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논문분류	춘계학술대회 초록집
제목	GLP-1 receptor activation by DPP-4 inhibitor in chronic kidney disease rat with myocardial infarction
저자	*Soon kil KWON, Seung JUNG, Do HEE, Sun MON, Hye-young KIM, Soon kil KWON
출판정보	2017; 2017(1):
키워드	Chronic kidney disease, myocardial infarction, GLP-1 receptor, linagliptin
초록	Objectives : Chronic kidney disease (CKD) is closely related to cardiovascular disease, which has a highly associated with mortality. GLP-1 is an incretin hormone, and renal GLP-1 activity is increased in the chronic kidney disease, also GLP-1 receptor (GLP-1R) activation is related with renal and cardiovascular protection. It is not clear that GLP-1R change in CKD and CKD with myocardial ischemia/reperfusion (MI/R). We investigated difference of renal GLP-1 activity in the CKD rat model with MI/R. Methods : Male Sprague Dawley rat was used and 5/6 nephrectomy was used for CKD. For myocardial ischemia, LAD was ligated 1 weeks after 5/6 nephrectomy. 30 Minutes after ligation, vessel was released for reperfusion. Linagliptin-treated groups were treated for 8 weeks after surgery. Renal cortical and myocardium GLP-1R activity was measured via immunohistochemistry and WB. Phosphrylation of Akt, ERK 1/2 and Bcl-2 activity was mesured via WB. Results : Western blot density of GLP-1R in the renal cortex extract showed increased level 2 weeks after 5/6 nephrectomy, then decreased 8 weeks after surgery comparing with control. Linagliptin increased the ranal expression of GLP-1R. In chronic kidney disease and chronic kidney disease rat with myocardial ischemia/reperfusion injury decreased the renal and cardiac expression of GLP-1R. The 5/6 nephrectomy with myocardial ischemia reperfusion injury lead to dephosporylation Akt, ERK1/2 and decreased expression of Bcl-2, whereas linagliptin treatment reversd these changes, resulting in phosporylation Akt, ERK1/2 and increased expression of Bcl-2. Conclusions : In chronic kidney disease and chronic kidney disease rat with myocardial ischemia/reperfusion injury, linagliptin attenuated renal dysfunction and increased GLP-1R activity. Altogether, these results suggest that expression of GLP-1 in kidney has a role in the chronic kidney disease with myocardial infarction and GLP-1 activity may provide cario and renoprotective effects independent of its hypoglycemic effects.
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