| Objective To investigate the cerebral vascular structure and function change of ratwith Hhcy and the interventional effects after giving the B vitamins.Methods Forty SD rats were randomly divided into four groups, including thecontrol group, Hhcy model group, Therapy group, Prevent group, each group hadten rats. Plain feedstuff, homomethionin feedstuff, homomethionin feedstuff feed fourweeks and then added B vitamins for eight weeks, homomethionin feedstuff and Bvitamins simultaneously feed were separately given to those four groups. The time ofexperiment was 12 weeks. The concentration of the total homocysteine in bloodplasma, MDA, NO level in blood serum and brain homogenate, SOD vigor weremeasured. The histological change Of cerebral vascular was observed with electronmicroscope.Results1 When the homomethionin feedstuff was feed to rats for four weeks, thehyperhomocysteinemia could be induced, the level of tHcy in blood plasma was-increased from 13.19±3.10gmol/l to 20.76±5.49μmol/l in the Hhcy model group.After the hyperhomocysteinemia model (21.01±6.55μmol/l) was made at the forthweek, B vitamins were given to intervene for 8 weeks in Therapy group. The leveloftHcy in blood plasma was 10.28±5.05μmol/l at the 12th week, and had nosignificant difference with the normal group (13.27±3.63μmol/l, P＞0.05). At theforth week, the level of tHcy in blood plasma was 16.40±4.15gmol/l in the Preventgroup, and was obviously lower than the Hhcy model group (22.85±4.92μmol/l) atthe same time. At the 12th week, the level oftHcy in blood plasma was 10.20± 2.25μmol/l, and had no significant difference with the normal group (13.27±3.63μmol/1, P＞0.05).2 The MDA level in blood serum of the Hhcy model group at the forth andtwelfth week was 13.80±3.86nmol/ml and 13.47±3.34nmol/ml separately, and wassignificant higher than that in normal group(7.81±2.61nmol/ml, 7.03±1.58 nmol/ml,P＜0.01), The MDA level in blood serum of the T group at the twelfth week was 6.82±1.51nmol/ml. It was lower than that at the forth week (13.11±2.70nmol/ml, P＜0.01), and had no significant difference with the normal group (7.03±1.58nmol/ml,P＞0.05). The MDA level in blood serum of the Prevent group at the forth week was10.35±2.74nmol/ml, and was lower than that in H model group(13180±3.86nmol/ml,P＜0.05). The MDA level in blood serum at the twelfth week (7.85±1.79nmol/ml)had no significant difference with the normal group (7.03±1.58nmol/ml, P＞0.05).3 The SOD vigor in blood serum of the Hhcy model group at the forth andtwelfth week was 123.70±22.30U/ml and 124.37±22.06 U/ml separately, and waslower than that in normal group(153.57±23.71 U/ml, 151. 21±5.27U/ml. P＜0.01),The SOD vigor in blood serum of the Therapy group at the twelfth week was 160.21±17.01U/ml. It was higher than that at the forth week (134.66±20.06 U/ml, P＜0.05), and there was no significant difference with the normal group (151.21±5.27U/ml, P＞0.05). The SOD vigor in blood serum of the Prevent group at the forthweek was 147.15±16.54 U/ml, and was higher than that in H model group (123.70±22.30 U/ml, P＜0.05), The SOD vigor in blood serum at the forth (147.15±16.54U/ml) and twelfth week (156.46±13.91U/ml) had no significant difference with thenormal group (153.57±23.71 U/ml, 151.21±5.27 U/ml, P＞0.05).4 The NO level in blood serum of the H model group at the forth and twelfthweek was 14.26±4.64μmol/l and 12.90±5.44μmol/l separately, and was lower thanthat in normal group(26.40±8.27μmol/l, 28.53±7.42μmol/1, P＜0.01), The NO level in blood serum of the Therapy group at the twelfth week was 21.77±5.85μmol/l. Itwas higher than that at the forth (14.84±6.75μmol/l, P＜0.05) and twelfth weekof Hhcy group (12.90±5.44μmol/l,P＜0.05),but still was lower than that in normalgroup (28.53±7.42μmol/l,P＜0.05). The NO level in blood serum of the Preventgroup at the forth week was 17.62±8.58μmol/l, and was higher than that in H modelgroup (14.26±4.64μmol/l, P＜0.05).The NO level in blood serum at the twelfthweek (26.80±8.31μmol/l) had no significant difference with that in normal group(28.53±7.42μmol/l, P＞0.05)5 The MDA level in brain homogenate of the H model group at the twelfthweek was2.10±0.43nmol/mgprot, and was higher than that in normal group(1.66±0.32 nmol/mgprot,P＜0.01), Therapy group (1.70±0.31 nmol/mgprot,P＜0.05) andPrevent group (1.65±0.24 nmol/mgprot, P＜0.01).The MDA level in Therapy groupand Prevent group had no significant difference with that in normal group(P＞0.05);The SOD vigor in H model group was 36.07±13.81U/mgprot,and was lower thanthat in normal group (50.87±13.51U/mgprot,P＜0.05),in Therapy group (55.78±13.51U/mgprot,P＜0.01) and in Prevent group (49.19±13.88U/mgprot, P＜0.05).The SOD vigor in Therapy group and Prevent group had no significantdifference with that in normal group(P＞0.05 ). The NO level in brain homogenate ofthe Hhcy model group(6.91±2.91μmol/mgprot) and Therapy group (10.86±5.21μmol/mgprot) was lower than that in normal group(16.33±6.00μmol/mgprot,P＜0.05), the NO level in Prevent group (16.04±6.84μmol/gprot) had no significantdifference with that in normal group (P＞0.05).6 On electron microscope, we observed that in the middle cerebral artery ofHhcy model group,the endothelial cell was degenerated, the endothelial cellmembrane was soluted and vague, the electron density was lowed, the cavitation ofintracytoplasm was formed, the cell organelles was annihilated,inner elasticity membrane was demixed by smooth muscle cell and showed worm-eclipsed change, the smoothmuscle cell nucleus were coacervated, and so on. We could also observed that in thecerebral cortex of Hhcy rats, the basement membrane of blood capillary was soluted,the endothelial cell nucleus were coacervated and allaxis, the baseboard was swollen,the cytoplasmic swelled, no cell organelles in cytoplasm and chromatinolysis, and soon. In Therapy group and Prevent group, we could observed that in the middlecerebral artery, the endothelial cell was vacuolated, the endothelial cell membraneinclined to be more thicker. In the cerebral cortex of T group and P group, we couldobserved that the small vessel wall was partially damaged,some cell organelles couldstill be recognized, the glial cells were damaged,the baseboard swelled, and so on.Conclusion The Hhcy that was induced by homomethionin feedstuff can damagethe cerebral vascular of rats. Giving the B vitamins can reduce the cerebral vasculardamage that caused by Hhcy, through reducing the tHcy level, oxidative stress andincreasing the NO level in blood serum. |
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