Antithrombin III Attenuates AKI Following Acute Severe Pancreatitis. Shock 2018 May;49(5):572-579
Date
07/19/2017Pubmed ID
28719489DOI
10.1097/SHK.0000000000000946Scopus ID
2-s2.0-85024501640 (requires institutional sign-in at Scopus site) 22 CitationsAbstract
BACKGROUND: Antithrombin III (ATIII), the predominant coagulation factor inhibitor, possesses anti-inflammatory properties and exerts renoprotective effects on renal ischemia-reperfusion injury in animal models. However, the ATIII's protective effects of ATIII on acute kidney injury (AKI) following severe acute pancreatitis (SAP) need to be confirmed.
METHODS: We assessed the association between ATIII activities and the incidence of AKI in patients with SAP, and explored therapeutic effects and potential mechanisms of ATIII on kidney injury in sodium taurocholate induced SAP rat model. Rats were intravenously injected with ATIII (500 μg/kg) before or after the induction of SAP.
RESULTS: The results demonstrated ATIII did not attenuate pancreatic injury, but significantly ameliorate renal dysfunction and renal histological injury. ATIII administration alleviated renal inflammation response, oxidative stress, and cell apoptosis. Moreover, ATIII attenuated tumor necrosis factor α (TNFα)-stimulated intercellular cell adhesion molecule 1(ICAM-1) and monocyte chemotactic protein 1 (MCP-1) upregulation in cultured renal tubular epithelial cells.
CONCLUSION: ATIII appears to ameliorate SAP-induced kidney injury by inhibiting inflammation, oxidative stress, and apoptosis. ATIII supplementation may have a potential prophylactic and therapeutic effect on SAP induced AKI.
Author List
Kong Y, Yin J, Cheng D, Lu Z, Wang N, Wang F, Liang MMESH terms used to index this publication - Major topics in bold
Acute DiseaseAcute Kidney Injury
Animals
Antithrombin III
Apoptosis
Cell Line
Chemokine CCL2
Humans
Incidence
Intercellular Adhesion Molecule-1
Male
Malondialdehyde
Pancreatitis
Rats
Rats, Sprague-Dawley
Real-Time Polymerase Chain Reaction
Superoxide Dismutase
