13 - PROTECTIVE EFFECT of CYMBOPOGON CITRATUS ESSENTIAL OIL on KIDNEY CELL INJURY Induced by ISCHEMIA and REPERFUSION: IN VITRO STUDY

Poster Board Number: 13
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Abstract Body : Kidney injury by ischemia and reperfusion (I/R) is one of the main causes of acute kidney injury (AKI) with progression related to oxidative damage, inflammation and cell death, mainly tubular cells. Different signaling pathways are involved in this process, such as the Ras/Raf1/ERK and Nrf2-Keap1 transcription pathways. Several antioxidant strategies have been studied in order to prevent or minimize the damage caused by I/R. The essential oil of Cymbopogon citratus has citral as its major component, formed by geometric isomers: trans-geranial and cis-neral. These are described as having anti-inflammatory and antioxidant activity and the potential to modulate the aforementioned transcription pathways. The aim of this study was to evaluate the cytoprotective effect of Cymbopogon citratus essential oil on proximal tubular cells of the LCC-MK2 lineage in an in vitro I/R model. The cells were exposed to a medium deprived of glucose, pyruvate and fetal bovine serum and submitted to 24 hours of hypoxia, using an anaerobic chamber. Then, reoxygenation and supplementation of the culture medium were performed, followed by treatment with the essential oil for another 24 hours. Cell viability was assessed by the 3-(4,5-Dimethylthiazol-2-yl)-2,5-Diphenyltetrazolium (MTT) reduction assay. To evaluate the mechanism of cell death, intracellular ROS production and changes in the mitochondrial transmembrane potential, flow cytometry techniques were used. A marker of renal injury from proximal tubular cells, kidney injury molecule-1 (KIM-1), was determined from cell supernatant. Ultrastructural changes were analyzed by scanning electron microscopy (SEM). The results showed a cytoprotective effect of Cymbopogon citratus essential oil by increasing cell viability, reducing intracellular ROS and reestablishing the mitochondrial transmembrane potential after ischemia and reoxygenation. Treatment at a concentration of 125 μg/ml decreased KIM-1 release and attenuated the ultrastructural damage caused by I/R.