Table 1.
Experimental studies evaluating the impact of different preservation solutions in the preservation of steatotic livers.
| Author, Year | Intervention | Experimental Model | Findings |
|---|---|---|---|
| Ben Mosbah et al., 2006 [64] | IGL-1 (vs. UW) |
24 h SCS followed by 2 h normothermic reperfusion in Zucker rat livers | Lower perfusate transaminase, MDA, and GLDH levels; improved bile production; lower vascular resistance. Inhibition of NO production suppressed IGL-1 effects. |
| Ben Mosbah et al., 2007 [78] | UW (+trimetazidine +aminoimidazole-4-carboxamide ribonucleoside) | 24 h SCS followed by 2 h normothermic reperfusion in Zucker rat livers | Lower perfusate transaminase, MDA, and GLDH levels; improved bile production; lower vascular resistance. Increased AMPK activation. Inhibition of AMPK suppressed the protective effects. |
| Ben Mosbah et al., 2010 [79] | UW (+carvedilol) |
24 h SCS followed by 2 h normothermic reperfusion in Zucker rat livers | Lower perfusate transaminase, MDA, and GLDH levels; improved bile production; lower vascular resistance; increased ATP. Increased AMPK activation. |
| Zaouali et al., 2010 [67] | IGL-1 (+trimetazidine) |
24 h SCS followed by 2 h normothermic reperfusion in Zucker rat livers | Lower perfusate transaminase, MDA, and GLDH levels; improved bile production; lower vascular resistance. Increased levels of HIF-1α and downstream genes. Better results and HIF-1α induction after addition of trimetazidine. Inhibition of NO production suppressed the protective effects. |
| Zaouali et al., 2010 [66] | IGL-1 (+IGF-1) |
24 h SCS followed by 2 h normothermic reperfusion in Zucker rat livers | Compared to IGL-1 alone: increased NO production, lower perfusate transaminase, MDA, and GLDH levels; improved bile production; lower vascular resistance, reduced oxidative stress. |
| Zaouali et al., 2010 [65] | IGL-1 (+EGF) |
24 h SCS followed by 2 h normothermic reperfusion in Zucker rat livers | Compared to IGL-1 alone: increased NO production, lower perfusate transaminase, MDA, and GLDH levels; improved bile production; lower vascular resistance, reduced oxidative stress; increased ATP. |
| Eipel et al., 2012 [82] | HTK (+erythropoietin) |
24 h SCS followed by 2 h normothermic reperfusion in ob/ob mice livers | Compared to HTK alone: lower perfusate AST; improved endothelial integrity; higher oxygen consumption. |
| Bejaoui et al., 2014 [70] | IGL-1 (+bortezomib) |
24 h SCS followed by 2 h normothermic reperfusion in Zucker rat livers | Compared to IGL-1 alone: activation of AMPK signaling, lower perfusate transaminase; improved bile production; lower vascular resistance, apoptosis inhibition. Inhibition of AMPK expression reduced IGL-1 protective effects. |
| Zaouali et al., 2013 [80] | UW (+bortezomib) |
24 h SCS followed by 2 h normothermic reperfusion in Zucker rat livers | Lower perfusate transaminase, MDA, and GLDH levels; improved bile production; lower vascular resistance. Increased AMPK activation. |
| Bejaoui et al., 2015 [71] | IGL-1 (+carbonic anhydrase II) |
24 h SCS followed by 2 h normothermic reperfusion in Zucker rat livers | Compared to IGL-1 alone: activation of AMPK signaling, lower perfusate transaminase; improved bile production; increased ATP; downregulation of MAPK and UPR pathway; apoptosis inhibition. |
| Bejaoui et al., 2015 [62] | PEG preconditioning | 24 h SCS followed by 2 h normothermic reperfusion in Zucker rat livers | Lower perfusate transaminase, and GLDH levels; lower vascular resistance. Increased AMPK activation. |
| Tabka et al., 2015 [69] | IGL-1 (vs. Celsior) |
24 h SCS followed by 2 h normothermic reperfusion in Sprague-Dawley rats rat livers | Increased NO production, lower perfusate transaminase, MDA, and GLDH levels; improved bile production; lower vascular resistance, reduced oxidative stress, downregulation of MAPK pathway. |
| Zaouali et al., 2017 [68] | IGL-1 (+trimetazidine) |
24 h SCS followed by 2 h normothermic reperfusion in Zucker rat livers | Compared to IGL-1 alone: lower perfusate transaminase and GLDH levels; increased levels of sirtuin 1 and reduced levels of HMGB1 and TNFα. |
| Zaouali et al., 2017 [75] |
IGL-1 (vs. UW) |
24 h SCS followed by 2 h normothermic reperfusion in Zucker rat livers | Lower perfusate transaminase and GLDH levels; increased ATP; reduced levels of HMGB1 and TNFα. Proteasome inhibition. |
| Panisello-Roselló et al., 2017 [56] | IGL-1 (vs. HTK) |
24 h SCS of Zucker rat livers | Lower perfusate transaminase and GLDH levels; increased ATP; reduced levels of HMGB1 and TNFα. Proteasome inhibition. Increased AMPK activation. |
| Panisello-Roselló et al., 2018 [76] | IGL-1 (vs. HTK vs. UW) |
24 h SCS of Zucker rat livers | Lower perfusate transaminase levels; increased ATP; reduced apoptosis. ALDH2 upregulation. |
| Panisello-Roselló et al., 2018 [74] | IGL-1 (vs. HTK) |
24 h SCS of Zucker rat livers | Lower perfusate transaminase and GLDH levels; reduced membrane mitochondrial depolarization; reduced apoptosis; reduced levels of HMGB1; increased autophagy. |
| Lopez et al., 2018 [86] | IGL-1 (vs. HTK vs. IGL-0 *) |
24 h SCS of Zucker rat livers | Lower perfusate transaminase levels, preserved glycocalyx integrity. |
| Bardallo et al., 2021 [83] | IGL-2 (vs. IGL-1, vs. IGL-0 *) |
24 h SCS of Zucker rat livers | Lower perfusate transaminase and GLDH levels; increased ATP; increased autophagy; ALDH2 upregulation. |
| Bardallo et al., 2022 [85] | IGL-2 (vs. IGL-1, vs. IGL-0 *) |
24 h SCS of Zucker rat livers | Increased ATP; reduced succinate accumulation; increased complex I and complex II levels: increased HO-1; increase glutathione levels; reduced oxidative stress. |
| Asong-Fontem et al., 2022 [84] | IGL-2 (vs. UW) |
24 h SCS +/− 2 h HOPE followed by 2 h normothermic reperfusion in Zucker rat livers | Lower perfusate AST; preserved glycocalyx integrity; reduced levels of HMGB1; increased weight loss (surrogate of edema formation). |
* IGL-0 was IGL-1 solution without polyethilen glycol. Abbreviations: ALDH2, aldehyde dehydrogenase 2; AMPK, adenosine monophosphate-activated protein kinase; EGF, epidermal growth factor; GLDH, glutamate dehydrogenase; HIF-1α, hypoxia-inducible factor 1-alpha; HMGB1, high mobility group box 1; HO-1, heme oxygenase 1; HOPE, hypothermic oxygenated perfusion; MAPK, mitogen-activated protein kinase; MDA, malondialdehyde; NO, nitric oxide; SCS, static cold storage; TNFα, tumor necrosis factor alpha; UPR, unfolded protein response.