Shi Jian-Xin, Cai Xiao-Qun, Zhao Ze-Hao, Deng Yu, Zhou Zhi-Kun
Department of Pharmacy, Guangdong Medical University, No. 1, Xincheng Dadao, Songshan Lake Science and Technology Industry Park, Dongguan 523808, China.
Huizhou Women's and Children's Hospital Affiliated to Guangdong Medical University, No. 10, Daling Road, Huicheng District, Huizhou 516001, China.
Evid Based Complement Alternat Med. 2022 Jun 8;2022:8769531. doi: 10.1155/2022/8769531. eCollection 2022.
Osteoclasts (OCs) have been the unique cell type exhibiting the bone-resorption activity in body. It is important to identify drugs to resist osteoclastogenesis to manage the bone-loss disorders. Huangqi Sanxian decoction (HQSXD) is utilized for the treatment of postmenopausal osteoporosis (PMOP) for a long history in East Asia. This work aimed to examine HQSXD's activity in OC differentiation. Based on staining with tartrate-resistant acid phosphatase (TRAP), it was found that HQSXD suppressed OC generation under the induction of RANKL produced in the bone marrow-derived monocytes/macrophages (BMMs), with no cytotoxic effect. Later analysis like molecular exploration and network pharmacology (NP) suggested the role of HQSXD in suppressing genes associated with osteoclastogenesis via PI3K/Akt-mediated mechanism dose-dependently. This work might illustrate the molecular pharmacological mechanism involved in HQSXD's effect on treating OC-associated disorders. Moreover, NP was found to modernize traditional Chinese medicine (TCM) research.
破骨细胞(OCs)是体内唯一具有骨吸收活性的细胞类型。识别抗破骨细胞生成的药物对于治疗骨质流失疾病至关重要。黄芪三仙汤(HQSXD)在东亚地区长期用于治疗绝经后骨质疏松症(PMOP)。这项工作旨在研究HQSXD在破骨细胞分化中的活性。基于抗酒石酸酸性磷酸酶(TRAP)染色,发现HQSXD在骨髓来源的单核细胞/巨噬细胞(BMMs)产生的RANKL诱导下抑制破骨细胞生成,且无细胞毒性作用。随后的分子探索和网络药理学(NP)等分析表明,HQSXD通过PI3K/Akt介导的机制剂量依赖性地抑制与破骨细胞生成相关的基因。这项工作可能阐明了HQSXD治疗OC相关疾病作用的分子药理机制。此外,发现网络药理学使传统中药(TCM)研究现代化。