HAO Hong, WANG Wei-na. Interventions of Taurine and Vitamin in Atherosclerosis Induced by Hyperhomocysteine in Rabbits[J]. Chinese journal of experimental traditional medical formulae, 2011, 17(11): 227-229.
HAO Hong, WANG Wei-na. Interventions of Taurine and Vitamin in Atherosclerosis Induced by Hyperhomocysteine in Rabbits[J]. Chinese journal of experimental traditional medical formulae, 2011, 17(11): 227-229.DOI:
Objective: To investigate the interventions of taurine and vitamin in atherosclerosis (AS) induced by hyperhomoaysteine(HHcy) in rabbits. Method: The model groups with HHcy were respectively fed with taurine
folic acid
vitamin B6 and vitamin B12-a high L-methionine diet.Compared with the control group(NC)
the serum of the model groups were tested respectively in the 4th week and 8th week to determine the content of Hcy
MDA
TC
TG
NO
TXB2 and the activity of SOD and the changes in abdominal artery disease by vascular ultrasound and histologyical observation. Result: The contents of Hcy
MDA
ET and TXB2 in the serum of the rabbits having received methionine increased a lot(P<0.01
P<0.05) in the 4 week and 8 week than that of the control group
but the content of NO and the activity of SOD were much lower(P<0.01)
compared with the NC group in the same period.Hcy in the rabbits having received taurine were much higher
but Hcy in the rabbits having received vitamin displayed on change in the 8 week.And the contents of MDA
ET and TXB2 in both model groups were much lower (P<0.01) than the group with methionine
but the contents of NO and the activity of SOD were much higher(P<0.01).In the group with methionine Hcy could obviously induce abdominal arterial lesions with intimal thickening
smooth muscle cell hyperplasia
elastic fiber fracture
sort disorder and fatty plaque.Compared with the NC group
the rabbits received taurine and those received vitamin displayed no arterial lesions
no fatty plaque with neat structure. Conclusion: Taurine can resist the destrucion induced by Hcy.Vitamin can promote Hcy metabolism
inhibit vascular damage induced by Hcy and delay or prevent AS.