From: Molecular mechanisms underlying the renal protective effects of coenzyme Q10 in acute kidney injury
Study/references | Research object | Types of injury | CoQ10 administration | Associated genes/pathways and agents | Main findings |
---|---|---|---|---|---|
Yenilmez et al. 2010 [25] | Rats | Induced by ochratoxin A (2.2 mg/kg, gastric gavage) | 10 mg/kg, intraperitoneally | NA | CoQ10 treatment ameliorated the ochratoxin A-induced renal oxidative injuries |
Fouad et al. 2010 [41] | Mice | Acute cisplatin (5 mg/kg, i.p.) nephrotoxicity injury | 10 mg/kg, intraperitoneally | Downregulating iNOS, NF-κB, caspase-3, and p53 | CoQ10 protects against acute cisplatin nephrotoxicity by decreasing the expression of iNOS, NF-κB, caspase-3, and p53 in renal tissue |
Ahmadvand et al. 2014 [26] | Rats | Gentamicin-induced nephrotoxicity injury | 15 mg/kg, intraperitoneally | Downregulating PON1 | CoQ10 alleviated gentamicin-induced nephrotoxicity by reducing the elevated serum lipid peroxidation, lipid profile and atherogenic index, and PON1 activity |
Carrasco et al. 2014 [42] | Patients (n = 100) | ESWL-induced kidney injury | 200 mg/day, orally administered during the week before ESWL and for 1 week after | Clinical trial | Compared with placebo group, CoQ10 significantly increased glomerular filtration (P = 0.013) and decreased albumin/creatinine and β2-microglobulin level (P = 0.02) |
Fatima et al. 2015 [43] | Rats | Cisplatin-induced oxidative stress injury | 10 mg/kg, intraperitoneally | CoQ10 combined with EGCG was more effective in attenuating renal injury | CoQ10 was effective against cisplatin-induced nephrotoxicity, resulted in a significant reduction of BUN and serum creatinine level |
Fatima et al. 2016 [44] | Rats | Cisplatin-induced nephrotoxicity injury (7 mg/kg, i.p.) | 5 mg/kg, intraperitoneally | Combined with 15 mg/kg EGCG | Combined CoQ10 and EGCG significantly attenuated cisplatin-induced oxidative stress, nitrosative stress, and inflammatory and apoptotic parameters |
Ozer et al. 2017 [45] | Rats | Cecal ligation and puncture-induced sepsis | 10 mg/kg, intraperitoneally | NA | CoQ10 showed protective effects against sepsis-induced kidney injury by anti-inflammatory and antioxidative effects |
Arany et al. 2017 [46] | Renal proximal tubule cell line | Nicotine-induced renal cell injury (cells treated with 200 µM nicotine) | 10 µM | Serine 36 phosphorylation | CoQ10 significantly inhibited nicotine-mediated production of reactive oxygen species (ROS) and consequent apoptosis |
Ustuner et al. 2017 [47] | Rats | Gentamicin-induced kidney damage (80 mg/kg/day, i.p.) | 10 mg/kg, intraperitoneally | NA | Necrotic tubuli rate and hyalin accumulation in tubuli were decreased after CoQ10 treatment |
Shamardl et al. 2017 [48] | Rats | L-NAME hypertensive kidney injury (40 mg/kg, i.p.) | 10 mg/kg, intraperitoneally | Combination with vitamin D had further effects on all parameters | CoQ10 decreased systolic, diastolic, and mean arterial pressure, total cholesterol, LDL-C, creatinine, TNF-α, and malondialdehyde level |
Chen et al. 2018 [49] | Patients (n = 150), rats (n = 45) | Contrast-induced nephropathy | Patients: 20 mg three times daily from 2 days before to 3 days after procedure; rats: 20 mg/kg | Combined with 20 mg trimetazidine | Incidence of contrast-induced nephropathy was significantly lower in CoQ10 plus trimetazidine group compared with control group (6.67% versus 21.3%, P = 0.01); CoQ10 and trimetazidine significantly reduced oxidation stress in an AKI animal model |
Akbulut et al. 2019 [50] | Rats | Renal ischemia–reperfusion injury | 10 mg/kg, intraperitoneally | NA | CoQ10 decreased tissue oxidative stress levels and scores of histopathology and apoptosis |
Albadrany et al. 2019 [51] | Broiler chickens | Diclofenac-induced renal injury (1 and 2 mg/kg, i.p.) | 30 mg/kg, orally | NA | CoQ10 could not alleviate diclofenac-induced renal injury, but worsened impaired renal function |
Kennedy et al. 2020 [52] | Mice | Khat-induced nephrotoxicity (1500 mg/kg, gastric gavage) | 200 mg/kg, orally | Normalization of GSH and TNF-α expression | CoQ10 decreased creatinine levels and reduced tubular necrosis and tubular epithelium injury |
Megrin et al. 2020 [53] | Rats | Lead-acetate-induced renal injury | 10 mg/kg, intraperitoneally | Upregulation Nrf2/HO-1 pathway | CoQ10 reduced the deleterious cellular side effects of lead acetate exposure owing to its antioxidant, anti-inflammatory, and anti-apoptotic effects |
Abdeen et al. 2020 [54] | Rats | Piroxicam-induced oxidative injury | 10 mg/kg, orally | NA | CoQ10 attenuated the piroxicam-inflicted deleterious oxidative harm and apoptosis, improving mitochondrial function and reducing ROS, which might be ascribed to the free-radical scavenging activity of CoQ10 |
Liu et al. 2020 [55] | Mice | Renal ischemia–reperfusion injury | 50 mg/kg, NA | NA | CoQ10 reduced oxidative damage in vitro and in vivo, inhibited renal cell apoptosis, and attenuated inflammatory response in renal I/R injury model, thus improving renal function |
Liu et al. 2021 [56] | Mice | Renal ischemia–reperfusion injury | 50 mg/kg, tail vein injection | NA | The mitochondria-targeted triphenylphosphine CoQ10 nanoparticles alleviated mtDNA damage, suppressed inflammatory and apoptotic responses, and improved renal function |
Alshogran et al. 2021 [57] | Rats | Contrast-induced kidney injury | 20 mg/kg, orally | Combined with 10 mg/kg atorvastatin | Pretreatment with CoQ10/atorvastatin showed regenerative effect on distal tubules with mild kidney histology alterations as compared with contrast-induced nephropathy rats |
Couto et al. 2021 [58] | Rats | Contrast-induced acute kidney injury | 10 mg/kg, intraperitoneally | NA | CoQ10 ameliorated renal function, prevented hemodynamic changes, neutralized oxidative damage, and prevented the progression of histologic damage |