Objective: To investigate the effect of 2, 2, 6, 6-tetramethyl-4-piperidinol (temPol) on NF-κB signaling pathway in rat cardiac hypertrophy.
Methods: A rat model of myocardial hypertrophy was established by intraperitoneal injection of isoPrenaline (ISO) (5 mg/kg, twice a day for 2 weeks). 42 SD male rats were randomly divided into 3 groups : Normal control group, myocardial hypertrophy model group (ISO + normal saline group), temPol intervention group (ISO + temPol group)? After 8 weeks of corresponding drug intervention, measure the heart weight index (HWI) and left ventricular weight Left ventricular weight index (LVWI), HE staining was used to observe the morphology and fibrosis of cardiomyocytes, Masson staining was used to detect myocardial fibrosis in rats, and qRT-PCR method was used to detect TNF-α?IL-6 mRNA in myocardial tissues. Transcription level, Western blot was used to determine the expression level of IκBα, P-P65, and P65 protein in rat myocardial tissue.
Results: Compared with the normal control group, the HWI and LVWI of the model group increased (P<0.05), the transcription level of TNF-α and IL-6 mRNA, the expression of P-P65/P65 were significantly increased, and the NF-κB inhibitory protein IκBα Expression decreased (P <0.05), myocardial HE staining showed muscle fiber thickening? Myocardial structure disorder? Myocardial cell surface area increased, myocardial Masson staining showed increased myocardial fibrosis and myocardial interstitial collagen fibers; compared with the model group, HWI in the temPol group LVWI decreased (P <0.05), the transcription level of TNF-α, IL-6 mRNA, and the expression of P-P65/P65 decreased to varying degrees, and the expression of IκBα increased (P <0.05). Myocardial structure is disordered? The degree of myocardial cell hypertrophy is reduced, and the degree of myocardial fibrosis is improved by Masson staining, and the interstitial collagen fibers are reduced?
Conclusion: TemPol can improve ISO-induced cardiac hypertrophy, which may be closely related to the inhibition of NF-κB signaling pathway activity?