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Fig. 5 | Cardiovascular Diabetology

Fig. 5

From: Empagliflozin suppressed cardiac fibrogenesis through sodium-hydrogen exchanger inhibition and modulation of the calcium homeostasis

Fig. 5

Intracellular Ca2+ signaling in empagliflozin or cariporide-treated atrial fibroblasts. Representative intracellular Ca2+ tracing from cariporide alone (10 μmol/L, left upper panels), and cariporide (10 μmol/L) mixed with empagliflozin (1 μmol/L, right upper panels). Where indicated, thapsigargin was added to the calcium-free buffer to induce ER Ca2+ depletion. After the intracellular Ca2+ surge induced by thapsigargin (ER calcium) was returned to the steady state, the extracellular Ca2+ concentration was then increased to 2 mmol/L to measure Ca2+ entry. F340/F380 was expressed as the relative intracellular Ca2+. The left lower panel displays the change (∆ F340/F380) of Ca2+ measured by area under curve of Ca2+ tracing (AUC, statistic test by unpaired t-test), the change from baseline to peak calcium amplitude (statistic test by statistic test by unpaired t-test), and the decay time of Ca2+ entry (T50, calculated from the peak to the 50% of the decay or the end of the calcium image recording, statistic test by unpaired t-test) in cariporide alone (n = 5) and cariporide mixed with empagliflozin-treated atrial fibroblasts (n = 5)

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