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Spermidine activates RIP1 deubiquitination to inhibit TNF-α-induced NF-κB/p65 signaling pathway in osteoarthritis
Zhong Chen1, Chuang-Xin Lin1,2, Bin Song1
1Department of Orthopedics, Sun Yat-sen Memorial Hospital, Sun Yat-Sen University, Guangzhou, 510120, P. R. China.
Abstract:
Spermidine has been known to inhibit the production of pro-inflammatory cytokines. However, there are no reports about anti-inflammatory effects of spermidine on osteoarthritis (OA). Herein, we examined whether OA progression could be delayed by intraperitoneal injection (i.p.) of spermidine in the anterior cruciate ligament transection (ACLT) and TNF-α induced arthritis (TIA) mouse models. During the process, human FLS cells (H-FLS) were used to investigate the potential ubiquitination mechanism of spermidine-mediated RIP1 in TNF-α-induced NF-κB/p65 signaling. We found that spermidine attenuated synovitis, cartilage degeneration and osteophyte formation, resulting in substantially lower OARSI scores and TNF-α scores in spermidine-treated ACLT and TIA mice. In terms of the mechanism, 9 μM spermidine did not affect the viability, proliferation, cell cycle and apoptosis of H-FLS, and exerted inhibitory effects by activating CYLD-mediated RIP1 deubiquitination on TNF-α-induced NF-κB/p65 signaling in H-FLS. From these data, we can conclude that spermidine attenuates OA progression by the inhibition of TNF-α-induced NF-κB pathway via the deubiquitination of RIP1 in FLS. Therefore, intake of spermidine could be a potential therapy for preventing OA.
Insights
Spermidine, a natural compound, was found to delay osteoarthritis progression in mouse models by reducing inflammation. It works by inhibiting the TNF-α-induced NF-κB pathway through RIP1 deubiquitination in fibroblast-like synoviocytes.
Area of Science:
- Biochemistry
- Immunology
- Rheumatology
Background:
- Osteoarthritis (OA) is a degenerative joint disease characterized by inflammation.
- Spermidine is known to inhibit pro-inflammatory cytokines, but its effects on OA are not well-documented.
Purpose of the Study:
- To investigate the potential anti-inflammatory effects of spermidine on osteoarthritis progression.
- To explore the underlying molecular mechanisms of spermidine's action in OA models.
Main Methods:
- Utilized anterior cruciate ligament transection (ACLT) and TNF-α induced arthritis (TIA) mouse models.
- Administered spermidine via intraperitoneal injection (i.p.).
- Investigated spermidine's effect on human fibroblast-like synoviocytes (H-FLS) and TNF-α-induced NF-κB/p65 signaling.
Main Results:
- Spermidine treatment significantly attenuated synovitis, cartilage degeneration, and osteophyte formation in OA mouse models.
- Spermidine treatment led to lower Osteoarthritis Research Society International (OARSI) and TNF-α scores.
- Spermidine activated CYLD-mediated RIP1 deubiquitination, inhibiting TNF-α-induced NF-κB/p65 signaling in H-FLS without affecting cell viability or proliferation.
Conclusions:
- Spermidine effectively attenuates osteoarthritis progression in mouse models.
- The mechanism involves the inhibition of the TNF-α-induced NF-κB pathway via RIP1 deubiquitination in fibroblast-like synoviocytes.
- Dietary spermidine intake may represent a potential therapeutic strategy for preventing osteoarthritis.
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