摘要
Objectives To observe the effects of telmisartan and rosiglitazone and explore the mechanism on early atherogenesis in male rats with type 2 diabetes mellitus. Methods Forty male SD rats were randomly and equally divided into four groups： control group, type 2 diabetes mellitus group, telmisartan group and rosiglitazone group. High lipid and high glucose were used for inducing DM in SD rats. The rats were raised for sixteen weeks. TC, TG, LDL-C and BG, PGI were measured. The aortae were collected for histopathlogical and immunohistochemical studies. Immunohisto-chemistry was used to analyze the expression of PPAR-γ, VCAM-1 and ICAM-1 in the arterial vessel wall. Results Compared with the control group, the level of TC, TG, LDL-C, and BG in blood were increased significantly （P 〈 0. 01 ） in type 2 Diabetic group. The telmisartan and rosiglitazone treatment decreased blood TC, TG, LDL-C and BG. The expression of PPAR-γ in type 2 diabetic group, telmisartan and rosiglitazone groups had significant differences compared with the control group, but there wasn＇t any significant differences （ P 〉 0. 05 ） among those three groups. Expression of VCAM-1, ICAM-1 and the monocytes infilitrating into the intima of the aortas telmisartan and rosiglitazone group was significantly lower than those in diabetic group （P 〈 0.01 ）. The endothelial damage of the aortae in telmisartan and rosiglitazone group was less severe than that in diabetes mellitus group. Conclusion Telmisartan and rosiglitazone can prevent early atherogenesis through alleviating the damage to the arterial wall by increasing the activation of PPAR-γ and inhibiting the VCAM-1, ICAM-1 expression and the monocytes infilitrating into the arterial wall. （S Chin J Cardio12009 ; 10（4） ： 216 -221 ）
Objectives To observe the effects of telmisartan and rosiglitazone and explore the mechanism on early atherogenesis in male rats with type 2 diabetes mellitus. Methods Forty male SD rats were randomly and equally divided into four groups： control group, type 2 diabetes mellitus group, telmisartan group and rosiglitazone group. High lipid and high glucose were used for inducing DM in SD rats. The rats were raised for sixteen weeks. TC, TG, LDL-C and BG, PGI were measured. The aortae were collected for histopathlogical and immunohistochemical studies. Immunohisto-chemistry was used to analyze the expression of PPAR-γ, VCAM-1 and ICAM-1 in the arterial vessel wall. Results Compared with the control group, the level of TC, TG, LDL-C, and BG in blood were increased significantly （P 〈 0. 01 ） in type 2 Diabetic group. The telmisartan and rosiglitazone treatment decreased blood TC, TG, LDL-C and BG. The expression of PPAR-γ in type 2 diabetic group, telmisartan and rosiglitazone groups had significant differences compared with the control group, but there wasn＇t any significant differences （ P 〉 0. 05 ） among those three groups. Expression of VCAM-1, ICAM-1 and the monocytes infilitrating into the intima of the aortas telmisartan and rosiglitazone group was significantly lower than those in diabetic group （P 〈 0.01 ）. The endothelial damage of the aortae in telmisartan and rosiglitazone group was less severe than that in diabetes mellitus group. Conclusion Telmisartan and rosiglitazone can prevent early atherogenesis through alleviating the damage to the arterial wall by increasing the activation of PPAR-γ and inhibiting the VCAM-1, ICAM-1 expression and the monocytes infilitrating into the arterial wall. （S Chin J Cardio12009 ; 10（4） ： 216 -221 ）
