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The protective effect of acute pantoprazole pretreatment on renal ischemia/reperfusion injury in rats
Author(s) -
Kohansal Parichehr,
Rajai Nazanin,
Dehpour Ahmad Reza,
Rashidian Amir,
Shafaroodi Hamed
Publication year - 2019
Publication title -
fundamental and clinical pharmacology
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 0.655
H-Index - 73
eISSN - 1472-8206
pISSN - 0767-3981
DOI - 10.1111/fcp.12451
Subject(s) - pantoprazole , creatinine , malondialdehyde , oxidative stress , medicine , renal function , renal ischemia , ischemia , blood urea nitrogen , kidney , endocrinology , pharmacology , reperfusion injury , inflammation , omeprazole
Renal ischemia/reperfusion injury ( IRI ), which occurs in many pathological conditions, is associated with high rate of morbidity and mortality. Activation of inflammatory responses and oxidative stress contribute to induce organ damage following IRI . Pantoprazole, a proton pump inhibitor, which is mostly prescribed for gastroesophageal reflux disease ( GERD ) has been shown to exert anti‐inflammation effects. In order to evaluate the effects of pantoprazole on renal ischemia/reperfusion injury, four different doses of pantoprazole (4.5, 9, 18, and 36 mg/kg) were administered 30 min before the induction of IRI in male Wistar rats. Serum concentration of creatinine and blood urea nitrogen (BUN) were measured to assess renal function. Histopathological changes, malondialdehyde (MDA) level and toll‐like receptor 4 ( TLR ‐4) expression in renal tissue were determined and compared to control group. The results revealed that pretreatment with 18 and 36 mg/kg of pantoprazole leads to the significant decline in serum creatinine and BUN levels and the severity of necrosis grade in comparison with control group ( P < 0.05). Pantoprazole also reduced the MDA level and TLR ‐4 expression in renal tissue. In summary, pantoprazole attenuates renal injury following ischemia/reperfusion. This effect is mediated partially through inhibition of oxidative stress and TLR ‐4 signaling pathway.