Effect of urantide on expression of c-jun n-terminal kinase in thoracic aorta tissue of rats with atherosclerosis and its significance / 吉林大学学报(医学版)

ABSTRACT

Objective: To investigate the effects of Urantide on the expressions of c-Jun N-terminal kinase (JNK) mRNA and protein in the thoracic aorta tissue of the rats with atherosclerosis (AS) • and to elucidate the molecular mechanism and significance of prevention and treatment of AS. Methods: The AS rat models were established by intraperitoneal injection of Vitamin D combined with high-fat diet and control group was set up at the same time. A total of 150 AS model rats were divided into model group, simvastatin group. IJrantide 3 d group. Urantide 7 d group and Urantide 14 d group ( n= 30). The rats in simvastatin group were adminstrated with simvastatin by gavage for 14 d. and the rats in Urantide groups were injected with Urantide by caudal vein for 3. 7. and 14 d. The serum markers of the rats in various groups were detected by automatic biochemical analyzer; the morphology of rat thoracic aorta tissue was observed by HE staining; the expression levels of JNK mRNA and protein in the rat thoracic aorta tissue were detected by immunohistochemical staining. qRT-PCR and Western blotting methods. Results: Compared with control group, the serum levels of triglyceride (TG). total cholesterol (TC) and low density lipoprotein (LDL) of the rats in model group were increased (P<0. 05). and the level of high-density lipoprotein (HDL) was decreased ( P<.0. 05). The HE staining results showed the formation of bubbling cells in the thoracic aorta tissue, rupture of medullary elastic fibers and calcification of the rats in model group; compared with model group, the pathological symptoms of the thoracic aorta tissue of the rats in simvastatin group and Urantide groups were improved. The immunohistochemistry results showed that the JNK positive particles were weakly expressed in the rat thoracic aorta tissue in control group; the expression intensity of JNK in the rat thoracic aorta tissue in model group was increased ( P<0. 05); compared with model group, the expression intensities of JNK in the rat thoracia aorta tissue in Urantide groups were significantly decreased (P∗C0. 05). The qRT-PCR and Western blotting results showed that the expression levels of JNK mRNA and protein in the rat thoracic aorta tissue in model group were significantly increased ( Pcontrol group; compared with model group, the expression levels of JNK mRNA and protein in simvastatin group and Urantide groups were gradually decreased ( P<0. 05); compared with simvastatin group, the expression levels of JNK mRNA and protein in the rat thoracic aorta tissue in Urantide groups were significantly decreased (P<. 0. 05). Conclusion; Urantide can improve the pathological damage of the thoracic aorta in the AS rats, and its mechanism may be related to the inhibition of JNK signaling pathway expression.