Myricetin Alleviates Pathological Cardiac Hypertrophy via TRAF6/TAK1/MAPK and Nrf2 Signaling Pathway
Myr prevented NRCM hypertrophy in vitro. (a) Immunofluorescence (IF) staining of NRCM in different groups; (b) calculated cell surface area (>100 cells per group); (c–e) mRNA expression levels of ANP, BNP, and β-MHC, respectively; Nrf2 knockdown (f) and its downstream genes including HO-1 (g), NQQ-1 (h), and GCLC (i), respectively. All mRNA expressions of target genes were normalized to GAPDH; (j) DCF fluorescence was quantified to present the reactive oxygen species after different treatments indicated in the pictures; (k) representative western blots for SOD1, CAT, and 4-HEN after different treatments indicated in the pictures; (l) quantified SOD1, CAT1, and 4-HEN after normalized to GAPDH. Cellular experiments were repeated three times independently. versus the group indicated in the picture.