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Endogenous glucocorticoids decrease the acinar cell sensitivity to apoptosis during cerulein pancreatitis in rats

K Kimura¹, T Shimosegawa, H Sasano

¹Third Department of Internal Medicine, Tohoku University School of Medicine, Sendai, Miyagi, Japan.

Gastroenterology

|February 7, 1998

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Endogenous glucocorticoids protect pancreatic acinar cells from cell death during acute pancreatitis. Blocking glucocorticoid receptors increases apoptosis, highlighting their crucial role in cell survival.

Area of Science:

Endocrinology
Gastroenterology
Cell Biology

Background:

The hypothalamus-pituitary-adrenal axis activation may mitigate acute pancreatitis.
The precise mechanism involving endogenous glucocorticoids in pancreatic acinar cell death requires clarification.

Purpose of the Study:

To investigate the role of endogenous glucocorticoids in pancreatic acinar cell death during acute pancreatitis.

Main Methods:

Studied apoptosis in adrenalectomized rats with or without cerulein-induced pancreatitis.
Examined the effects of a glucocorticoid-receptor antagonist (RU38486) on cultured acinar cells (AR42J).
Utilized terminal deoxynucleotidyl transferase-mediated deoxyuridine triphosphate-biotin nick-end labeling (TUNEL) and electron microscopy.

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Main Results:

Adrenalectomy increased acinar cell apoptosis, which was reversed by glucocorticoid replacement.
Cerulein-induced pancreatitis exacerbated apoptosis in adrenalectomized rats.
RU38486 induced dose-dependent apoptosis in cultured acinar cells.

Conclusions:

Endogenous glucocorticoids are vital for pancreatic acinar cell survival.
Glucocorticoids protect acinar cells by reducing their susceptibility to cell death induction in acute pancreatitis.