Fig 1: The GLP-1 receptor agonist, exendin-4, preserves heart function and hemodynamics. (A) Echocardiographic data for the sham-operated, MI, MI+Ex-4 and MI+Ex-4+Ex9-39 groups (n=9 animals per group). MV E/A, LADd, LADs and LAFS were analyzed using echocardiography. (B) LW/TL ratios and the plasm levels of ANP in the sham-operated, MI, MI+Ex-4 and MI+Ex-4+Ex9-39 groups (n=9 animals per group). (C) Representative recordings of dp/dt and the statistical analyses of dP/dtmax, dP/dtmin, SBP, DBP, MBP in the sham-operated, MI, MI+Ex-4 and MI+Ex-4+Ex9-39 rat hearts at 4 weeks following sham or MI surgery (n=9 animals per group). *P<0.05 vs. the sham-operated group, #P<0.05 vs. the MI group, §P<0.05 vs. the MI+Ex-4 group. MI, myocardial infarction; Ex-4, exendin-4; Ex9-39, exendin9-39; LW/TL, lung weight to tibia length ratio; MV E/A, mitral valve E/A; LADd, LA dimension in ventricular diastole; LADs, LA dimension in ventricular systole; LAFS, LA fractional shortening; ANP, atrial natriuretic peptide; SBP, systolic blood pressure; DBP, diastolic blood pressure; MBP, mean blood pressure.
Fig 2: The GLP-1 receptor agonist, exendin-4, improves atrial electrophysiological function properties. (A) Representative recordings of action potentials and quantitative analysis of the APD20, APD50 and APD90 of LAA in the sham-operated, MI, MI+Ex-4 and MI+Ex-4+Ex9-39 rat hearts at four weeks following sham or MI surgery (n=12 animals per group). (B) Representative recordings of burst pacing-induced atrial tachyarrhythmias in the sham-operated, MI, MI+Ex-4 and MI+Ex-4+Ex9-39 rat hearts at four weeks following sham or MI surgery and statistical analyses of these data (n=12 animals per group). *P<0.05 vs. the sham-operated group, #P<0.05 vs. the MI group, §P<0.05 vs. the MI+Ex-4 group. MI, myocardial infarction; Ex-4, exendin-4; Ex9-39, exendin9-39; APD, action potential duration; LAA, left atrial appendage.
Fig 3: Exendin-4 inhibits the PI3K/AKT signaling pathway. (A) Plasma GLP-1 levels and (B) GLP-1 receptor mRNA expression as determined by reverse transcription-quantitative PCR in the sham-operated, MI, MI+Ex-4 and MI+Ex-4+Ex9-39 rat atrial tissues 4 weeks following sham or MI surgery. (C) Representative western blots of atrial tissues probed for GLP-1 receptor, total PI3K, phosphorylated PI3K, total AKT and phosphorylated AKT in the sham-operated, MI, MI+Exendin-4 and MI+Exendin-4+Ex9-39 rat hearts four weeks following sham or MI surgery and statistical analysis of the expression levels of these proteins, which were normalized to those of GAPDH (n=5 animals per group). *P<0.05 vs. the sham-operated group, #P<0.05 vs. the MI group, §P<0.05 vs. the MI+Ex-4 group. MI, myocardial infarction; Ex-4, exendin-4; Ex9-39, exendin9-39; GLP-1, glucagon-like peptide-1 receptor; p-, phosphorylated; t-, total.
Fig 4: PCA ameliorated the oxidative stress, liver damage, and the downregulated GLP-1 in IR/D rats. (A–C) The antioxidant enzymes and oxidative stress markers including GSH (A), SOD (B), and MDA (C) in the liver tissues of IR/D rats pretreated with PCA or not were examined by ELISA. (D–F) TNF-α, IL-1β and IL-6 in the sera of IR/D rats pretreated with PCA or not were examined by ELISA. (G) The histopathological changes in liver tissues of IR/D rats pretreated with PCA or not were also examined using hematoxylin-eosin staining. (H) Steatosis scores of the liver in different groups. (I) The GLP-1 positive cells in terminal ileum of IR/D rats pretreated with PCA or not were detected by immunohistochemistry. (***p < 0.001 vs. Control; ++p < 0.01, +++p < 0.001 vs. Vector; ∧p < 0.05, ∧∧p < 0.01 or ∧∧∧p < 0.001 vs. 15 mg/kg). (ELISA: Enzyme-linked Immunosorbent Assay, PCA: Protocatechuic Acid, IR/D: insulin resistance type 2 diabetic, GSH: glutathione, SOD: superoxide dismutase, MDA: malondialdehyde, GLP-1: glucagon‐like peptide-1, TNF-α: tumor necrosis factor α).
Supplier Page from Abcam for Anti-GLP1 antibody [EPR4042-407]