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目的探究不同n-3/n-6系多不饱和脂肪酸(PUFAs)是否能够调节视网膜细胞的高糖损伤,并探讨其可能的作用机制。方法以APRE-19细胞系作为研究对象,建立高糖损伤环境,筛选细胞能耐受的5种PUFAsα-亚麻酸(ALA)、亚油酸(LA)、花生四烯酸(AA)、二十碳五烯酸(EPA)、二十二碳六烯酸(DHA)的最高安全浓度,并以此浓度分别协同高糖处理细胞,测定细胞炎性因子肿瘤坏死因子-α(TNF-α)、白介素-4(IL-4)、白介素-6(IL-6)、脂氧素A4(LXA4)的分泌量及胞内抗氧化酶超氧化物歧化酶(SOD)、过氧化氢酶(CAT)活力。结果 APRE-19细胞株对上述五种PUFAs耐受量存在差异,100μmol/L是其均可耐受的最高安全浓度。与高糖协同处理时,LA、EPA显著下调TNF-α分泌,LA、ALA、EPA、DHA显著下调IL-6分泌,LA、ALA、AA、DHA显著下调IL-4分泌,ALA显著上调LXA4分泌(P<0.05);ALA恢复SOD酶活力至正常水平,ALA、LA和DHA上调CAT酶活力。结论 PUFAs能够调节高糖对视网膜色素上皮细胞的损伤,抑制炎症反应发生可能是其主要的机制之一,氧化应激调控也发挥了一定作用。
Objective To investigate whether different n-3 / n-6 polyunsaturated fatty acids (PUFAs) can regulate high glucose injury in retinal cells and explore its possible mechanism. Methods The APRE-19 cell line was used as the research object to establish a high sugar-damaged environment. Five PUFAsα-linolenic acid (ALA), linoleic acid (LA), arachidonic acid (AA) (EPA) and docosahexaenoic acid (DHA). The cells were treated with high glucose in this concentration, and the cytokines such as tumor necrosis factor-α (TNF-α) (IL-4), interleukin-6 (IL-6) and lipoxygenin A4 (LXA4) and the activities of intracellular antioxidant enzymes superoxide dismutase (SOD), catalase (CAT) vitality. Results The APRE-19 cell lines differed in the tolerance of these five PUFAs, with 100 μmol / L being the safest tolerable dose. ALA, EPA and DHA significantly down-regulated IL-6 secretion while LA, ALA, AA and DHA significantly down-regulated IL-4 secretion while ALA significantly up-regulated LXA4 secretion (P <0.05). ALA restored SOD enzyme activity to normal level, and ALA, LA and DHA up-regulated CAT enzyme activity. Conclusions PUFAs can regulate the damage of retinal pigment epithelial cells by high glucose and inhibit the inflammatory reaction may be one of the main mechanisms. The regulation of oxidative stress also plays a role.