Abstract
Figures and Tables
Fig. 1
Blood glucose level in the three groups after 72 hours. Diabetes was induced by a single intraperitoneal injection streptozotocin followed by intraperitoneal administration of nicotinamide in the group II and III. After 72 hours, blood glucose concentration was measured. ALA, alpha-lipoic acid. a)P<0.05 vs. control.
![acb-52-176-g001](/upload/SynapseData/ArticleImage/1049ACB/acb-52-176-g001.jpg)
Fig. 2
Microscopic photography of aorta abdominal of rats (H&E staining; A and B, ×100; C, ×400). (A) Normal. (B, C) Atherosclerosis lesion induced by diabetes. 1, increased intimal wall thickness; 2, foam cell.
![acb-52-176-g002](/upload/SynapseData/ArticleImage/1049ACB/acb-52-176-g002.jpg)
Fig. 3
The effect of alpha-lipoic acid on the concentration of plasma oxidated low-density lipoprotein (oxLDL). The animals were organized into the following groups: I, negative control group without diabetes induction; II, positive control group with diabetes induction; and III, treatment group received alpha-lipoic acid (ALA) orally. DM, diabetes mellitus. a)P<0.05 vs. control. b)P<0.05 vs. DM.
![acb-52-176-g003](/upload/SynapseData/ArticleImage/1049ACB/acb-52-176-g003.jpg)
Fig. 4
Immunoreactivity of VCAM-1 in abdominal aortic from rats. Diaminobenzidine stains the VCAM-1 brown. Slides were counterstained with H&E, ×400 original magnification. Showing the expression of VCAM-1 (black arrows) was significantly lower in DM+ALA (C) than in DM (B). Expression of abdominal aortic adhesion molecule was assessed by calculation with Adobe Photoshop CS3 for percentage of area and intensity. (A) Normal: histogram present intensity, 28.71; area percent=8.02%. (B) DM: histogram present intensity, 58.26; area percent, 21.26%. (C) DM+ALA: histograms present intensity, 43.53; area percent,13.46%. L, lumen side; VACM-1, vascular cell adhesion molecule-1; DM, group with streptozotocin/nicotinamide-induced diabetes; DM+ALA, group with streptozotocin/nicotinamide/alpha-lipoic acid-induced diabetes.
![acb-52-176-g004](/upload/SynapseData/ArticleImage/1049ACB/acb-52-176-g004.jpg)
Table 1
Distribution of aortic atherosclerosis in the 3 groups
![acb-52-176-i001](/upload/SynapseData/ArticleImage/1049ACB/acb-52-176-i001.jpg)
Lesion scores | Group I (n=6) | Group II (n=6) | Group III (n=6) |
---|---|---|---|
0 | 6 | 0 | 4 |
1 | 0 | 0 | 1 |
2 | 0 | 6 | 1 |
3 | 0 | 0 | 0 |
The animals were organized into the following groups: I, negative control group without diabetes induction; II, positive control group with diabetes induction; and III, treatment group received alpha-lipoic acid orally. Atherosclerosis was scored as follows: 0, normal; 1, widening of elastic fibers with few foam cells; 2, fragmentation of elastic lamellae with numerous foam cells and fibrosis/classification, vascular smooth muscle cells proliferation, medial lipid infiltration; and 3, ulcerated plaque/thrombus.
Table 2
VCAM-1 expression in the 3 groups
![acb-52-176-i002](/upload/SynapseData/ArticleImage/1049ACB/acb-52-176-i002.jpg)
Group | Percentage area (%) | Intensity (index) |
---|---|---|
I | 5.68±0.9 | 33.81±2.4 |
II | 10.12±1.8a) | 43.79±1.8a) |
II | 5.77±1.3b) | 43.95±4.2a) |
Rats were segregated into three groups labeled as I control group, II diabetes mellitus group and III diabetes mellitus+alpha-lipoic acid group. Expression of abdominal aortic adhesion molecule was assessed by calculation with Adobe Photoshop CS3 for percentage of area and intensity. Values are presented as mean±SD. VACM-1, vascular cell adhesion molecule-1. a)P<0.05 vs. I. b)P<0.05 vs. II.
Acknowledgements
References
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