动物造模,心肌肥厚大鼠NF-κB信号通路 z-bio 2021-07-22 442

　　Objective: How to study the effect of 2,2,6,6-tetramethyl-4-piperidinol (temPol) on the NF-κB signaling pathway in rat cardiac hypertrophy?

　　Method: IsoPrenaline (ISO) (5mg)/kg intraperitoneally injected twice a day for 2 weeks) How to establish a rat model of myocardial hypertrophy? 42 SD male rats were randomly divided into three groups: normal control group, cardiac hypertrophy model group (ISO+normal saline) group, temPol intervention group (ISO+temPol group)? After 8 weeks of corresponding drug intervention, the heart weight index (HWI) and left ventricular weight index (left ventricular weight index, LVWI) were measured, and the rat myocardium HE staining was performed for morphology and myocardial fiber quality staining. qRT-PCR to detect fibrosis? Detect the transcription level of IL-6 mRNA and use Western blot IκBα? Measure the expression of P-. Rat myocardial tissue P65? P65 protein. grade?

　　Result: Compared with the normal control group, HWI and LVWI of the model group increased (Pu003c0.05), and the transcription level of TNF-α and IL-6 mRNA increased. Is the expression of P-P65/P65 significantly increased, and the expression of NF-κB inhibitory protein IκBα decreased (Pu003c0.05), and HE staining of myocardium shows thickening of muscle fibers? Myocardial structure disorder? The surface area of myocardial cells increased, and Masson staining of myocardium showed that myocardial fibrosis and myocardial interstitial collagen fibers increased. Compared with the model group, the HWI and LVWI of the temPol group were decreased (Pu003c0.05), and the transcription levels of TNF-α and IL-6 mRNA and P -P65/ expression decreased. All P65 decreased to varying degrees, and the expression of IκBα increased (Pu003c0.05). HE staining of myocardium can be seen. Myocardial structure disorder? Cardiomyocyte hypertrophy is reduced. Masson staining improves the degree of myocardial fibrosis. Does the interstitial collagen fiber decrease?

　　Conclusion: TemPol can improve myocardial hypertrophy caused by ISO. Could this be closely related to the inhibition of F-κB signaling pathway activity?