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Effect of verapamil and lidocaine on TRPM and NaV1 9 gene expressions in renal ischemia-reperfusion #MMPMID24507022
Dusmez D; Cengiz B; Yumrutas O; Demir T; Oztuzcu S; Demiryurek S; Tutar E; Bayraktar R; Bulut A; Simsek H; Dagli SN; Kilic T; Bagci C
Transplant Proc 2014[Jan]; 46 (1): 33-9 PMID24507022show ga
BACKGROUND: To determine effects on calcium and sodium channels of Ca(2+) and Na(+) channel blockers in the present study, expression levels of TRPM1, TRPM2, TRPM3, TRPM4, TRPM5, TRPM6, TRPM7, TRPM8, and NaV1.9 genes were evaluated in kidney tissues after induced ischemia-reperfusion. MATERIAL AND METHODS: Forty albino Wistar male rats were equally divided into 4 groups as follows: group I: control group (n = 10), group II: ischemia group (60 minutes of ischemia + 48 hours of reperfusion; n = 10), group III: ischemia (60 minutes of ischemia + 48 hours of reperfusion) + calcium channel blocker (n = 8), group IV: ischemia (60 minutes of ischemia + 48 hours of reperfusion) + sodium channel blocker (n = 8). RESULTS: When compared to ischemia group expression levels of TRPM2, TRPM4, TRPM6, and NaV1.9 in Ca(2+) and Na(+) channel blocker groups were increased, whereas that of TRPM7 was decreased. However, expression levels of TRPM1, TRPM3, TRPM5, and TRPM8 were not determined in kidney tissue. Histologically, the Ca(2+) channel blocker verapamil and the Na(+) channel blocker lidocaine inhibited the cell death in kidney tissue compared to control. CONCLUSION: Our study suggested that verapamil and lidocaine significantly reduce the degree of ischemia-reperfusion injury due to effects to TRPM and Nav1.9 genes.