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. 2024 Sep 16;16(18):3130. doi: 10.3390/nu16183130

Figure 5.

Figure 5

The effects and mechanisms of polyunsaturated fatty acids against osteoarthritis. n-3 PUFAs could increase SIRT1 and inhibit the HMGB1-RAGE/TLR4-NF-κB signaling pathway, while n-6 PUFAs could promote the pathway, which was associated with increasing the level of NLRP3 and inflammatory factors, like IL-1β and TNF-α. n-3 PUFAs could increasing JNK, p38 MAPK pathways expression and Bcl-2 to suppress apoptosis. n-3 PUFAs could raise the level of Beclin-1 by inhibiting the expression of the mTOR pathway to promote autophagy. n-3 PUFAs could lower the expression of RANKL and NFATc1 to suppress osteoclast differentiation and reduce VEGF and its receptor to inhibit vessel formation. Bcl-2—B-cell lymphoma-2; HMGB1—high-mobility group box 1; IL-1β—interleukin-1β; JNK—c-Jun N-terminal kinase; MAPK—mitogen-activated protein kinase; mTOR—mammalian target of rapamycin; NF-κB—nuclear factor-κ-gene binding; NFATc1—nuclear factor of activated T-cells cytoplasmic 1; NLRP3—NOD-like receptor protein 3; PUFA—polyunsaturated fatty acid; RAGE—receptor for advanced glycation end products; RANKL—receptor activator of nuclear factor κB ligand; SIRT1—sirtuin 1; TLR4—toll-like receptor 4; TNF-α—tumor necrosis factor-α; VEGF—vascular endothelial growth factor; VEGFR—vascular endothelial growth factor receptor.