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| Author, year of publication | Hormone | Species | Preservation solution modification/cold ischemia/key settings of the experiment | Outcome measures, n (intervention, I/control, C) | Hormone dose | Drugs/substances used simultaneously/dose | Effects of hormone |
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| Zaouali et al., 2011 [1] | Melatonin | Rat | IGL-1/24 h, 4°C/normothermic reperfusion: 2 h, 37°C | I: IGL + MEL; n = 16
C1: Ringer’s lactate; n = 16
C2: IGL-1; n = 16
C3: UW; n = 16 | 100 μmol/L | — | (i) Lower transaminase levels (AST/ALT)
(ii) Higher bile production
(iii) Higher BSP clearance
(iv) Reduced vascular resistance
(v) Increased nitrites/nitrates
(vi) Prevention of oxidative stress |
| Zaouali et al., 2013 [2] | Rat | IGL-1/24 h, 4°C/normothermic reperfusion: 2 h, 37°C | I: IGL + MEL + TMZ;
C1: Ringer’s lactate;
C2: IGL-1;
C3: UW;
C4: IGL + MEL + TMZ + araA | 100 μmol/L | TMZ
10−3 μm/L | (i) Decreased GRP78, pPERK, and CHOP activation after reperfusion
(ii) Inhibition of AMPK induced an increase in ER stress
(iii) Significant reduction in autophagy |
| Gunal et al., 2010 [3] | Rat | UW/48 h, 4°C | I: UW + MEL; n = 10
C: UW; n = 10 | 30 mg/L | — | (i) Lower transaminase levels (LDH, AST, and ACP)
(ii) Induced heat-shock protein (HSP 70)
(iii) Decreased lipid peroxidation
(iv) Prevented Kupffer cell activation and inflammation |
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| Ryszka et al., 2004 [4] | Prolactin | Rabbit | Ringer/24 h, 4–6°C | I: Ringer + PRL; n = 5
C: Ringer; n = 5 | 100 IU/L | — | (i) Lower transaminase levels (AST and ALT)
(ii) Slowing the rate of transaminase release |
| Dolińska et al., 2011 [5] | Pig | HTK/24 h, 4–6°C | I: HTK + PRL; n = 5
C: HTK; n = 5 | 100 IU/L | — | (i) Lower transaminase levels (AST and ALT)
(ii) Slowing the rate of transaminase release |
| Ryszka et al., 2011 [6] | Pig | HTK/24 h, 4–6°C/cold reperfusion | I: HTK + PRL; n = 6
C: HTK; n = 6 | 3 IU/L | Cys
0.3 mmol/L | (i) Lower levels of AST, ALT, LDH, and lactic acid
(ii) Less release of K+, Mg2+
(iii) Greater release of Na+, Ca2+ |
| Szulc-Musioł et al., 2018 [7] | Rabbit | HTK/in situ | I: HTK + PRL; n = 10
C: HTK; n = 10 | 2.5 μg/g liver | — | (i) Inhibition of liver cell cytolysis |
| Budziński et al., 2011 [8] | Pig | HTK/12 h, 4°C | I: HTK + PRL; n = 6
C: Ringer; n = 6
C: UW; n = 6
C: HTK; n = 6 | 20 IU/L | — | (i) High apoptosis level |
| Budziński et al., 2011 [9] | | Pig | HTK
/12 h, 4°C | I: HTK + PRL; n = 6
C: Ringer; n = 6
C: UW; n = 6
C: HTK; n = 6 | 20 IU/L | — | (i) Significantly decreased dopamine and adrenaline concentrations |
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| Koetting et al., 2010 [10] | Dopamine | Rat | HTK
/18 h, 4°C/normothermic reperfusion: 2 h, 37°C | I: HTK + DA; n = 6
C: HTK; n = 6 | 10 μmol/L
50 μmol/L 100 μmol/L | — | (i) Reduction in ALT, LDH, GLDH release
(ii) Reduced histologic signs of tissue injury
(iii) Doubled bile production and tissue ATP |
| Minor et al., 2011 [11] | Rat | HTK
/20 h, 4°C/HMP, normothermic reperfusion: 2 h, 37°C | I: HTK + DA; n = 6 C: HTK; n = 6 | 10 μmol/L 50 μmol/L 100 μmol/L | — | (i) Reduction in ALT release
(ii) Enhanced bile flow
(iii) Reduced lipid peroxidation |
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| Eipel et al., 2012 [12] | Erythropoietin | Mouse | HTK
/24 h, 4°C/normothermic reperfusion: 2 h | I: HTK + EPO; n = 6
C: HTK; n = 6
C: livers without cold storage; n = 6 | 10 IU/mL | — | (i) Prevented induced denudation of the endothelial lining in steatotic livers, but aggravated in lean livers
(ii) Enzyme (AST, LDH, GLDH) release reduced to 50% in steatotic livers, but not in lean livers
(iii) Steatotic livers presented with lower oxygen consumption than lean livers
(iv) Reduced MAPK-dependent Erk phosphorylation in lean livers |
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| Li et al., 2003 [13] | Insulin | Rat | UW/24 h, 4°C | I: UW + Ins; n = 14
C: UW; n = 20 | 40 IU/L | — | (i) Higher transaminase levels (AST and ALT)
(ii) Repressed expression of 215 genes
(iii) Exacerbated graft ischemic injury |
| Li et al., 2004 [14] | | Rat | UW/24 h, 0–4°C | I: UW + Ins; n = 5
C: UW; n = 5 | 40 IU/L | — | (i) Deteriorated energy regeneration
(ii) Acceleration of lipoprotein metabolism through upregulation of the activity of apolipoprotein C‐III (Apo C‐III)
(iii) Inhibition of the insulin‐like growth factor‐binding protein‐1 pathway |
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| Minor et al., 1998 [15] | Glucagon | Rat | UW/24 h, 4°C/normothermic perfusion: 45 min, 37°C | I: UW + Gluc; n = 5
C: UW; n = 5 | 0.5 μg/mL | — | (i) Enhanced endogenous cAMP signal
(ii) Reduction in ALT release
(iii) Threefold increase in hepatic bile production
(iv) Restored ATP tissue levels |
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| Zaouali et al., 2010 [16] | IGF-1 | Rat | IGL-1/24 h, 4°C/warm reperfusion: 2 h, 37°C | I: IGL-1 + IGF-1; n = 8
C: IGL-1, n = 8 | 10 μg/L | — | (i) Lower transaminase levels (ALT, AST)
(ii) Increased bile clearance
(iii) Reduction in vascular resistance
(iv) Activation of AKT
(iv) Constitutive endothelial nitric oxide synthase |
|
| Zaouali et al., 2010 [17] | EGF-1 | Rat | IGL-1/24 h, 4°C/warm reperfusion: 2 h, 37°C | I: IGL-1 + EGF-1; n = 8
C: IGL-1, n = 8 | 10 μg/L | — | (i) Lower transaminase levels
(ii) Greater bile production
(iii) Ameliorated flow rates |
|
| Zaouali et al., 2010 [18] | IGF-1
EGF | Rat | UW/24 h, 4°C/normothermic reperfusion: 2 h, 37°C | I1: UW + IGF-1; n = 16
I2: UW + EGF; n = 16
I3: UW + IGF-1 + EGF; n = 16
C: UW; n = 16 | 10 μg/LIGF-1
10 μg/LEGF | AKT inhibitor
1.5 mg/L | (i) IGF‐I could be a more appropriate clinical therapy than EGF
(ii) EGF and IGF‐1 upregulated AKT
(iii) EGF and IGF-I (separately or in combination) reduced hepatic injury and improved survival in recipients |
| Ambiru et al., 2004 [19] | IGF-1
EGF
NGF | Pig | UW/18 h, 4°C/cold reperfusion | I: UW + IGF-1 + EGF + NGF; n = 7
C: UW; n = 7 | 10 μg/LEGF
10 μg/LIGF-1
20 μg/L(NGF)-β | Bactenecin:
1 mg/L
SP: 2.5 mg/L | (i) Transaminases (AST, ALT) were comparable between the two groups
(ii) Higher ATP levels
(iii) Less haemorrhagic necrosis
(iv) Cold ischemic time extended to 18 h |
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| Takeda et al., 1999 [20] | hrHGF | Rat | UW | I: UW + hrHGF
C: UW | 0.3 μg/mL | 100 μg/body hrHGF was injected | (i) Reduced injury in SEC
(ii) Prevented expansion of fatty droplets
(iii) Protective effect |
| Takeda et al., 2003 [21] | Rat | UW/24 h, 4°C | I: UW + hrHGF
C: UW | 0.1 μg/mL or 1 μg/mL | — | (i) Decreased transaminase levels
(ii) Diminished hepatocellular damage in histological examination |
|
| Boehnert et al., 2005 [22] | hr relaxin-2 | Rat | UW/3.5 h, 4°C or 3.5 h, 20°C/cold reperfusion: 4°C or warm reperfusion: 20°C | I: UW + hrRLX-2; n = 10
C: UW; n = 10 | 32 ng/mL (reperfusion solutions)
64 ng/mL (preservation solution) | — | (i) Decreased MDA activity
(ii) Decreased MPO activity |
| Boehnert et al., 2008 [23] | Rat | HTK/5 h, 4°C or 5 h, 20°C/cold reperfusion: 4°C or warm reperfusion: 20°C | I: HTK + hrRLX-2; n = 20
C: HTK; n = 10 | 64 ng/mL | — | (i) Decreased MDA activity
(ii) Decreased MPO activity |
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| Aliosmanoglu et al., 2013 [24] | Prostaglandin E-1 | Rat | HTK/12 h, 4°C UW/12 h, 4°C | I1: HTK + PGE-1; n = 6
I2: UW + PGE-1; n = 6
C1: Ringer’s lactate; n = 6
C2: HTK; n = 6 C3:UW; n = 6 | 20 μg/kg | — | (i) Decreased transaminase levels
(ii) Decreased pathologic injury |
| Morioka et al., 2003 [25] | Rat | HTK/2 h or 6 h, 4°C
Ringer’s lactate/2 h or 6 h, 4°C | I1: HTK + PGE-1; Ringer’s lactate + PGE-1
C1: fatty livers + 0.3 mg/kg FK506
C2: fatty livers | 1 μg/mL | — | (i) 75% 7-day survival
(ii) Decreased ALT and hyaluronic acid levels
(iii) Reduced tissue injury |
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