Gastrin ameliorates heart failure and suppresses myocardial remodeling via the JAK2/STAT3 and ERK1/2 pathways
Fig 7
Mechanism of gastrin in alleviating ISO-induced cardiomyocyte hypertrophy.
In the control,gastrin, ISO, and ISO+gastrin groups:(A)The protein expression levels of JAK2,p-JAK2, STAT3, p-STAT3, ERK1/2, p-ERK, and GAPDH by Western blot; (B)The level of p-JAK2/ JAK2; (C)The level of p-STAT3/ STAT3;(D)The level of p-ERK/ERK. In the control, ISO, ISO+ gastrin, and ISO+gastrin+ CI-988 groups: (E)The protein expression levels of JAK2,p-JAK2, STAT3, p-STAT3, ERK1/2, p-ERK, and GAPDH by Western blot;(F)The level of p-JAK2/ JAK2;(G)The level of p-STAT3/ STAT3;(H)The level of p-ERK/ERK. The expression of ANP(I),BNP(J), protein ERK1/2, p-ERK(K) and the ratio of p-ERK/ERK (L)after the addition of ERK agonist mSIRK. The expression of ANP(M),BNP(N), protein STAT3,p-STAT3(O) and the ratio of p-STAT3/STAT3 (P)after the addition of STAT3 agonist colevelin.*P < 0.05, **P < 0.01. ***P < 0.001. ****P < 0.0001. The data are presented as the mean±SEM. One-way ANOVA with Tukey’s post-hoc was conducted for (Panel B-D,F–-H,L,P). Welch’s one-wayANOVA analysis was performed of (Panel I,J,M,N).