Kuo Dar-Chih, Hsu Shih-Ping, Chien Chiang-Ting
Department of Cardiovascular Surgery, Kuang-Tien General Hospital, Taichung, Taiwan.
J Biomed Sci. 2009 Feb 2;16(1):15. doi: 10.1186/1423-0127-16-15.
Increased reactive oxygen species (ROS) and hyperlipidemia can promote arterial thrombus. We evaluated the potential of a partially hydrolyzed guar gum (PHGG) as dietary fiber on lipid profiles and FeCl3-induced arterial thrombosis in the high fat-diet fed hamsters. Our in vitro results found that PHGG is efficient to scavenge O2-*, H2O2, and HOCl. High fat-diet increased plasma triglyceride, total cholesterol, LDL, VLDL, methylguanidine and dityrosine level and accelerated FeCl3-induced arterial thrombosis formation (from 463 +/- 51 to 303 +/- 45 sec). Low dose PHGG supplement significantly decreased the total cholesterol, LDL, methylguanidine and dityrosine level and delayed the time for arterial thrombosis formation (528 +/- 75 sec). High dose PHGG supplement decreased the level in triglyceride, total cholesterol, LDL and VLDL and further delayed the time for arterial thrombus (671 +/- 36 sec). The increased Bax protein and decreased Bcl-2 and HSP-70 protein expression was found in the carotid and femoral arteries of high fat-diet hamsters. Low and high dose of PHGG supplement decreased Bax expression and increased Bcl-2 and HSP-70 protein expression. We found that FeCl3 significantly enhanced intercellular adhesion molecule-1 and 4-hydroxynonenal expression in the endothelial site of damaged artery after 150-sec FeCl3 stimulation. PHGG supplement decreased the endothelial ICAM-1 and 4-hydroxynonenal expression after 150-sec FeCl3 stimulation. Based on these results, we conclude that PHGG supplement can increase antioxidant protein expression and thus decrease oxidative stress induced arterial injury.
活性氧(ROS)增加和高脂血症可促进动脉血栓形成。我们评估了部分水解瓜尔胶(PHGG)作为膳食纤维对高脂饮食喂养的仓鼠血脂水平和FeCl3诱导的动脉血栓形成的影响。我们的体外实验结果发现,PHGG能有效清除超氧阴离子(O2-*)、过氧化氢(H2O2)和次氯酸(HOCl)。高脂饮食会增加血浆甘油三酯、总胆固醇、低密度脂蛋白(LDL)、极低密度脂蛋白(VLDL)、甲基胍和二酪氨酸水平,并加速FeCl3诱导的动脉血栓形成(从463±51秒缩短至303±45秒)。低剂量补充PHGG可显著降低总胆固醇、LDL、甲基胍和二酪氨酸水平,并延迟动脉血栓形成时间(528±75秒)。高剂量补充PHGG可降低甘油三酯、总胆固醇、LDL和VLDL水平,并进一步延迟动脉血栓形成时间(671±36秒)。在高脂饮食仓鼠的颈动脉和股动脉中,发现促凋亡蛋白Bax表达增加,抗凋亡蛋白Bcl-2和热休克蛋白70(HSP-70)表达降低。低剂量和高剂量补充PHGG均可降低Bax表达,并增加Bcl-2和HSP-70蛋白表达。我们发现,在给予FeCl3刺激150秒后,受损动脉内皮部位的细胞间黏附分子-1(ICAM-1)和4-羟基壬烯醛(4-HNE)表达显著增强。补充PHGG可降低FeCl3刺激150秒后内皮ICAM-1和4-HNE的表达。基于这些结果,我们得出结论,补充PHGG可增加抗氧化蛋白表达,从而减少氧化应激诱导的动脉损伤。