Skip to main content
. 2011 Nov 1;15(9):2407–2424. doi: 10.1089/ars.2010.3751

FIG. 3.

FIG. 3.

Effect of in vivo TN challenge (3 mg/kg, i.p. for 48 h) on endoplasmic reticulum (ER) stress, cell survival, mitochondrial integrity (aconitase activity), and phosphorylation of Akt and glycogen synthase kinase 3β (GSK3β) in WT and MyAkt mice. A cohort of WT mice were injected with the ER stress inhibitor tauroursodeoxycholic acid (TUDCA) (50 mg/kg, i.p.) at the time of TN challenge. (A) Gadd153 expression; (B) GRP78 expression; (C) cell survival; (D) aconitase activity; (E) pAkt-to-Akt ratio; and (F) pGSK3β-to-GSK3β ratio. Insets: Representative gel blots depicting the ER stress proteins Gadd153 and GRP78, as well as pan and phosphorylated Akt and GSK3β using specific antibodies (β-actin was used as the loading control). All protein expressions were normalized to that of β-actin. Mean±SEM, n=5–7 hearts per group, *p<0.05 versus WT group, #p<0.05 versus WT-TN group.