【Animal modeling】-Tempol's effect on NF-κB signaling pathway in rats with cardiac hypertrophy

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

  Method: How to establish a rat model of myocardial hypertrophy with isoPrenaline (isoPrenaline, ISO) (5mg/kg, twice a day for 2 weeks)? 42 SD rats were randomly divided into 3 groups: normal control group, cardiac hypertrophy model group (ISO + normal saline) group, temPol intervention group (ISO + temPol group)? Eight weeks after the corresponding drug intervention, we measured the heart weight index (HWI) and left ventricular weight index (LVWI), and used HE staining to observe myocardial cell morphology and fiber Masson staining of rat myocardial fibers. To detect the disease, we used qRT- PCR was used to detect the transcription level of TNF-αβIL-6mRNA in myocardial tissue, and Western blot was used to detect the expression of IκBαβ-P65βP65 protein in rat myocardial tissue.

  Results: Compared with the normal control group, the HWI and LVWI of the model group increased (P\u003c0.05), the transcription level of TNF-α and IL-6 mRNA, and the expression of P-P65/P65 NF-κB inhibitor protein IκBα The expression of myocardium is significantly increased (P\u003c0.05), does myocardial HE staining show muscle fiber thickening? The surface area of myocardial structure increased, and Masson staining of myocardium showed that myocardial fibrosis and myocardial matrix collagen fibers increased; compared with the model group, the HWI and LVWI of the temPol group decreased (P\u003c0.05). ), TNF-α, IL-6 mRNA transcription level and P-P65/P65 expression all decreased to varying degrees, while the expression of IκBα increased (P\u003c0.05). Myocardial structure is abnormal? Does reduced myocardial hypertrophy and Masson stain show improved myocardial fibrosis and reduced interstitial collagen fibers?

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