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. Sep-Oct 2012;12(5):451-7.
doi: 10.1016/j.pan.2012.07.017. Epub 2012 Aug 9.

Severe Acute Pancreatitis Is Associated With Upregulation of the ACE2-angiotensin-(1-7)-Mas Axis and Promotes Increased Circulating angiotensin-(1-7)

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Severe Acute Pancreatitis Is Associated With Upregulation of the ACE2-angiotensin-(1-7)-Mas Axis and Promotes Increased Circulating angiotensin-(1-7)

Yan Wang et al. Pancreatology. .

Abstract

Background/objectives: Angiotensin-converting enzyme 2 (ACE2), its product angiotensin-(1-7) and its receptor Mas may counteract the adverse effects of the ACE-angiotensin receptor II-AT(1) axis in many diseases. We examined the expression of these novel components of the rennin-angiotensin system in an experimental mouse model of severe acute pancreatitis (SAP).

Methods: SAP was induced by six intraperitoneal injections of caerulein, and mice were sacrificed at 2, 12, 24, 48 and 72 h post disease-induction (normal control group mice were sacrificed at 2 h post disease-induction). Tissue and blood were collected for biochemical detection, gene and protein expression by qRT-PCR and western blot analysis, enzyme-linked immunosorbent assay and immunohistology detection.

Results: Pancreatic ACE2 gene and protein expression, plasma and pancreatic angiotensin-(1-7) levels and Mas receptor gene and protein expression were significantly increased (p < 0.05) following SAP induction compared with the normal control group.

Conclusions: Severe acute pancreatitis is associated with upregulation of the ACE2-angiotensin-(1-7)-Mas axis and promotes increased circulating angiotensin-(1-7). These results support the presence of an ACE2-angiotensin-(1-7)-Mas axis in pancreatitis.

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