Dietary L-arginine attenuates expression of vascular cell adhesion molecule-1 in the aortae of hypercholesterolemic rats

Objective To determine whether the antiatherogenic effect of L arginin e is due to an inhibition of vascular cell adhesion molecule 1 (VCAM 1) expres sion in the aortae of hypercholesterolemic rats. Methods Twenty four male Wistar rats were randomized into three gr oups : Group NC with normal diet (NC, n=8), Group CC with 4% cholesterol and 1% choli c acid diet (CC, n=8), Group AC with 4% cholesterol and 1% cholic acid diet supp lemented with 3% L arginine HCl in the drinking water (AC, n=8). Eight weeks la ter, the blood samples were collected for biochemical studies, and the aortae we re harvested for RT PCR and immunohistochemical studies.Results The results showed that dietary L arginine supplementation red uced expression of VCAM 1 in protein level and mRNA level. Conclusion Inhibitory effect of dietary supplementation of L argin ine on VCAM 1 expression may be one of the mechanisms of its antiatherosclerosis.

Doseeffect of dietary Larginine supplementation on burn woundhealing in rats

Objective To investigate the dose effect of dietary L arginine supplementation on burn wound healing in rats Methods 218 Sprague Dawley rats (weighing 200-250?g) were subjected to 10% deep partial thickness scald burns and were randomized into six groups Groups A, B, C, D, E and F received 800, 400, 200, 100, 50 and 0?mg·kg -1 ·d -1 L arginine in the form of L arginine solution, and 0, 727, 1090, 1272, 1364, and 1454?mg·kg -1 ·d 1 glycine, respectively Each solution was isonitrogenous The times of completing re epithelization were recorded The contents of hydroxyproline (OHP) in burn wound area (index of reparative collagen synthesis) and the ratios of type Ⅰ and type Ⅲ collagen were examined in all groups Results The times of completing re epithelization (day) in groups A, B, C, D, E, and F were 24 9±1 95, 22 5±2 0, 20 2±2 4, 23 5±2 6, 23 8±3 5, and 24 7±2 3, respectively The contents of hydroxyproline in groups B, C and D were higher than in groups A, E and F on PBD 7, 10 and 14 The ratios of typeⅠ and type Ⅲ collagen in groups B, C and D were lower than in groups A, E and F Conclusion Oral dietary L arginine supplementation from 100?mg·kg -1 ·d -1 to 400?mg·kg -1 ·d -1 shortened the times of re epithelization, increased amounts of hydroxyproline, and accelerated the synthesis of reparative collagen in burn rats

Interelation between nitric oxide and endothelin-1 in an experimental acute hypoxia in rats and its intervention

Objectives To study the interrelation between nitric oxide (NO) and endothelin 1 (ET 1) in experimental acute hypoxic rats, and to evaluate the mechanism of acute hypoxic pulmonary hypertension affected by NO and ET 1 and its intervention.Methods Nicotinamide adenine dinucleotide phosphate (NADPH) diaphorase histochemical staining method, Griess biochemical assay and radioimmune assay were applied to investigate the changes of nitric oxide syntheses (NOS), NO and ET 1 in normal, hypoxic, and L Arginine (L Arg) and dexamethasone treated hypoxic rats.Results In normal rats, the NOS stain was localized in pulmonary vascular endothelium, and in the hypoxic rats, the activity of NOS was significantly lower. The level of plasma NO was significantly lower during acute hypoxia, but L Arg as well as dexamethasone could prevent the drop of plasma NO. The level of plasma ET 1 rose up significantly in the acute hypoxic rats, but after L Arg therapy, it was significantly reduced, however, dexamethasone could not affect plasma ET 1. The level of plasma cyclic guanosine monophosphate (cGMP) was significantly lower in the acute hypoxic rats, and L Arg could prevent the drop of plasma cGMP, but dexamethasone could not prevent the drop of plasma cGMP. Conclusions NO and ET 1 may modulate hypoxic pulmonary hypertension and acute hypoxia can result in acute hypoxic pulmonary hypertension. L Arg can reverse the acute hypoxic pulmonary hypertension. Further study is needed if dexamethasone is beneficial in acute hypoxic diseases. NO may play an important role in physiology of the lung and acute hypoxic diseases.