Journal
MOLECULAR BIOLOGY REPORTS
Volume 48, Issue 2, Pages 1735-1743Publisher
SPRINGER
DOI: 10.1007/s11033-021-06214-2
Keywords
Curcuminoid nanoparticle; Renal ischemia; reperfusion; Oxidative stress; Caspase-3; MAPKs; Rat
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Funding
- Shiraz University of Medical Sciences, Shiraz, Iran [98-01-57-22109]
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The study demonstrated that nanomicellar curcuminoids pretreatment significantly improved renal function and histopathological damages, reduced renal oxidative stress and suppressed apoptosis and MAPKs pathways induced by renal ischemia/reperfusion injury.
Renal ischemia/reperfusion (I/R) injury is considered as a main problem in clinical practice. Curcuminoids, the active constituents of turmeric, seem to have potential renoprotective effects. However, the poor bioavailability of curcuminoids restricts their therapeutic effects. In the present study, the effect of nanomicellar curcuminoids (NC) treatment on renal function, histology, total antioxidant capacity (TAC), total oxidative stress (TOS), caspase-3 level as well as mitogen activated protein kinases (MAPKs: JNK, p38 and ERK) phosphorylation were evaluated following renal I/R. Adult male Sprague-Dawley rats were administered NC at the dose of 25 mg/kg 1 h before renal ischemia induction. The animals were subjected to bilateral renal ischemia for 60 min and reperfusion for 24 h. Subsequently, blood urea nitrogen (BUN), creatinine (Cr), renal histopathology, TAC, TOS, and oxidative stress index, cleaved caspase-3 level, Bax and MAPKs signaling were evaluated. The results indicated that NC pretreatment at the dose of 25 mg/kg significantly improved renal function as well as histolopatholgical damages. Moreover, NC reduced the level of renal oxidative stress, cleaved caspase-3 and Bax (as the proapoptotic proteins) and suppressed the activated Jun N-terminal Kinase (JNK), p38 and extracellular receptor kinase (ERK) signaling induced by renal I/R. The findings of the current study indicate that NC might prevent the injury induced by renal I/R through suppression of oxidative stress, apoptosis and MAPKs pathways.
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