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Am J Physiol Gastrointest Liver Physiol 291: G95-G101, 2006. First published April 6, 2006; doi:10.1152/ajpgi.00520.2005
0193-1857/06 $8.00
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HORMONES AND SIGNALING

Crambene induces pancreatic acinar cell apoptosis via the activation of mitochondrial pathway

Yang Cao,1,* Sharmila Adhikari,1,* Abel Damien Ang,1 Marie Véronique Clément,2 Matthew Wallig,3 and Madhav Bhatia1

Department of 1Pharmacology and 2Biochemistry, National University of Singapore, Singapore; and 3Department of Pathobiology, University of Illinois at Urbana Champaign, Urbana, Illinois

Submitted 7 November 2005 ; accepted in final form 16 March 2006

We investigated the apoptotic pathway activated by crambene (1-cyano-2-hydroxy-3-butene), a plant nitrile, on pancreatic acinar cells. As evidenced by annexin V-FITC staining, crambene treatment for 3 h induced the apoptosis but not necrosis of pancreatic acini. Caspase-3, -8, and -9 activities in acini treated with crambene were significantly higher than in untreated acini. Treatment with caspase-3, -8, and -9 inhibitors inhibited annexin V staining, as well as caspase-3 activity, pointing to an important role of these caspases in crambene-induced acinar cell apoptosis. The mitochondrial membrane potential was collapsed, and cytochrome c was released from the mitochondria in crambene-treated acini. Neither TNF-{alpha} nor Fas ligand levels were changed in pancreatic acinar cells after crambene treatment. These results provide evidence for the induction of pancreatic acinar cell apoptosis in vitro by crambene and suggest the involvement of mitochondrial pathway in pancreatic acinar cell apoptosis.

caspases; cytochrome c; membrane potential


Address for reprint requests and other correspondence: M. Bhatia, Dept. of Pharmacology, National Univ. of Singapore, Yong Loo Lin School of Medicine, Bldg. MD2, 18 Medical Drive, Singapore 117597 (e-mail: mbhatia{at}nus.edu.sg)






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