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[Protective effect of diosgenin on chondrocytes mediated by JAK2/STAT3 signaling pathway in mice with osteoarthritis]
Abstract:
Objective: To investigate the effect of diosgenin (Dgn) on chondrocytes and its relation to JAK2/STAT3 signaling pathway in mice with osteoarthritis (OA).Methods: Fifteen male C57BL/6 mice were randomly divided into three groups:control group, OA group and OA+Dgn group. After 4 weeks of treatment, the histopathological changes of cartilage tissue were observed by toluidine blue staining under light microscopy and the ultrastructure of chondrocytes was observed under electron microscopy. The primarily cultured chondrocytes of OA mice were randomly divided into 4 groups:(1) OA group, (2) Dgn group, (3) Dgn+AG490 group, (4) AG490 group. The expression of p-JAK2, p-STAT3, Bax, succinate dehydrogenase (SDH) and cytochrome c oxidase (COX) were detected by Western blotting, and superoxide dismutase (SOD) was detected using colorimetric method. Results: The morphological observation showed that the chondrocytes of OA group presented considerable pathological changes, while the chondrocytes in OA+Dgn group maintained intact membrane. Electron microscopy observation found obvious injury in cartilage tissues of OA group, while that in OA+Dgn group remained smooth. Compared with OA group, the expressions of p-JAK2 and p-STAT3 in chondrocytes of Dgn group were increased (all P<0.05), and the expressions of Bax protein, SDH, COX and SOD were decreased (all P<0.05). While compared with Dgn group, the expressions of p-JAK2, p-STAT3, SDH, COX and SOD in chondrocytes of Dgn+AG490 group were decreased (all P<0.05), and the expression of Bax protein was increased (P<0.05). Conclusion: Diosgenin can inhibit apoptosis and increase mitochondrial oxidative stress capacity of chondrocytes in mice with osteoarthritis, which is closely related to the activation of JAK2/STAT3 signaling pathway.
Insights
Diosgenin (Dgn) protects chondrocytes in osteoarthritis (OA) mice by inhibiting apoptosis and enhancing mitochondrial function. This effect is linked to the activation of the Janus kinase 2/signal transducer and activator of transcription 3 (JAK2/STAT3) signaling pathway.
Area of Science:
- Biochemistry
- Cell Biology
- Pharmacology
Background:
- Osteoarthritis (OA) is a degenerative joint disease characterized by cartilage breakdown and chondrocyte apoptosis.
- The JAK2/STAT3 signaling pathway plays a crucial role in cellular processes, including inflammation and cell survival, and is implicated in OA pathogenesis.
- Diosgenin (Dgn), a natural steroid saponin, has shown potential therapeutic properties, but its specific effects on chondrocytes in OA and its underlying molecular mechanisms require further investigation.
Purpose of the Study:
- To elucidate the therapeutic effects of diosgenin (Dgn) on chondrocytes in a mouse model of osteoarthritis (OA).
- To investigate the involvement of the JAK2/STAT3 signaling pathway in the protective mechanisms of Dgn against OA-induced chondrocyte damage.
Main Methods:
- Osteoarthritis was induced in male C57BL/6 mice, which were then treated with diosgenin (Dgn).
- Histopathological and ultrastructural changes in cartilage and chondrocytes were assessed using toluidine blue staining and electron microscopy.
- The expression levels of key proteins, including phosphorylated JAK2 (p-JAK2), phosphorylated STAT3 (p-STAT3), Bax, succinate dehydrogenase (SDH), and cytochrome c oxidase (COX), were determined by Western blotting.
- Superoxide dismutase (SOD) activity was measured using a colorimetric method.
Main Results:
- Diosgenin treatment preserved chondrocyte morphology and cartilage integrity in OA mice compared to untreated OA controls.
- Dgn treatment significantly increased the expression of p-JAK2 and p-STAT3 in chondrocytes.
- Dgn treatment reduced the expression of pro-apoptotic Bax protein and enhanced mitochondrial function markers (SDH, COX, SOD).
- Inhibition of the JAK2/STAT3 pathway with AG490 reversed the protective effects of Dgn, decreasing p-JAK2, p-STAT3, SDH, COX, and SOD, while increasing Bax.
Conclusions:
- Diosgenin exhibits chondroprotective effects in osteoarthritis by inhibiting apoptosis and enhancing mitochondrial oxidative stress capacity.
- The therapeutic actions of diosgenin in OA are closely associated with the activation of the JAK2/STAT3 signaling pathway.
- Diosgenin represents a potential therapeutic agent for osteoarthritis, targeting chondrocyte survival and mitochondrial function via JAK2/STAT3 modulation.
