School of Health Sciences, College of Health, Massey University, Palmerston North, New Zealand.
School of Health Sciences, College of Health, Massey University, Palmerston North, New Zealand.
Prog Lipid Res. 2021 Jul;83:101113. doi: 10.1016/j.plipres.2021.101113. Epub 2021 Jul 2.
Long-chain polyunsaturated fatty acids (LCPUFAs) and their metabolites are considered essential factors to support bone and joint health. The n-6 PUFAs suppress the osteoblasts differentiation via increasing peroxisome proliferator-activated receptor gamma (PPARγ) expression and promoting adipogenesis while n-3 PUFAs promote osteoblastogenesis by down-regulating PPARγ and enhancing osteoblastic activity. Arachidonic acid (AA) and its metabolite prostaglandin E2 (PGE2) are key regulators of osteoclast differentiation via induction of the receptor activator of nuclear factor kappa-Β ligand (RANKL) pathway. Marine-derived n-3 LCPUFAs have been shown to inhibit osteoclastogenesis by decreasing the osteoprotegerin (OPG)/RANKL signalling pathway mediated by a reduction of pro-inflammatory PGE2 derived from AA. Omega-3 PUFAs reduce the expression of cartilage degrading enzyme matrix metalloproteinase-13 (MMP-13) and a disintegrin and metalloprotease with thrombospondin motifs-5 (ADAMTS-5) protein, oxidative stress and thereby apoptosis via nuclear factor kappa-betta (NF-kβ) and inducible nitric oxide synthase (iNOS) pathways. In this review, a diverse range of important effects of LCPUFAs on bone cells and chondrocyte was highlighted through different mechanisms of action established by cell cultures and animal studies. This review allows a better understanding of the possible role of LCPUFAs in bone and chondrocyte metabolism as potential therapeutics in combating the pathological complications such as osteoporosis and osteoarthritis.
长链多不饱和脂肪酸（LCPUFAs）及其代谢产物被认为是支持骨骼和关节健康的重要因素。n-6PUFAs 通过增加过氧化物酶体增殖物激活受体γ（PPARγ）的表达和促进脂肪生成来抑制成骨细胞分化，而 n-3PUFAs 通过下调 PPARγ和增强成骨细胞活性来促进成骨细胞生成。花生四烯酸（AA）及其代谢产物前列腺素 E2（PGE2）通过诱导核因子 kappa-B 配体（RANKL）途径是破骨细胞分化的关键调节剂。已经表明，海洋衍生的 n-3LCPUFAs 通过减少源自 AA 的促炎 PGE2 来抑制破骨细胞生成，从而减少骨保护素（OPG）/RANKL 信号通路。ω-3PUFAs 通过核因子 kappa-betta（NF-kβ）和诱导型一氧化氮合酶（iNOS）途径减少软骨降解酶基质金属蛋白酶-13（MMP-13）和解整合素金属蛋白酶与凝血酶 5 型（ADAMTS-5）蛋白的表达、氧化应激和细胞凋亡。在这篇综述中，通过细胞培养和动物研究建立的不同作用机制，强调了 LCPUFAs 对骨细胞和软骨细胞的多种重要影响。这篇综述使人们更好地理解了 LCPUFAs 在骨和软骨细胞代谢中的可能作用，作为对抗骨质疏松症和骨关节炎等病理并发症的潜在治疗方法。
