Green tea catechins inhibit pancreatic phospholipase A2 and intestinal absorption of lipids in ovariectomized rats
Green tea catechins inhibit pancreatic phospholipase A2 and intestinal absorption of lipids in ovariectomized rats
复制标题
DOI：
10.1016/j.jnutbio.2006.03.004
复制
发表时间：
2006-07-01
影响因子：
5.6
通讯作者：
Koo, Sung I.
中科院分区：
文献类型：
--
作者：
Wang, Shu;Noh, Sang K.;Koo, Sung I.
本研究旨在研究绿色茶抑制肠道脂质吸收是否与其儿茶素对胰腺磷脂酶A（2）（PLA（2））的抑制作用有关。使用不同浓度（0.075-1.80 μ mol/L）的1，2-二油酰磷脂酰胆碱（DOPC）、猪胰腺PLA 2和儿茶素测定PLA（2）活性。通过HPLC测定释放的1-油酰基-2-羟基磷脂酰胆碱的量。0.6 μ mol儿茶素对PLA（2）的抑制率依次为（-）-表儿茶素（23.3%）、（+）-儿茶素（CAT; 24.8%）、（-）-表没食子儿茶素（25.7%）、（-）-表儿茶素没食子酸酯（39.7%）和（-）-表没食子儿茶素没食子酸酯（EGCG; 64.9%）。在体内研究中，用含有[二油酰-1-C-14]-磷脂酰胆碱、DOPC、α-生育酚（α TCH）和视黄醇（ROH）的三油酸甘油酯乳剂在没有（CAT 0）或具有CAT或EGCG的情况下经尿道内输注具有淋巴套管的卵巢切除大鼠8小时。与CAT（56.2 +/- 5.2%剂量）和卡托（64.7 +/- 2.0%剂量）相比，EGCG（45.5 +/- 4.9%剂量）显著降低了淋巴总C-14放射性。EGCG（24.1%剂量）中小肠腔和盲肠中残留的C-14放射性高于CAT（9.5%剂量）和CAT 0大鼠（9.0%剂量）。在EGCG大鼠中，淋巴三酰甘油和胆固醇酯中的C-14放射性显著减少。作为极疏水脂质标记物的α-TOH吸收在EGCG（7.8 +/- 1.7 μ mol）中显著低于CAT（14.4 +/- 2.8 μ mol）和卡托大鼠（16.8 +/- 2.1 μ mol）。ROH的吸收不受影响，而在EGCG大鼠中油酸输出较低。结果表明，EGCG抑制脂质的肠吸收，这部分与其抑制磷脂酰胆碱水解有关。数据表明，表没食子儿茶素没食子酸酯可以抑制其他高度亲脂性有机化合物的吸收。
This study was conducted to examine whether the inhibition of intestinal lipid absorption by green tea is associated with the inhibitory effect of its catechins on pancreatic phospholipase A(2) (PLA(2)). PLA(2) activity was assayed by using 1,2-dioleoylphosphatidylcholine (DOPC), porcine pancreatic PLA2 and catechins at varying concentrations (0.075-1.80 mu mol/L). The amount of 1-oleoyl-2-bydroxyphosphatidylcholine liberated was determined by HPLC. The percentage of inhibition of PLA(2) by catechins at 0.6 mu mol increased in the order of (-)-epicatechin (23.3%), (+)-catechin (CAT; 24.8%), (-)-epigallocatechin (25.7%), (-)-epicatechin gallate (39.7%) and (-)-epigallocatechin gallate (EGCG; 64.9%). In an in vivo study, ovariectomized rats with lymph cannula were infused intraduodenally for 8 h with a triolein emulsion containing [dioleoyl-l-C-14]-phosphatidylcholine, DOPC, alpha-tocopherol (alpha TCH) and retinol (ROH) without (CAT0) or with CAT or EGCG. The lymphatic total C-14-radioactivity was significantly lowered by EGCG (45.5 +/- 4.9% dose) compared with CAT (56.2 +/- 5.2% dose) and CATO (64.7 +/- 2.0% dose). The C-14-radioactivity remaining in the small intestinal lumen and cecum was higher in EGCG (24.1% dose) than in CAT (9.5% dose) and CAT0 rats (9.0% dose). Significantly less C-14 radioactivity was incorporated into lymph triacylglycerol and cholesteryl ester in EGCG rats. The absorption of alpha TOH, used as a marker of extremely hydrophobic lipids, was significantly lower in EGCG (7.8 +/- 1.7 mu mol) than in CAT (14.4 +/- 2.8 mu mol) and CATO rats (16.8 +/- 2.1 mu mol). The absorption of ROH was unaffected, whereas oleic acid output was lower in EGCG rats. The results show that EGCG inhibits the intestinal absorption of lipids, which is in part associated with its inhibition of phosphatidylcholine hydrolysis. Data suggest that EGCG may inhibit the absorption of other highly lipophilic organic compounds.