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Glycyrrhizic acid alters the hyperoxidative stress-induced differentiation commitment of MSCs by activating the
Huihui Xu1,2, Liang Fang1,2, Qinghe Zeng1,2
1The First College of Clinical Medicine, Zhejiang Chinese Medical University, Hangzhou, Zhejiang, 310053, China.
Abstract:
This study aimed to examine the in vivo and in vitro therapeutic effects of glycyrrhizic acid (GA) on steroid-induced osteonecrosis of the femoral head (SONFH), which is caused by the overuse of glucocorticoids (GCs). Clinically, we identified elevated oxidative stress (OS) levels and an imbalance in osteolipogenic homeostasis in SONFH patients compared to femoral neck fracture (FNF) patients. In vivo, we established experimental SONFH in rats via lipopolysaccharides (LPSs) combined with methylprednisolone (MPS). We showed that GA and Wnt agonist-S8320 alleviated SONFH, as evidenced by the reduced microstructural and histopathological alterations in the subchondral bone of the femoral head and the decreased levels of OS in rat models. In vitro, GA reduced dexamethasone (Dex)-induced excessive NOX4 and OS levels by activating the Wnt/β-catenin pathway, thereby promoting the osteogenic differentiation of mesenchymal stem cells (MSCs) and inhibiting lipogenic differentiation. In addition, GA regulated the expression levels of the key transcription factors downstream of this pathway, Runx2 and PPARγ, thus maintaining osteolipogenic homeostasis. In summary, we demonstrated for the first time that GA modulates the osteolipogenic differentiation commitment of MSCs induced by excessive OS through activating the Wnt/β-catenin pathway, thereby ameliorating SONFH.
Insights
Glycyrrhizic acid (GA) shows therapeutic potential for steroid-induced osteonecrosis of the femoral head (SONFH). GA treatment reduced oxidative stress and promoted bone health by activating the Wnt/β-catenin pathway in preclinical models.
Area of Science:
- Biomedical research
- Orthopedics
- Pharmacology
Background:
- Steroid-induced osteonecrosis of the femoral head (SONFH) is a debilitating condition linked to glucocorticoid overuse.
- Elevated oxidative stress (OS) and disrupted osteolipogenic homeostasis are observed in SONFH patients.
Purpose of the Study:
- To investigate the therapeutic effects of glycyrrhizic acid (GA) on SONFH.
- To elucidate the underlying mechanisms involving oxidative stress and the Wnt/β-catenin pathway.
Main Methods:
- In vivo studies using a rat model of SONFH induced by lipopolysaccharides and methylprednisolone.
- In vitro experiments with mesenchymal stem cells (MSCs) treated with dexamethasone.
- Assessment of microstructural, histopathological, oxidative stress, and molecular markers.
Main Results:
- GA treatment alleviated SONFH in rats, reducing bone damage and OS levels.
- In vitro, GA mitigated dexamethasone-induced OS by activating the Wnt/β-catenin pathway.
- GA promoted osteogenic differentiation and inhibited lipogenic differentiation of MSCs, regulating Runx2 and PPARγ.
Conclusions:
- Glycyrrhizic acid demonstrates therapeutic efficacy against SONFH.
- GA ameliorates SONFH by modulating MSC osteolipogenic differentiation via the Wnt/β-catenin pathway and reducing oxidative stress.
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