The Scientific World Journal / 2014 / Article / Tab 2

Review Article

Caffeic Acid Phenethyl Ester as a Protective Agent against Nephrotoxicity and/or Oxidative Kidney Damage: A Detailed Systematic Review

Table 2

In vivo studies showing several types of action, animals recruited, doses applied, and reported outcomes of CAPE in some disease models of kidney.

The type of studyTarget organAnimals usedThe dose appliedType of actionReported outcomesReference

Renal I/R modelKidneyAlbino Wistar rats10  mol/kg, i.p.Inhibits neutrophil sequestrationAttenuation in renal damage after I/R[6]

Renal I/R modelKidneyAlbino Wistar rats10  mol/kg, i.p.Alters the indices of oxidative stressPartially alleviates renal damage after I/R[5]

Renal I/R modelKidneyAlbino Wistar rats10  mol/kg, i.p.Suppressed I/R-induced renal lipid peroxidationTherapeutic advantage in acute injury setting[19]

Cisplatin-induced nephrotoxicityKidneyFemale albino Wistar rats10  mol/kg/day, i.p.Free oxygen radical scavenging activityMarked reduction in the extent of tubular damage[7]

Paraquat-induced acute nephrotoxicityKidneyFemale albino Wistar rats10  mol/kg, i.p.Attenuates the oxidative stress caused by paraquatProtects acute nephrotoxicity induced by paraquat[74]

Acute urogenital injury following pneumoperitoneumKidney, testis, prostateAlbino Wistar rats10  mol/kg, i.p.Affects TAC and TOS levelsPrevents adverse effects of intra-abdominal pressure on kidney and testis[108]

Toluene-induced nephrotoxicityKidneyMale albino Wistar rats10  mol/kg/day, i.p.By showing antioxidant, antitoxic, and nephroprotective effectPrevents renal damage[109]

Cadmium-induced kidney mitochondrial injuryKidneyMale Wistar rats10  M final conc. to the isolated mitochondriaAntioxidant potentialHas therapeutic benefits in the setting of nephrotoxicity caused by cadmium[63]

Acetylsalicylic acid toxicityKidneyAlbino Wistar rats20  g/kg/day, p.o.Reduces the concentration of oxidant products and supports the antioxidant systemProtects kidneys from ASA-induced nephrotoxicity[68]

Aging-related oxidative damageKidneySprague Dawley rats15 mg/bw/day, i.p.Antioxidant and high cellular protective effectsBeneficial in delaying age-related cellular changes[82]

Renal I/RKidneyMale Wistar rats10  mol/kg, i.p.Antioxidant effectPromotes greater functional and anatomic renal injury[28]

Cd-induced renal damageKidneyAdult Cumming mice0.1 and 1  mol/kg/day, i.p.Reduces the levels of oxidative stress and altering the antioxidant defense systemProtects the oxidative renal damage induced by Cd in a dose-dependent manner[64]

Methotrexate-induced hepatorenal oxidative injuryKidneyBoth sexes albino Wistar rats10  mol/kg/day, i.p. for 5 days Anti-inflammatory and antioxidant effectsCapable of reducing methotrexate-induced hepatorenal oxidative injury[43]

Gentamycin-induced oxidative nephrotoxicityKidneyFemale albino Wistar rats10  mol/kg/day, i.p. for 12 daysModulator effect on oxidative stress and antioxidant redox systemNephrotoxicity may be significantly reduced[47]

Renal dysfunction by cyclosporine AKidneyMale Wistar rats10 and 30  mol/kg, i.p. for 10 daysInhibits renal lipid peroxidation and enhances and maintaining the antioxidant GSH contentProtects against cyclosporine A nephrotoxicity[33]

Cyclosporine A-induced nephrotoxicityKidneyFemale albino Wistar rats10  mol/kg/day, i.p. for 11 daysInhibits lipid peroxidation via inhibition of oxidative processProtects kidney from cyclosporine A-induced damage[34]

Vancomycin-induced nephrotoxicityKidneyMale albino Wistar rats10  mol/kg/day, i.p. for 7 daysDecreases lipid peroxidation and increases antioxidant enzyme activityReduction of the nephrotoxic effects of vancomycin[54]

Methotrexate-induced renal oxidative stressKidneyAlbino Wistar rats10  mol/kg/day, i.p. for 7 daysShows a potent scavenging effect of free radicalsReduces renal impairment[44]

Lithium-induced renal toxicityKidneyMale albino Wistar rats10  mol/kg/day, i.p. for 4 weeksSignificant increase in the activities of antioxidant enzymes and decrease in lipid peroxidationReduces Li-induced oxidative stress mediated renal tubular damage[44]

Long-term mobile phone exposure/renal impairmentKidneyMale Sprague-Dawley rats10  mol/kg/day, i.p. for 3 monthsFree radical scavenging and antioxidant propertiesProtects renal tissue from oxidative damage and prevents organ impairment[90]

Amikacin-induced nephrotoxicityKidneyFemale Wistar rats10  mol/kg/day, i.p. for 2 daysDecreases MDA levels showing lipid peroxidation-preventive effectsProtects kidney tissue against oxidative damage[58]

Shock wave-induced renal tubular oxidative stressKidneyWhite rabbits10  mol/kg/day, i.p. for 10 daysReduces significantly MDA levels, urine NAG activity, uric acid and white cell count in renal tissueAvoiding the side effects of ESWL applications[93]

Carbon tetrachloride-induced renal toxicityKidneyMale albino Wistar rats10  mol/kg, i.p. for every other day for one monthReduces MDA levels by antioxidant propertiesProtective effect on CCl4-induced kidney damage[71]

Oxidative organ damage due to thermal traumaKidneyMale albino Wistar rats10  mol/kg/day, i.p. for max. 7 daysScavenges free oxygen radicals, decreases MPO activity in neutrophils, increases antioxidant enzymeA potential beneficial agent in humans who suffer from thermal injury[84]

Doxorubicin-induced nephrotoxicityKidneyMale Sprague-Dawley rats10  mol/kg/body weight/day, i.p. for 12 daysAntioxidant and anti-inflammatory effectsProtects renal tissues against DXR-induced toxicity[8]

ASA: acetylsalicylic acid, CAPE: caffeic acid phenethyl ester, CCl4: carbon tetrachloride, Cd: cadmium, DXR: doxorubicin, ESWL: extracorporeal shock wave lithotripsy, GSH: glutathione, i.p.: intraperitoneal, I/R: ischemia/reperfusion, Li: lithium, MDA: malondialdehyde, MPO: myeloperoxidase, NAG: N-acetyl- -D-glucosaminidase, p.o.: per oral, TAC: total antioxidant capacity, TOS: total oxidant status.

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