrease in the muscle weight and grip strength and increased the regenerating capacity of injured muscles and the serum insulin-like growth factor-1 levels compared with controls. In vitro, using isolated satellite cells from aged mice, pRJ treatment increased the cell proliferation rate, promoted cell differentiation, and activated Akt intracellular signaling pathway compared with controls. These findings suggest that RJ/pRJ treatment had a beneficial effect on age-related sarcopenia.

Original languageEnglish
Pages (from-to)1482-1492
Number of pages11
JournalJournals of Gerontology - Series A Biological Sciences and Medical Sciences
Volume68
Issue number12 A
DOIs
Publication statusPublished - 2013

Keywords

  • Aged mice
  • Akt signaling
  • Ins lin
  • Like growth factor 1
  • Royal jelly
  • Sarcopenia
  • Satellite cells

ASJC Scopus subject areas

  • Ageing
  • Geriatrics and Gerontology

Fingerprint Dive into the research topics of 'Royal jelly prevents the progression of sarcopenia in aged mice in vivo and in vitro'. Together they form a unique fingerprint.

Cite this