Abstract
Background and purpose: Ischemia–reperfusion injury is encountered in numerous processes such as cardiovascular diseases or kidney transplantation; however, the latter involves cold ischemia, different from the warm ischemia found in vascular surgery by arterial clamping. The nature and the intensity of the processes induced by ischemia types are different, hence the therapeutic strategy should be adapted. Herein, we investigated the protective role of tannic acid, a natural polyphenol in a rat model reproducing both renal warm ischemia and kidney allotransplantation. The follow-up was done after 1 week. Experimental approach: To characterize the effect of tannic acid, an in vitro model of endothelial cells subjected to hypoxia–reoxygenation was used. Key results: Tannic acid statistically improved recovery after warm ischemia but not after cold ischemia. In kidneys biopsies, 3 h after warm ischemia–reperfusion, oxidative stress development was limited by tannic acid and the production of reactive oxygen species was inhibited, potentially through Nuclear Factor erythroid-2-Related factor 2 (NRF2) activation. In vitro, tannic acid and its derivatives limited cytotoxicity and the generation of reactive oxygen species. Molecular dynamics simulations showed that tannic acid efficiently interacts with biological membranes, allowing efficient lipid oxidation inhibition. Tannic acid also promoted endothelial cell migration and proliferation during hypoxia. Conclusions: Tannic acid was able to improve renal recovery after renal warm ischemia with an antioxidant effect putatively extended by the production of its derivatives in the body and promoted cell regeneration during hypoxia. This suggests that the mechanisms induced by warm and cold ischemia are different and require specific therapeutic strategies.
Highlights
Ischemia is the cessation of blood flow to an organ and reperfusion is its restoration.The combination of both processes induces a range of lesions at the cellular and organ level, leading to increased cell death and immunogenicity, assembled under the term Ischemia–Reperfusion Injury (IRI)
Interleukin 6 (IL-6), Interleukin 10 (IL-10) and tumor necrosis factor alpha (TNFa) levels were determined in blood with Enzyme-Linked ImmunoSorbent Assay (ELISA) kit assays (Quantikine, RD Sytem, Minneapolis, United States) following the manufacturer’s instructions
To mimic the ischemia–reperfusion found in vivo, we used a standard protocol of hypoxia–reoxygenation in human aortic endothelial cells (HAEC, Gibco, Courtaboeuf, France), cultured as recommended by the manufacturer [12]
Summary
Ischemia is the cessation of blood flow to an organ and reperfusion is its restoration. The combination of both processes induces a range of lesions at the cellular and organ level, leading to increased cell death and immunogenicity, assembled under the term Ischemia–Reperfusion Injury (IRI). AOnxtisdyastitveems.tress is an imbalance between reactive oxygen species (ROS) production and eliTmaninnaitcioancibdyisanatipolxaindta-dntersiyvsetedmpso.lyphenol from the family of hydrolysable tannins It is composed of a penTtaa-nOn-igcalalcoiydl-biseta-Dp-lganlut-cdoesreiv(PedGGp)onlyupchleeunsolanfrdosmevtehreal fgaamllilcyacoifd hmyodireotileyss.abItlehatsanshnoinws.n Isteviseral benceofimcpiaolsedffeocftas,pseunctha-aOs-greadllouycli-nbgetas-eDru-gmlucohsoele(PstGeGro)lnauncdletursigalnydcesreivdeerallevgaellsi,caasciwd emlloaiestiaens.tiIot xhiadsant actisvhiotwiens [s3e–v5e]r.al Tbheneemficuialtliepflfeecptsh, esnuochl garsoruedpuscaint gitsserpuemripchheorleystceoronltrainbdutterigtolycthereidsetalbevileizlsa,taios nweolfl its oxiadsizaendti(orxaiddiacnatl) afoctrimvisti,evsia[3e–l5e]c.trTohneic mdeulloticpalleizpathieonnoilngtrhoeuπp-scoant juitgsapteedripsyhsetreymc.oTnhtriisbmutaekteos ttahnenic acidstaabnidliziatstidoneroivf aittsivoexsideiffizecdie(nratdRicOaSl) sfcoarmvesn, gveiarse,leincttruonrnicrdeedluoccainligzaItRioIn[4in,6]th(eFiπg-ucroen1ju)g. This makes tannic acid and its derivatives efficient ROS scavengers, in turn reducing IRI [4,6] (Figure 1). Determination of Blood Tannic Acid and Derivatives Levels after Intraperitoneal Administration.
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