摘要
Aim To investigate the mechanism of RhoA/ROCK signaling pathway in abnormal aortic contractility in type 2 diabetes (T2DM) mice. Methods The experiment was divided into two groups, the control group (db/m mice) and the model group (db/db mice). Changes of the response to different methods were measured in aorta rings using a Multi Myograph System. At the same time, the protein expression changes of aortic smooth muscle contraction signaling pathway in mice were determined by Western method. Results Compared with the control group, the blood glucose and body weight levels of the mice in the T2DM group significantly increased, and the cardiac function was abnormal (P <0. 01). The contractile response of the aorta of the diabetic mice induced by the contractile agents Phe, 5-HT and CaCl2 significantly increased (P < 0. 05). The aortic vasoconstriction responses mediated by L-type calcium channels, calcium release and SOC channels were higher in the T2DM group than in the control group (P <0. 05). Compared with the control group, the inhibition rate of ROCK inhibitor Y27632 on Phe-induced aortic constriction was more significant in the T2DM group (P < 0. 05), while the PKC inhibitor G66983 had no significant difference between the two groups (P >0. 05); Y27632 significantly inhibited SOCC-mediated aortic constriction (P < 0. 05). The protein expressions of RhoA, ROCK1, Cavl. 2 and Orail in T2DM aortic tissue increased (P <0. 05), while the expression of α1-AR had no significant difference (P >0. 05). There was no significant difference in the expression of Cavl. 2 and Orail protein in the aortic tissue incubated with 10 μmol ? L-1 Phe (P > 0. 05), and there was no significant difference in the expression of RhoA and ROCK1 protein in the aortic tissue incubated with 1 μmol ? L-1 nifedipine (P > 0. 05). Conclusions The hyperresponsiveness of aortic smooth muscle to contractile agents in type 2 diabetic mice is closely related to the enhancement of RhoA/ROCK kinase-mediated calcium signaling. ? 2023 Publication Centre of Anhui Medical University.
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