Effect and mechanism of Bajitianwan on preventing D-galactose-induced osteoblast bone loss
10.12206/j.issn.2097-2024.202202030
- VernacularTitle:巴戟天丸防治D-半乳糖损伤成骨细胞骨丢失的作用及机制研究
- Author:
Weifan XU
1
,
2
;
Wumu XU
2
;
Luying DING
2
;
Yiping JIANG
2
;
Tianshuang XIA
2
;
Hailiang XIN
1
,
2
Author Information
1. School of Pharmacy, Fujian University of Traditional Chinese Medicine, Fuzhou 350122, China
2. Department of Pharmacognosy, School of Pharmacy, 2b. Department of Pharmacy, Changhai Hospital, Naval Medical University, Shanghai 200433, China.
- Keywords:
Bajitianwan;
D-galactose;
osteoblast;
reactive oxygen species;
Nrf2
- From:
Journal of Pharmaceutical Practice
2023;41(3):155-159
- CountryChina
- Language:Chinese
-
Abstract:
Objective To explore the effect and mechanism of Bajitianwan on preventing D-galactose (D-gal)-induced osteoblast bone loss. Methods Osteoblasts isolated from 24 h old Wistar rats were injured by D-gal and intervened with Bajitianwan extract. The osteoblastic proliferation and differentiation were determined by MTT and alkaline phosphatase (ALP), respectively. The cell reactive oxygen species (ROS) levels were detected by DCFH-DA fluorescent probes. The expression of cellular oxidation-related protein nuclear factor erythroid 2-related factor 2 (Nrf2), phosphorylated protein kinase B (p-AKT), protein kinase B (AKT), heme oxygenase-1 (HO-1), and NADPH quinone oxidoreductase 1 (NQO1) were detected by Western blotting. The intranuclear expression of Nrf2 protein was measured by immunofluorescence. Results Bajitianwan extract had significantly increased the osteoblastic proliferation and differentiation, and significantly reduced the intracellular ROS level. Bajitianwan extract had activated the PI3K/AKT pathway via activating the phosphorylation of AKT in osteoblasts, and promoted NQO1 and HO-1 expression. In addition, Bajitianwan had significantly promoted the expression of Nrf2 in the nucleus of osteoblasts, activating Nrf2 signaling pathway, and further promoted bone formation. Conclusion This study confirmed that Bajitianwan could prevent D-gal injured osteoblastic bone loss for the first time. The mechanism might be related to the regulation of oxidative stress associated PI3K/AKT and Nrf2 signaling pathway.
