Ethanolic extract of Actaea racemosa (black cohosh) potentiates bone nodule formation in MC3T3-E1 preosteoblast cells

• Published in: Bone (New York, N.Y.) N.Y.), 2008-09, Vol.43 (3), p.567-573
• Main Authors: Chan, B.Y, Lau, K.S, Jiang, B, Kennelly, E.J, Kronenberg, F, Kung, A.W.C
• Format: Article
• Language: English
• Subjects: Actaea; Actaea racemosa; Animals; Biological and medical sciences; Black cohosh; Bone and Bones - metabolism; Cell Proliferation; Cimicifuga - metabolism; Cimicifuga racemosa; Core Binding Factor Alpha 1 Subunit - biosynthesis; Dose-Response Relationship, Drug; Estradiol - analogs & derivatives; Estradiol - pharmacology; Estrogen Antagonists - pharmacology; Estrogen receptor; Ethanol - pharmacology; Fundamental and applied biological sciences. Psychology; ICI 182 780; MC3T3-E1; Mice; Orthopedics; Osteoblast; Osteoblasts - cytology; Osteoblasts - metabolism; Osteocalcin - biosynthesis; Osteogenesis - drug effects; Plant Extracts - pharmacology; Receptors, Androgen - metabolism; Vertebrates: anatomy and physiology, studies on body, several organs or systems
• ISSN: 8756-3282; 1873-2763
• DOI: 10.1016/j.bone.2008.04.018

Abstract Aceaea racemosa (formerly Cimicifuga racemosa , black cohosh, AR) extracts have been widely used as an alternative to hormonal replacement therapy for menopausal symptoms. Recent evidences suggest AR extracts are also effective in protecting against postmenopausal bone loss. To determine whether AR has any direct anabolic effect on osteoblasts, we investigated the ethanolic extract of AR on bone nodule formation in mouse MC3T3-E1 preosteoblast cells. AR did not stimulate osteoblast proliferation. Rather, at high doses of 1000 ng/mL for 48 h, AR suppressed (7.2 ± 0.9% vs. control) osteoblast proliferation. At 500 ng/mL, a significant increase in bone nodule formation was seen with Von Kossa staining. Using quantitative PCR analysis, AR was shown to enhance the gene expression of runx2 and osteocalcin. Co-treatment with ICI 182,780, the selective estrogen receptor antagonist, abolished the stimulatory effect of AR on runx2 and osteocalcin gene induction, as well as on bone nodule formation in MC3T3-E1 cells. This is a first report of the direct effect of AR on enhancement of bone nodule formation in osteoblasts, and this action was mediated via an estrogen receptor-dependent mechanism. The results provide a scientific rationale at the molecular level for the claim that AR can offer effective prevention of postmenopausal bone loss.