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Taraxasterol inhibits inflammation in osteoarthritis rat model by regulating miRNAs and NF-κB signaling pathway
Zikang Xie1, Bin Wang1, Chong Zheng1
1Department of Orthopaedics, Changzhou Traditional Chinese Medicine Hospital, Changzhou, 213000, PR China.
Abstract:
Osteoarthritis (OA) has a high incidence rate in the elderly population and is a cause of chronic degenerative joint disease. Current therapeutic approaches to OA are effective but come with some side effects. Therefore, it is urgent to find new safe and effective OA treatments. This study aimed to clarify the function of taraxasterol (TAX) isolated from Taraxacum officinale in the papain-induced rat OA model. We observed that TAX alleviated the typical OA-caused phenomena in the joint. The expression of serum inflammatory mediators such as TNF-α, IL-6, and IL-1β was also repressed by TAX. In addition, NF-κB signaling pathway was repressed by TAX. Furthermore, two microRNAs: miR-140 and miR-146a were elevated after TAX treatment in OA rat model. Interestingly, several common targets of miR-140 and miR-146a, including HSPA4L, ST5, and ERBB4, were confirmed to be regulated by TAX. Inflammatory response related genes including S100A8, CCL3, A2M, LBP, and CCR1 were repressed by TAX in OA rat model. In summary, TAX inhibits inflammation in osteoarthritis rat model. Inflammatory mediators, NF-κB pathway and miR-140/miR-146a targets mediate the function of TAX.
Insights
Taraxasterol (TAX) effectively treats osteoarthritis (OA) by reducing joint inflammation and suppressing key inflammatory pathways. This natural compound offers a promising, safe alternative for managing degenerative joint disease.
Area of Science:
- Biomedical Science
- Pharmacology
- Molecular Biology
Background:
- Osteoarthritis (OA) is a prevalent degenerative joint disease in the elderly.
- Current OA treatments have limitations and potential side effects.
- There is a need for novel, safe, and effective OA therapies.
Purpose of the Study:
- To investigate the therapeutic potential of taraxasterol (TAX), a compound from Taraxacum officinale, in a rat model of osteoarthritis.
- To elucidate the molecular mechanisms underlying TAX's anti-osteoarthritis effects.
Main Methods:
- Induction of osteoarthritis in rats using papain.
- Administration of taraxasterol (TAX) to the OA rat model.
- Assessment of joint pathology, inflammatory mediator levels (TNF-α, IL-6, IL-1β), NF-κB pathway activation, microRNA expression (miR-140, miR-146a), and target gene regulation.
Main Results:
- TAX treatment alleviated OA-induced joint damage.
- TAX significantly reduced serum levels of pro-inflammatory cytokines TNF-α, IL-6, and IL-1β.
- TAX inhibited the NF-κB signaling pathway.
- TAX upregulated miR-140 and miR-146a expression.
- TAX regulated common targets of miR-140/miR-146a, including HSPA4L, ST5, and ERBB4.
- TAX repressed inflammatory genes such as S100A8, CCL3, A2M, LBP, and CCR1.
Conclusions:
- Taraxasterol (TAX) demonstrates significant anti-inflammatory and chondroprotective effects in an experimental osteoarthritis model.
- TAX exerts its therapeutic benefits by modulating inflammatory mediators, inhibiting the NF-κB pathway, and regulating specific microRNAs and their target genes.
- TAX represents a potential natural therapeutic agent for osteoarthritis management.
