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ω-3(n-3)多不饱和脂肪酸在自然发生疾病模型中对骨关节炎的调节作用。

Regulation of osteoarthritis by omega-3 (n-3) polyunsaturated fatty acids in a naturally occurring model of disease.

机构信息

Matrix Biology, Div. VPII, University of Bristol, Veterinary School, Langford, Bristol BS40 5DU, UK.

出版信息

Osteoarthritis Cartilage. 2011 Sep;19(9):1150-7. doi: 10.1016/j.joca.2011.06.005. Epub 2011 Jul 1.

DOI:10.1016/j.joca.2011.06.005
PMID:21723952
原文链接:https://pmc.ncbi.nlm.nih.gov/articles/PMC3176911/
Abstract

OBJECTIVE

To examine effects of high omega-3 (n-3) polyunsaturated fatty acid (PUFA) diets on development of osteoarthritis (OA) in a spontaneous guinea pig model, and to further characterise pathogenesis in this model. Modern diets low in n-3 PUFAs have been linked with increases in inflammatory disorders, possibly including OA. However, n-3 is also thought to increases bone density, which is a possible contributing factor in OA. Therefore we aim to determine the net influence of n-3 in disease development.

METHOD

OA-prone Dunkin-Hartley (DH) Guinea pigs were compared with OA-resistant Bristol Strain-2s (BS2) each fed a standard or an n-3 diet from 10 to 30 weeks (10/group). We examined cartilage and subchondral bone pathology by histology, and biochemistry, including collagen cross-links, matrix metalloproteinases (MMPs), alkaline phosphatase, glycosaminoglycan (GAG), and denatured type II collagen.

RESULTS

Dietary n-3 reduced disease in OA-prone animals. Most cartilage parameters were modified by n-3 diet towards those seen in the non-pathological BS2 strain - significantly active MMP-2, lysyl-pyridinoline and total collagen cross-links - the only exception being pro MMP-9 which was lower in the BS2, yet increased with n-3. GAG content was higher and denatured type II lower in the n-3 group. Subchondral bone parameters in the DH n-3 group also changed towards those seen in the non-pathological strain, significantly calcium:phosphate ratios and epiphyseal bone density.

CONCLUSION

Dietary n-3 PUFA reduced OA in the prone strain, and most disease markers were modified towards those of the non-OA strain, though not all significantly so. Omega-3 did not increase markers of pathology in either strain.

摘要

目的

研究高ω-3(n-3)多不饱和脂肪酸(PUFA)饮食对自发性豚鼠骨关节炎(OA)发展的影响,并进一步研究该模型的发病机制。现代饮食中 n-3 PUFA 含量低与炎症性疾病的增加有关,包括 OA。然而,n-3 也被认为可以增加骨密度,这可能是 OA 的一个促成因素。因此,我们旨在确定 n-3 在疾病发展中的净影响。

方法

将易患 OA 的 Dunkin-Hartley(DH)豚鼠与不易患 OA 的 Bristol Strain-2s(BS2)进行比较,从 10 周到 30 周(每组 10 只),两组均喂食标准饮食或 n-3 饮食。我们通过组织学和生物化学方法检查软骨和软骨下骨病理学,包括胶原蛋白交联、基质金属蛋白酶(MMPs)、碱性磷酸酶、糖胺聚糖(GAG)和变性 II 型胶原蛋白。

结果

n-3 饮食可减轻易患 OA 动物的疾病。大多数软骨参数通过 n-3 饮食向非病理性 BS2 品系的方向改变,显著的活性 MMP-2、赖氨酰吡啶啉和总胶原蛋白交联——唯一的例外是 pro MMP-9,它在 BS2 中较低,但随着 n-3 的增加而增加。n-3 组的 GAG 含量较高,变性 II 型胶原蛋白较低。DH n-3 组的软骨下骨参数也向非病理性品系的方向改变,显著的钙:磷比和骺骨密度。

结论

n-3 PUFA 饮食可减轻易患 OA 豚鼠的 OA 发生,大多数疾病标志物向非 OA 品系的方向改变,但并非所有标志物都显著改变。ω-3 并未增加两品系的病理学标志物。

https://cdn.ncbi.nlm.nih.gov/pmc/blobs/1f3e/3176911/62de9d4f682d/gr4.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/1f3e/3176911/78e901c25fdf/gr1.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/1f3e/3176911/bb6edea7040c/gr2.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/1f3e/3176911/7cc8526a758e/gr3.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/1f3e/3176911/62de9d4f682d/gr4.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/1f3e/3176911/78e901c25fdf/gr1.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/1f3e/3176911/bb6edea7040c/gr2.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/1f3e/3176911/7cc8526a758e/gr3.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/1f3e/3176911/62de9d4f682d/gr4.jpg

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