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. 2020 Jan 18;9(1):263. doi: 10.3390/jcm9010263

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© 2020 by the authors.

Licensee MDPI, Basel, Switzerland. This article is an open access article distributed under the terms and conditions of the Creative Commons Attribution (CC BY) license (http://creativecommons.org/licenses/by/4.0/).

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Effect of altering calcium on caerulein-induced (A–D), and changing Cai on LA-induced (E–H) acinar cell injury. (A) Extracellular calcium (1, 2 mM) had no effect on intracellular calcium peak and plateau levels induced by 100 nM caerulein and (B) did not modulate the lack of mitochondrial depolarization with caerulein treatment. (C) Extracellular calcium did not reduce caerulein-induced acinar cell injury, while (D) intracellular calcium chelation with BAPTA-AM (50 μM) or ryanodine receptor antagonization with dantrolene (100 μM) caused caerulein-induced injury to be nonsignificant versus control. (E) BAPTA-AM (50 μM), (F) Dantrolene (100 μM), and (G) thapsigargin (1 μM) all reduced intracellular calcium elevation after 100 μM LA treatment, while BAPTA-AM (E’) partially limiting mitochondrial depolarization Dantrolene (F’) and thapsigargin (G’) had no effect on mitochondrial depolarization. (H): Despite effects on calcium elevation, BAPTA-AM, Dantrolene, and Thapsigargin did not significantly affect LA-induced injury in acinar cells, as measured by LDH release.