Objective To explore the effects of drugs on functions of mitochondria in retinal nerve cells, and to lay a foundation of the investigation of drug protection for retinal nerve cells. Methods Cultivation of the retinal nerve cells of 8 eyes of neonatal calves was performed. The changes of fluorescent density of the mitochondria of cultured cells labeled by dye rhodamine 123 (Rh123) before and after the activation of the medicines, including ferulic acid (FA), arginine, glycine,taurine, vitamine E and brain derived neurotrophic factor( BDNF) respectively, were detected by laser-scanning confocal microscopy. Results FA with the concentration of 500 μg/ml led the diphasic variation of the fluorescent intensity of mitochondria. After scanning for 60.772 seconds when treated with FA firstly, the fluorescent intensity decreased rapidly (from 45.425±4.153 to 22.135±5.293); while after 112.774 seconds when treated secondly, the in tensity increased obviously (from 19.655±4.383 to 28.247±4.764), and after 168.773 seconds when treated thirdly the intensity still increased. After scanning for 56.457 seconds when treated with vitamin E (12.5 mg/ml), the fluorescent in tensity increased obviously (from 88.255±5.039 to 111.273±4.529), which suggested that vitamin E with the concentration of 12.5 mg/ml strengthen the fluorescent intensity. After scanning for 58.147 and 134.148 seconds when treated with BDNF(50 ng/ml) respectively, the fluorescent intensity increased obviously (from 69.115±5.038 to 77.225±5.131) which suggested that BDNF with the concent ration of 50 ng/ml led the increase of the fluorescent intensity. Glycine (2.5 mg/ml) and arginine(30 mg/ml) didn’t affect the fluorescent intensity of mitochondria, and taurine (6.25 mg/ml) caused the appreciable decrease of the fluorescent intensity . Conclusion FA, BDNF and vitamin E may promote the metabolism of retinal nerve cells via the path of mitochondria, while amino acids may adjust the activation of retinal nerve cells through other ways. (Chin J Ocul Fundus Dis，2004，20：229-232)
PURPOSE: To probe the effect of taurine on lipid peroxidation,surperoxide dismutase(SOD) and glutathione peroxidase(GSH-Px)in retina in vitro. METHODS: The animal eye cups were put into media(divided into four groups:control,model,taurine and beta;-carotene) respectively,and incubated at 37deg;C in a humidified atmosphere of 5% CO2/95% air. After 24h or 48h ,the retinas were taken out from the media and the SOD,GSH-Px ,protein and malondialdehyde(MDA) were examined. RESULTS:Taurine could inhibite lipid peroxidation in retina ,decrease MDA level ,could not protect GSH-Px activity in retina. The effect of taurine on SOD activity in retina was also uncertain. CONCLUSION:Taurine can inhibit lipid peroxidation in retina in vitro,but the mechanism of that has nothing to do with the effect of taurine on SOD activity and GSH-Px activity. （Chin J Ocul Fundus Dis,1996,12: 183-185 ）
Objective To observe the effects of taurine on ventricular remodeling of rats with acute myocardial infarction (AMI) though the establishment of rat AMI model by ligating the left anterior descending coronary branch. Methods Sixty 8-week-old male Wistar rats were randomly divided into four groups: sham group, AMI group, small-dose and high-dose taurine group, with 15 rats in each. Rats in the AMI group and taurine groups received ligation of the anterior descending coronary branch to establish an animal model of AMI. Meanwhile, rats in the sham group were subjected to sham coronary ligature. From the next day of the operation, rats in the taurine groups were dosed orally per day with taurine 300 mg/kg or 400 mg/kg for 8 weeks, respectively. Echocardiographic images were acquired before and 8 weeks after the operation, to get the indexes such as left ventricular end systolic diameter (LVIDs), left ventricular end diastolic diameter (LVIDd), left ventricular posterior wall end diastolic thickness (LVPWd), left ventricular ejection fraction (LVEF), fractional shortening (FS), mitral inflow velocity E (E), mitral inflow velocity A (A), and E/A ratio, and all the measurements above were expressed as the average of 6 consecutive cardiac cycles. After the animals were executed, cardiac mass and left ventricular mass were measured, and cardiac mass index (CMI) and left ventricular mass index (LVMI) were calculated. Brain natriuretic peptide (BNP) in all groups were measured by enzyme-linked immunosorbent assay before and 8 weeks after the operation. Results In comparison with the AMI group, CMI, LVMI, LVIDd and LVIDs of the small-dose and high-dose taurine groups were lower, and LVPWd, LVEF, FS and E/A were higher (P<0.05). Plasma BNP level in the AMI group and two taurine-treated groups were higher than that in the sham group, and it was the highest in the AMI group (P<0.05). Conclusion Taurine has a protective effect on ventricular remodeling in rats with AMI, and the protective effect is dose-dependent.