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An Ultrasonic Tool for Nerve Conduction Block in Diabetic Rat Models
Published on: October 20, 2017
[Effect of cilostazol on adhesion molecules of STZ-induced diabetic rats]
Zhe Wang1, Jiajun Zhao, Ling Gao
1Department of Endocrinology, Shandong Provincial Hospital, Shandong University, Jinan, China.
Objective:
To investigate the effect of cilostazol on the expression of CD(54), CD(106), CD(62P) in kidney, aorta, surface of platelet, and mononuclear cell of blood in STZ-induced diabetic rats.
Methods:
Rats were randomly divided into four groups: normal control group (n = 8), diabetes control group (n = 8), insulin group (n = 7 subcutaneous injection of insulin, 1 approximately 4 U * d(-1)), and cilostazol group (n = 7, gastric infusion of cilostazol, 18 mg * kg(-1) * d(-1)). Sciatic nerve conductive velocity and level of CD(54)/CD(62p) on the surface of mononuclear cell/platelet were examined by flow cytometry. Immunohistochemistry was used to examine the expression of CD(54) and/or CD(106) in kidney and aorta.
Results:
The sciatic nerve conductive velocity was 20.3 +/- 2.2 m * s(-1) and 28.9 +/- 7.9 m * s(-1) in diabetic rats and cilostazol group respectively (P < 0.05). The mononuclear cell surface expression of CDa-a(c)54 was 69.1 +/- 14.9% and 25.9 +/- 8.6% in diabetic group and cilostazol group respectively (P < 0.05). The expression of CD(54)/CD(106) in kidney and aorta was decreased. The expression of CD(62p) on the surface of platelets was 40.4 +/- 8.7% in diabetic group and 28.5 +/- 3.7% in cilostazol group (P > 0.05).
Conclusion:
Cilostazol treatment delays the development of diabetic pathological change in kidney, aorta and sciatic nerve and decreases the expression of CD(54) and CD(106).
Insights
Cilostazol treatment improved nerve function and reduced inflammatory markers in diabetic rats. This suggests cilostazol may delay diabetic complications in the kidney, aorta, and sciatic nerve.
Area of Science:
- Biomedical Science
- Pharmacology
- Diabetology
Background:
- Diabetes mellitus is associated with microvascular complications.
- Inflammatory markers like CD54 and CD106 play a role in diabetic pathology.
- STZ-induced diabetic rats are a common model for studying diabetic complications.
Purpose of the Study:
- To evaluate the therapeutic effect of cilostazol on diabetic complications.
- To investigate the impact of cilostazol on specific inflammatory markers (CD54, CD106, CD62P).
- To assess cilostazol's influence on kidney, aorta, platelet, and mononuclear cell function in diabetic rats.
Main Methods:
- Rats were divided into normal, diabetes, insulin, and cilostazol groups.
- Sciatic nerve conductive velocity was measured.
- Flow cytometry and immunohistochemistry were used to analyze CD marker expression.
Main Results:
- Cilostazol significantly improved sciatic nerve conductive velocity in diabetic rats.
- Cilostazol reduced the expression of CD54 on mononuclear cells and CD54/CD106 in the kidney and aorta.
- No significant difference in CD62P expression on platelets was observed between diabetic and cilostazol groups.
Conclusions:
- Cilostazol treatment demonstrates a protective effect against diabetic pathological changes.
- Cilostazol effectively reduces key inflammatory markers implicated in diabetic complications.
- The findings suggest cilostazol as a potential therapeutic agent for managing diabetic vascular and nerve issues.

