The Effect And Mechanism Of Caveolin-1 To Diabetic Rats’ NO Of Tissue Ischemia

Aims:To evaluate the effect of diabetic rats’ e NOS and NO pathway of tissue ischemia by raised Caveolin-1.Method: Select healthy, male, SD rats from Animal Center of the University of South China, to whose enterocoelia inject STZ to build diabetic rat models, and cut off lift side-arteries femoralis and branches to build acute lower limb ischemia animal models. The next is to divide the models into 4 groups randomly by using Liposome transfect Caveolin-1 technique. The four groups are Sham-operation group, Ischemia group, Ischemia transfection group and Ischemia empty transfection group. After the operation, cutting the gastronomies’ muscle tissue of lower limbs in 14 days do the Immunohistochemical staining and HE staining,and the semi-quantitative analysis of Ischemia rats parts section by Image-Pro Plus(IPP) 6.0 image analysis system, and detect the NO standerd in the tissue homogenate by using NO detection kit.Result: The IHC semi- quantitative analysis and detection show that the expression of Caveolin-1 in ischemia group apparently increased compared with sham-operation group(P <0.05), and e NOS protein level has no change(P>0.05), while, the content of NO decreased(P <0.05); Compared with the sham operation group, the ischemia group and the empty transfection group, the ischemia transfection group’s expression of caveolin-1, e NOS and NO were significantly increased(P <0.05), which means successful transfection and decrease of Caveolin-1’s inhibition to e NOS/NO. This shows that Caveolin-1 has contradictory effect on diabetic rats’ e NOS and NO pathway of ischemic area, which would may be related to the fact that Caveolin-1’s impact to the signal pathway of AKT/e NOS/NO is stronger than its direct inhibition to e NOS.Conclusion: 1. The over-expression of caveolin-1 has auxo-action on diabetic rats’ e NOS/NO pathway of ischemic area; 2. Caveolin-1 can promote the angiogenesis of diabetic rats’ lower limb ischemia region,which may be related to the fact that Caveolin-1’s impact to the signal pathway of AKT is stronger than its direct inhibition to e NOS.