To investigate the effect of green tea extract (GTE) on oxygen-induced neovascularization (NV) in neonatal rat model, NV was induced by maintaining neonatal rats in 80% oxygen on a cycle of 23.5h oxygen/0.5h room air until postnatal day 12 (P12), when the rats were placed in room air. The control rats were maintained in room air. From P6 to P17, rats were treated once daily by oral administration of saline (50μl/10g body weight) that contained 25% GTE, 12.5% GTE, or nothing. On P18, the rats were sacrificed and the retinal samples were collected. Retinal NV was scored and avascular areas (AVAs) were measured in ADPase stained retinas. The retinal vascular endothelial cell growth factor (VEGF) contents were measured with immunoassay kit, and matrix metalloproteinase-2 (MMP-2) activity was determined by gelatin zymography. GTE (25%) treatment suppressed NV and slightly increased AVAs in oxygen-induced NV model compared with the control. VEGF contents in retina significantly increased on P13 and P15, but GTE treatment did not prevent the increase of VEGF contents. Oxygen-induced increases in MMP-2 activity on P13 and P15 were suppressed by GTE treatment. These results suggest that GTE suppressed oxygen-induced NV in the neonatal rat, possibly through inhibition of MMP-2 activity. It also suggests that orally administered green tea has the potential to inhibit neovascular disease.
The present study was designed to examine the influence of the early stage hepatopathy on blood fluidity by using a rat experimental system. F344 male rats, 4 weeks of age, were fed chow containing 3'-methyl-4-dimethylaminoazobenzene (DAB) at 0.06%. These rats were autopsied 8, 12, 16 and 20 weeks after starting DAB feeding. Blood samples were collected from the inferior vena cava under pentobarbital anesthesia and blood fluidity and platelet aggregation activity were examined by a Micro Channel Array Flow Analyzer and a platelet aggregometer, respectively. We also examined histological changes in the liver after staining with hematoxylin-eosin. Histological observation of the liver revealed early-stage hepathopathy when the organs were obtained from rats that fed DAB for more than 16 weeks. Although DAB-feeding of rats for 8 and 12 weeks barely affected blood fluidity, long-term intake (>16 weeks) caused decrease in fluidity. On the other hand, platelet aggregation activity was increased when rats were fed DAB for more than 16 weeks. The present results suggest that assaying for blood fluidity may be useful for the assessment of the degree of hepatopathy.
[Objective] Perspiration is almost only heat radiation mechanism under high temperature environments. And sudoriferous water is supplied from blood. Blood flow is determined by blood fluidity, blood volume and the cardiovascular system. It was reported that strong stress decreased blood fluidity.In this experiment, we investigated the relation between blood fluidity and water supply in rats loaded with forced exercise in high temperature environment.[Methods] SPF male Wistar rats weighing 250g were used. All animals were put in high temperature environment (Wet Bulb Globe Temperature; WBGT: 28°C) through whole experimental period. The rats were divided into four groups randomly; Suitable temperature environment-Exercise-Non water intake (SEN), High temperature environment-Exercise-Non water intake (HEN), High temperature environment-Exercise-Water intake (HEW) and Baseline (BL). In a group of water supply, distilled water was served before and later exercise by sonde forcibly. The blood was collected before or later of exercise and blood and erythrocyte suspension fluidity were measured.[Results] In the HEN, hydroperoxides, blood sodium, lactic acid and adrenaline increased while blood and erythrocyte suspension fluidity were decreased significantly compared with the BL. In addition, the hematocrit did not increase even if water equivalent to 4% of body weight lost it.[Conclusion] We speculate that exercise in high temperature environment decreases blood fluidity. However, the water supply in exercise that might not be sufficiently improve blood fluidity.
This study aimed to investigate the antioxidant effect of lutein, human macula pigment, and pycnogenol, which contains several flavonoids, on lipid peroxidation induced in 10% porcine retinal homogenate by the addition of 1 mM Ferric chloride (FeCl3), 50 mM 2,2'-azobis (2-amidino-propane) dihydrochloride (AAPH), or 25 mM 2,2'-azobis (2,4-dimethyl-valeronitrile) (AMVN). Lipid hydroperoxide concentration was determined from the amount of thiobarbituric acid reactive substances (TBARS) in the sample following treatment. After 60 min of oxidation with FeCl3, AAPH and AMVN, the TBARS content in the retinal homogenates increased from 28.6 ± 1.6 to 85.4 ± 0.9, from 27.9 ± 1.2 to 57.2 ± 1.1, and from 26.0 ± 1.0 to 77.5 ± 2.0 nmol MDA/mg protein, respectively. Lutein did not show remarkable antioxidant activity in this experimental system. However, IC50 of pycnogenol for TBARS formation was decreased by combining 10 μM lutein in each initiator; from 12 to 5 μg/mL in FeCl3, from 2.8 to 0.5 μg/mL in AAPH, from 465 to 110 μg/mL in AMVN. These results suggested that a combination treatment of lutein and pycnogenol is more effective for inhibiting lipid peroxidation in porcine retinal homogenate. This synergy might be due to efficient functional antioxidants acting in both hydrophilic and lipophilic cellular environments.
