Evidence map›Paper›PMID 40346551›Full record

ArticleJournal of orthopaedic surgery and research2025

Parthenolide ameliorates glucocorticoid-induced inhibition of osteogenic differentiation and osteoporosis by activating ERK signaling pathway.

Yanling Feng, Zhaoyang Li

Abstract read
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Article in Journal of orthopaedic surgery and research, 2025. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Not yet cited in PubMed.

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4 · The record

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5 · Who and what money

Authors and funding

2 authors.

Yanling FengDepartment of Endocrinology and Metabolism, The Second Hospital of Lanzhou University, No.82, Cuiyingmen, Lanzhou, 730030, Gansu Province, China. 18093192897@163.com.
Zhaoyang LiThe Second Clinical Medical School, Lanzhou University, Lanzhou, 730000, China.

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

backgroundParthenolide (PTL) is a natural sesquiterpene lactone that possesses significant effects on stimulating osteoblast differentiation. The present study focused on the potential of PTL in the treatment of glucocorticoid-induced osteoporosis (GIOP).

methodsMC3T3-E1 cells were treated with dexamethasone (DEX; 10 µM) or/and PTL (5, 10, and 20 µM). The changes in osteogenic differentiation were analyzed by conducting ALP and Alizarin Red staining and assessing the levels of osteogenic markers (Runx2, Osx, and OPN). PTL (3 and 10 mg/kg/day) was injected into rat models of GIOP induced by DEX. Bone formation was analyzed by assessing the levels of bone turnover markers (ALP, TRAP, OCN, and CTx) in the serum and osteoblast differentiation markers (BMP2 and Runx2) in the femurs. The pathological changes of the femurs were determined by H&E staining. Bone mass and osteoblast numbers in the femurs were measured. Western blotting evaluated ERK phosphorylation in vitro and in vivo.

resultsPTL promoted osteogenic differentiation and enhanced the levels of Runx2, Osx, OPN, and ERK phosphorylation in DEX-treated MC3T3-E1 cells. ERK inhibitor U0126 reversed the promoting effect of PTL on osteogenesis in DEX-treated MC3T3-E1 cells. After the administration of PTL in rat models of GIOP, the levels of ALP, TRAP, OCN, and CTx in the serum and the levels of BMP2, Runx2, and ERK phosphorylation in the femurs were restored. PTL increased trabecular bone number, reduced trabecular separation, and increased the number of osteoblasts in GIOP rat model.

conclusionOverall, PTL alleviates osteoporosis by promoting osteogenic differentiation via activation of ERK signaling.

Indexed as

Cell DifferentiationGlucocorticoidsMAP Kinase Signaling SystemOsteogenesisOsteoporosisSesquiterpenesAnimalsCell LineDexamethasoneMaleMiceOsteoblastsRatsRats, Sprague-DawleyDexamethasoneGlucocorticoidsparthenolideSesquiterpenesBone formationERKGlucocorticoidOsteoporosisParthenolide

Identifiers

PMID40346551
PMCPMC12063341

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Read under generation 80e0d062 · epoch 390. Bibliography from PubMed, PubMed Central and OpenAlex; grants from NIH RePORTER; trial links from ClinicalTrials.gov; estimates, votes and beliefs from the OpenQuestion graph.