Partially hydrolyzed guar gum supplement reduces high-fat diet increased blood lipids and oxidative stress and ameliorates FeCl3-induced acute arterial injury in hamsters

Abstract

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.

Figure 1

Chemical structure of partially hydrolysed guar gum (PHGG). The chemical structure of PHGG: mannose: galactose = 2:1.

Figure 2

The antioxidant activity against O₂•^-, H₂O₂, HOCl in control (distilled water), PHGG, catechins and vitamin C is demonstrated. Catechins, vitamin C and PHGG significantly reduced O₂•^-, H₂O₂, HOCl activity in an order of catechins > vitamin C > PHGG > control. Each test was performed 6 times. * P < 0.05 when compared to the control value.

Figure 3

Effect of PHGG on carolic intake and the increased body weight in the four groups of animals. Each group was performed in 11 animals. * P < 0.05 when compared to the control value or 0 week, respectively.

Figure 4

Effect of PHGG on 30% FeCl₃-induced 4-HNE, ICAM-1 and TTO in the injuried carotid artery of the hamsters with HF diet. Oxidative stress indicated by 4-HNE (A-D) and ICAM-1 (E-H) immunostaining of hamster carotid arterial sections subjected to 150 sec of FeCl₃-induced arterial injury. Significantly enhanced endothelial ICAM-1 (brown color in B) and and 4-HNE (brown color in F) are found in HF group subjected to FeCl₃ treated carotid artery. The amplified diagram in the right corner was displayed. Carotid arterial 4-HNE and ICAM-1 expression were significantly reduced in HFLP and HFHP groups. FeCl₃ induced time to occlusion (TTO) of carotid arteries obtained from control (n = 11), HF (n = 11), HFLP (n = 11) and HFHP (n = 11) groups is indicated in the I. HF shortened TTO, but was reversed by PHGG treatment. *P < 0.05 vs. control group. # P < 0.05 vs. HF group.

Figure 5

Effect of low and high dosage of PHGG on Bax, Bcl-2, and HSP-70 expression in the carotid artery and femoral artery of HF fed hamsters. HF increased Bax and decreased Bcl-2 and HSP-70 expression in the hamster carotid and femoral arteries. HFLP and HFHP treatment decreased Bax and increased Bcl-2 and HSP-70 expression in both carotid and femoral arteries. *P < 0.05 vs. control group. # P < 0.05 vs. HF group.