Triboulot C, Hichami A, Denys A, Khan N A
UPRES Lipids & Nutrition, Faculty of Life Sciences, Université de Bourgogne, Dijon 21000, France.
J Nutr. 2001 Sep;131(9):2364-9. doi: 10.1093/jn/131.9.2364.
After 10 wk of feeding an experimental diet enriched with (n-3) polyunsaturated fatty acids (PUFA), i.e., eicosapentaenoic acid [EPA, 20:5(n-3)] and [DHA, 22:6(n-3)] (EPAX), blood pressure in spontaneously hypertensive rats (SHR), but not in normotensive Wistar-Kyoto (WKY) rats was reduced relative to rats fed an unsupplemented control diet. Concanavalin A-stimulated T-cell proliferation was diminished in both strains of rats fed the PUFA/EPAX diet. The experimental diet lowered secretion of interleukin-2 in SHR, but not in WKY rats compared with rats fed the control diet. To determine whether there was a defect in calcium homeostasis in T cells during hypertension, we employed the following agents: caffeine, which recruits calcium from the cytosolic Ca(2+)-induced Ca(2+)-release pool; ionomycin, which at low concentrations opens calcium channels; and thapsigargin (TG), which mobilizes [Ca(2+)]i from the endoplasmic reticulum (ER) pool. Caffeine-induced increases in [Ca(2+)]i were not modified by the PUFA/EPAX diet. The ionomycin-induced increases in [Ca(2+)]i in T cells from SHR were greater than in those from WKY rats; consumption of the PUFA/EPAX diet did not modify Ca(2+) influx in cells of either strain. The TG-induced increases in [Ca(2+)]i in T cells from SHR were greater than those in cells from WKY rats. Interestingly, consumption of the experimental diet reduced TG-evoked increases in [Ca(2+)]i in T cells from SHR and increased those in T cells from WKY rats, indicating that the PUFA/EPAX diet could reverse the calcium mobilization from the ER pool in T cells. These results suggest that (n-3) PUFA exert antihypertensive effects and modulate T-cell calcium signaling during hypertension in rats.
在喂食富含（n-3）多不饱和脂肪酸（PUFA），即二十碳五烯酸[EPA，20:5（n-3）]和二十二碳六烯酸[DHA，22:6（n-3）]（EPAX）的实验性饮食10周后，自发性高血压大鼠（SHR）的血压相对于喂食未添加对照饮食的大鼠有所降低，但正常血压的Wistar-Kyoto（WKY）大鼠的血压未降低。喂食PUFA/EPAX饮食的两种品系大鼠中，伴刀豆球蛋白A刺激的T细胞增殖均减少。与喂食对照饮食的大鼠相比，实验性饮食降低了SHR中白细胞介素-2的分泌，但未降低WKY大鼠中白细胞介素-2的分泌。为了确定高血压期间T细胞钙稳态是否存在缺陷，我们使用了以下试剂：咖啡因，其从胞质Ca（2+）诱导的Ca（2+）释放池中募集钙；离子霉素，其在低浓度下打开钙通道；以及毒胡萝卜素（TG），其从内质网（ER）池中动员[Ca（2+）]i。咖啡因诱导的[Ca（2+）]i增加未被PUFA/EPAX饮食改变。离子霉素诱导的SHR T细胞中[Ca（2+）]i增加大于WKY大鼠T细胞中的增加；食用PUFA/EPAX饮食未改变任一品系细胞中的Ca（2+）内流。TG诱导的SHR T细胞中[Ca（2+）]i增加大于WKY大鼠细胞中的增加。有趣的是，食用实验性饮食降低了TG诱导的SHR T细胞中[Ca（2+）]i增加，并增加了WKY大鼠T细胞中的增加，表明PUFA/EPAX饮食可以逆转T细胞中内质网池的钙动员。这些结果表明，（n-3）PUFA在大鼠高血压期间发挥降压作用并调节T细胞钙信号传导。
