Search

Rice bran contains a number of compounds which have shown to present beneficial effects on cardiovascular system. The rennin-angiotensin system is suggested to play roles in insulin resistance and cardiovascular diseases. Rice bran products have been reported to ameliorate type 2 diabetes. The protein fraction from rice bran is a rich source of valuable nutrition, however, there is only few reports on its effects on angiotensin system. Rice protein hydrolysates (RBP) were prepared from defatted Hom-Mali rice cultivated in the North-East region of Thailand with controlled enzymatic hydrolysis. Murine macrophage RAW 264.7 cells were cultured in DMEM media supplemented with 10% fetal bovine serum. Exposure of RAW 264.7 cells to angiotensin-I (ANG-I) and ANG-II resulted in stimulation of superoxide formation, as detected by lucigenin enhanced chemiluminescent assay. RBP (20-400ug/mL) concentration-dependently suppressed the oxidant formation. The suppression effect may be in part due to the inhibition of angiotensin converting enzyme (ACE) activity, as shown by an in vitro assay using rabbit ACE and specific substrate. Thus, RBP possesses ACE inhibiting activity and Since ANG may participate in inflammatory processes in diabetes and metabolic syndrome, nitric oxide formation was measured as a marker of induction of iNOS. Rice bran protein hydrolysates (100-800 ug/mL) showed to suppress ANG-I and ANG-II-induced nitric oxide generation. This study suggests that rice bran protein hydrolysates could suppress angiotensin-mediated oxidative stress and may provide beneficial effect as food supplement in diseases with oxidative stress conditions. [ABSTRACT FROM AUTHOR]

Nitric oxide (NO) depletion induces hypertension, oxidative stress and arterial stiffness. Previous study has shown that tetrahydrocurcumin (THU), a major antioxidant and anti-inflammatory agent, improved aortic stiffening of rats with NO-deficiency, however, the associated mechanism remains unclear. The objective of this study was to determine whether THU could attenuate vascular dysfunction and aortic remodeling in NO-deficient rats. The procedures and experimental protocols were reviewed and approved by the Institutional Animal Ethics Committee of Khon Kaen University, Thailand. Male Sprague-Dawley rats weighing 200-220 g were divided into normotensive and hypertensive groups (n=6-8/group). Hypertension was induced by administering Nω-nitro-L-arginine methyl ester (L-NAME) at a dose of 50 mg/kg/day in their drinking water for 5 weeks. After 3 weeks, hypertension had been established and was sustained in all animals. During the last two weeks, L-NAME hypertensive rats were randomly divided into three treatment groups. Group 1 was intragastrically administered with polyethylene glycol (PG), a vehicle. Group 2 and 3 were intragastrically administered with THC for 2 weeks at doses of 50 and 100 mg/kg/day, respectively. The normotensive controls were received tap water ad libitum and intragastrically administered with PG. At the end of treatment, animals were anesthetized with pentobarbital sodium (60 mg/kg body weight, i.p.), arterial blood pressure and vascular response to acetylcholine (3, 10 and 30 nmol/kg, i.v.) were determined. Thereafter, rats were sacrificed by overdose of an anesthetic drug. The thoracic aortas were excised and used for quantitative morphometric analysis of structural changes and immunohistochemistry staining of MMP-2. Values are means ± S.E.M., compared by one way ANOVA. L-NAME significantly increased blood pressure, blunted vascular response and induced aortic remodeling. THU 50 and 100 mg/kg/day significantly decreased mean arterial pressure (174 ± 2 and 165 ± 2 mmHg, respectively vs. 189 ± 2 mmHg in L-NAME control rats; P < 0.01), and prevented the reduction in endothelium-dependent vasodilatation. THU reduced the increases in media thickness, cross-sectional area, smooth muscle cells proliferation and collagen accumulation in the aortic wall. Increased MMP-2 expression was found in the aortas of L-NAME, and THU at test doses significantly reduced it (P < 0.05). Our results suggest that MMP-2 plays a role in L-NAME hypertension and its structural and functional vascular changes, which were attenuated by THU. This study was supported by grants from the Faculty of Medicine, Khon Kaen University, the Thailand Research Fund (Grant No. DBG5380045) and the British Council PMI2 Grant (#RC53). [ABSTRACT FROM AUTHOR]

Curcumin, a major active component from turmeric (Curcuma longa), widely grown in tropical regions of Asia. Normally, it was used as a spice to give specific flavor and color of food. Moreover, curcumin is a medicinal plant which possesses neuroprotective, cardioprotective, anti-carciogenic, anti-inflammation, and antioxidant properties. Phenylhydrazine (PHZ) is a strong oxidant agent and has been used in an animal model of hemolytic anemia (1). PHZ oxidation causes free iron release resulting in massive free radicals generation, oxidative stress and vascular dysfunction (2). The aim of this study was to investigate the effect of curcumin on PHZ-induced hemolytic anemia in rats. Male Sprague-Dawley rats were obtained from National Animal Laboratory Center, Thailand, and were housed and treated at North-Eastern Laboratory Animal Center, Khon Kaen University, Thailand. All animal procedures were reviewed and approved by the Institutional Animal Ethics Committee of Khon Kaen University (AE 41/2555). Rats (n= 8/group) were exposed to PHZ (15 mg/kg/day; i.p.) and orally administered with curcumin (30 and 100 mg/kg/day)for 8 days. After 8 days of PHZ administration, rats were anaesthetized with pento-barbital sodium (60 mg/kg; i.p) then arterial blood pressures and hind limb blood flow (HBF) were measured. At the end of experiment, blood samples were collected from abdominal aorta for assays of hematocrit values, non-transferrin bound iron (NTBI), oxidative stress markers including, plasma malondialdehyde (MDA) and protein carbonyl levels. Tissue samples, heart, kidneys, and liver, were also removed to measure MDA and protein carbonyl levels. Subsequently, the thoracic aorta was excised rapidly from the animals and used for measurement of superoxide production. The systolic, diastolic and mean arterial blood pressure of PHZ treated rats were markedly decreased whereas HBF and serum NTBI level were dramatically increased when compared with normal controls. Interestingly, the restoration of hemodynamic disturbance and anemia during PHZ exposure were related to the alleviation of free iron release, superoxide production and oxidative stress status. Results in this study reveal the effects of curcumin that may offer potential advantage of practical use in prevention of vascular dysfunction and oxidative stress in PHZ treated rats. [ABSTRACT FROM AUTHOR]

Consumption of high-fat, high-carbohydrate diet mainly contributed in the development of metabolic syndrome, which is associated with obesity, insulin resistance, dyslipidemia, and high blood pressure. It is well established that asiatic acid, a natural triterpenoid compound derived from Centella asiatica, exhibited biological effects including, antiinflammation, antioxidant and antihyperglycemia. In the present study, we examined the metabolic, cardiovascular responses as well as antioxidant properties of asiatic acid in rats with metabolic syndrome (MS) induced by high-fat, high-carbohydrate (HFHC) diet. Male Sprague-Dawley rats (160-180 g) were fed with HFHC diet with 15% fructose in drinking water for 12 weeks to induce MS. Then, MS rats and normal rats received asiatic acid (10 mg/kg) or vehicle for further 3 weeks. Fasting serum insulin, fasting blood glucose (FBG), oral glucose tolerance test (OGTT) and systolic blood pressure (SBP) were measured once a month. At the end of treatment, rats were anaesthetized with peritoneal injection of pentobarbital-sodium (60 mg/kg) and hemodynamic status, lipid profiles and oxidative stress markers were evaluated. All procedures are complied with the standards for the care and use of experimental animals and approved by Animal Ethics Committee of Khon Kaen University, Khon Kaen, Thailand (AEKKU 36/2555). Data are expressed as the mean ± S.E.M., compared by ANOVA. Results showed that rats fed with HFHC diet had an impairment of OGTT, high homeostasis model assessment of insulin (HOMA-IR), high cholesterol, and high SBP, indicating metabolic syndrome (MS) in these rats (p<0.05). Moreover, mean arterial blood pressure (MAP) (MS: 114.61 ± 3.7 vs. 90.58 ± 1.7 mmHg control, p<0.05), hindlimb vascular resistance (HVR) (MS: 30.64 ± 2.5 vs. 11.46 ± 0.6 mmHg/min/100 g/ml control, p<0.05) were significantly increased, relating to the augmentation of vascular superoxide production (MS: 114.9 ± 15.1 vs. 56.9 ± 4.3 counts/min/mg dry weight control, p<0.05) and plasma MDA levels (MS: 5.8 ± 0.5 vs. 2.9 ± 0.2 µM control, p<0.05) in MS group. Treatment with asiatic acid significantly attenuated dyslipidemia and improved insulin sensitivity as shown by the decreased HOMA-IR (p<0.05). We found reductions in MAP (about 11 .4%) and HVR (about 36%) in MS rats received asiatic acid (p<0.05). Moreover, asiatic acid exhibited antioxidant properties by markedly reducing oxidative stress markers in vascular tissues and plasma in MS rats (p<0.05). In conclusion, asiatic acid improved metabolic and hemodynamic changes as well as oxidative stress in HFHC diet induced MS rats. [ABSTRACT FROM AUTHOR]