Post-treatment with JP-1302 protects against renal ischemia/reperfusion-induced acute kidney injury in rats

• Published in: Journal of pharmacological sciences 2019-03, Vol.139 (3), p.137-142
• Main Authors: Shimokawa, Takaomi, Tsutsui, Hidenobu, Miura, Takeshi, Takama, Masashi, Hayashi, Kohei, Nishinaka, Toru, Terada, Tomoyuki, Yoneda, Kozo, Yamagata, Masayo, Yukimura, Tokihito
• Format: Article
• Language: English
• Subjects: Acute kidney injury; Ischemia/reperfusion; JP-1302; Norepinephrine; α2C-adrenoceptor
• ISSN: 1347-8613; 1347-8648
• DOI: 10.1016/j.jphs.2018.12.008

Ischemia/reperfusion injury is the most common cause of acute kidney injury. We previously revealed that pre-treatment with yohimbine or JP-1302 attenuated renal ischemia/reperfusion injury by inhibition of α2C-adrenoceptor antagonist. The aim of the present study is to investigate the effects of post-treatment with JP-1302 on renal ischemia/reperfusion injury in rats. Male Sprague Dawley rats were randomly divided into four groups: sham operation, ischemia/reperfusion, pre-treatment with JP-1302 (3.0 mg/kg) and post-treatment with JP-1302 groups. In ischemia/reperfusion injury, renal functional parameters, such as blood urea nitrogen, plasma creatinine and creatinine clearance, deteriorated after reperfusion. Renal venous norepinephrine concentrations, as well as inflammatory molecules in the kidney increased after reperfusion. Both pre- and post-treatment with JP-1302 improved renal dysfunction, tissue damage, renal venous norepinephrine concentrations and inflammatory molecules expression in the kidney. In conclusion, these results suggest that post-treatment with JP-1302 protects on ischemia/reperfusion-induced acute kidney injury by suppressing cytokine upregulation via α2C-adrenoceptors.