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Regulatory Effect of Catalpol on Th1/Th2 cells in Mice with Bone Loss Induced by Estrogen Deficiency
Author(s) -
Lai Nannan,
Zhang Jianhai,
Ma Xingyan,
Wang Bin,
Miao Xiuming,
Wang Zhaoxia,
Guo Yuqi,
Wang Li,
Yao Chengfang,
Li Xia,
Jiang Guosheng
Publication year - 2015
Publication title -
american journal of reproductive immunology
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 1.071
H-Index - 97
eISSN - 1600-0897
pISSN - 1046-7408
DOI - 10.1111/aji.12423
Subject(s) - catalpol , estrogen , endocrinology , medicine , biology , chemistry , glycoside , stereochemistry
Problem Estradiol (E 2 ) deficiency can cause bone loss and the skew of Th1/Th2 cells. However, the correlation between the Th1/Th2 cells and the bone loss induced by estrogen deficiency remains unclear. Our aim was to investigate the role of Th1/Th2 in bone loss induced by estrogen deficiency and elucidated the therapeutical effect of catalpol in this condition. Method of Study Young, sham‐operated (Sham), ovariectomized (Ovx), and naturally aged mice, treated with catalpol at different doses or control vehicle, were used in this study as indicated in each experiment. ELISA assay, dual‐energy X‐ray absorptiometry, and flow cytometry were used to analyze E 2 , C‐terminal telopeptides of type I collagen ( CT x‐I), bone mineral density ( BMD ), and Th1/Th2 subsets, respectively. The mRNA and protein expressions of specific transcription factors for Th1/Th2 cells (T‐bet and GATA ‐3) were analyzed using real‐time quantitative PCR and Western blot, respectively. Results Bone mineral density and E 2 levels positively correlated with the proportion of Th2 subset while negatively correlated with that of Th1 subset and the ratio of Th1/Th2. Catalpol alleviated bone loss effectively by regulating Th1/Th2 polarization. Catalpol promoted the expression of Th2‐specific transcription factors while inhibited that associated with Th1. Conclusion Th1/Th2 skew is involved in bone loss induced by estrogen deficiency. Catalpol alleviates bone loss effectively by regulating Th1/Th2 paradigm.