Chinese Journal of Tissue Engineering Research ›› 2011, Vol. 15 ›› Issue (11): 1901-1904.doi: 10.3969/j.issn.1673-8225.2011.11.001

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Effects of recombinant human insulin-like growth factor on rat osteoblasts

Xu Ping1, Zhang Ke-qin2, Liu Chao2, Chen Jun-jian1, Yuan Guo-yue1, Yu Li1, Qian Fang-fang1   

  1. 1Department of Endocrinology, the Affiliated Hospital of Jiangsu University, Zhenjiang  212001, Jiangsu Province, China
    2Department of Endocrinology, the First Affiliated Hospital of Nanjing Medical University, Nanjing  210029, Jiangsu Province, China
  • Received:2010-09-07 Revised:2010-10-29 Online:2011-03-12 Published:2011-03-12
  • Contact: Zhang Ke-qin, Doctor, Chief physician, Department of Endocrinology, the First Affiliated Hospital of Nanjing Medical University, Nanjing 210029, Jiangsu Province, China keqzhang@hotmail.com
  • About author:Xu Ping★, Master, Attending physician, Department of Endocrinology, the Affiliated Hospital of Jiangsu University, Zhenjiang 212001, Jiangsu Province, China jennyxu1234@yahoo.com.cn
  • Supported by:

    the Natural Science Foundation of Jiangsu Province, No. BK2009208*

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Abstract:

BACKGROUND: Recombinant human insulin-like growth factor (rhIGF-Ⅰ) is rich in osteoblasts, which has close contact with bone mineral density. 
OBJECTIVE: To investigate the effects of rhIGF-Ⅰ on proliferation, apoptosis and synthesis of alkaline phosphatase (ALP) of rat osteoblasts in vitro.
METHODS: Rat calvaria cells were cultured in medium with or without rhIGF-Ⅰ. The living cell number was assessed by MTT colorimetric assay. Tumor necrosis factor α (TNF-α) was added in the medium to induce apoptosis. The cell cycle and apoptosis were analyzed by flow cytometry after the cells were incubated with medium containing TNF-α or TNF-α plus rhIGF-Ⅰ. The ALP content within osteoblasts was measured by PNPP method.
RESULTS AND CONCLUSION: The cell number of osteoblasts exposed to rhIGF-Ⅰ at 102-105 ng/mL significantly increased compared with control group (P < 0.05). TNF-α (102-105 ng/L) caused a dose-dependent increase of apoptosis (P < 0.05) and decreased the cell number in S phase (P < 0.05). rhIGF-Ⅰ inhibited the inducement of TNF-α for apoptosis. The ALP activity in rhIGF-Ⅰ-treated cells was higher than that in vehicle-treated cells (P  < 0.05). IGF-Ⅰ can stimulate proliferation of osteoblasts and inhibit apoptosis induced by TNF-α in vitro, these results suggested that increasing the cell number of osteoblasts might be one of the mechanisms for IGF-Ⅰ to promote bone formation. IGF-Ⅰ can increase ALP synthesis in osteoblasts in vitro, this result suggested that IGF-Ⅰ could probably promote the synthesis of organic matrix and mineralize action of bone.

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