Abstract P144: DHA is a Superior Treatment Over 12/15-lipoxygenase Inhibition in LPS-induced Acute Kidney Injury via Increased Resolvin D2 and IL-10 Levels

Hypertension ◽  
2016 ◽  
Vol 68 (suppl_1) ◽  
Author(s):  
Mohamed Katary ◽  
Nehal M Elsherbini ◽  
Ahmed S Ibrahim ◽  
Mohamed Al-Shabrawey ◽  
Ahmed A Elmarakby
Keyword(s):  
Oxidative Stress ◽  
Acute Kidney Injury ◽  
Urinary Excretion ◽  
Renal Injury ◽  
Kidney Injury ◽  
Intercellular Adhesion Molecule ◽  
Protective Mechanism ◽  
Thiobarbituric Acid Reactive Substance ◽  
Omega 3 ◽  
Renal Expression

Acute kidney injury (AKI) is characterized by loss of kidney function and is often associated with high mortality rate. The polyunsaturated, omega-3 fatty acid, docosahexaenoic acid (DHA), has a promising role in preventing AKI; however; DHA reno-protective mechanism remains unclear. Our aim is to investigate whether and how DHA attenuates lipopolysaccharide (LPS)-induced AKI. Four groups of wild type C57BL/6 (WT) mice were used; control, LPS injected (4 mg/kg i.p), LPS treated with the 12/15-lipoxygenase (12/15-LO) inhibitor baicalein (20 mg/kg i.p for 6 days) and LPS treated with DHA (50 mg/kg i.p for 6 days). LPS-injected mice showed significant elevation in markers of renal injury as urinary excretion levels of protein, podocalyxin and albumin were elevated compared to WT untreated mice (albuminuria was 112±4 vs. 8±1 μg/day and podocalyxin was 3.5±0.6 vs. 0.6±0.1 μg/day in LPS injected mice vs. control WT, P< 0.05). The elevation in renal injury markers were also associated with increases in urinary excretion of thiobarbituric acid reactive substance (TBARs), as a marker of oxidative stress and monocyte chemoattractant protein-1 (MCP-1), as a marker of inflammation, in LPS injected mice. Treatment of LPS injected mice with either DHA or baicalein significantly reduced markers of renal injury, inflammation and oxidative stress. DHA or baicalein treatment also significantly reduced the elevation in renal mRNA expression levels of intercellular adhesion molecule 1 (ICAM-1) and tumor necrosis factor-α (TNF-α) in LPS injected mice. DHA was superior over baicalein in reducing renal expression of Interleukin-6 (IL-6) and IL-1β and in increasing the renal expression of the anti-inflammatory cytokine IL-10 in LPS injected mice. DHA reduced renal tubular necrosis and vaculated cells and lowered renal expression of CD45, a marker of leucocyte adhesion, in LPS injected mice. DHA also restored the decrease in plasma resolvin D2 (RvD2) in LPS injected mice. In conclusion, our data suggest that 12/15-LO activation is involved in LPS-induced acute kidney injury and DHA is a superior treatment over 12/15-LO inhibitor in preventing LPS-induced kidney injury, at least in part, via 12/15-LO-induced resolvin D2.

scholarly journals Kahweol Ameliorates Cisplatin-Induced Acute Kidney Injury through Pleiotropic Effects in Mice

Biomedicines ◽  
2020 ◽  
Vol 8 (12) ◽  
pp. 572
Author(s):  
Jung-Yeon Kim ◽  
Jungmin Jo ◽  
Jaechan Leem ◽  
Kwan-Kyu Park
Keyword(s):  
Oxidative Stress ◽  
Acute Kidney Injury ◽  
Renal Injury ◽  
Manganese Superoxide Dismutase ◽  
Immune Cell ◽  
Nicotinamide Adenine Dinucleotide Phosphate ◽  
Kidney Injury ◽  
Pleiotropic Effects ◽  
Induced Apoptosis ◽  
Vascular Adhesion

Cisplatin is an effective chemotherapeutic agent, but its clinical use is frequently limited by its nephrotoxicity. The pathogenesis of cisplatin-induced acute kidney injury (AKI) remains incompletely understood, but oxidative stress, tubular cell death, and inflammation are considered important contributors to cisplatin-induced renal injury. Kahweol is a natural diterpene extracted from coffee beans and has been shown to possess anti-oxidative and anti-inflammatory properties. However, its role in cisplatin-induced nephrotoxicity remains undetermined. Therefore, we investigated whether kahweol exerts a protective effect against cisplatin-induced renal injury. Additionally, its mechanisms were also examined. Administration of kahweol attenuated renal dysfunction and histopathological damage together with inhibition of oxidative stress in cisplatin-injected mice. Increased expression of nicotinamide adenine dinucleotide phosphate oxidase 4 and decreased expression of manganese superoxide dismutase and catalase after cisplatin treatment were significantly reversed by kahweol. Moreover, kahweol inhibited cisplatin-induced apoptosis and necroptosis in the kidneys. Finally, kahweol reduced inflammatory cytokine production and immune cell accumulation together with suppression of nuclear factor kappa-B pathway and downregulation of vascular adhesion molecules. Together, these results suggest that kahweol ameliorates cisplatin-induced renal injury via its pleiotropic effects and might be a potential preventive option against cisplatin-induced nephrotoxicity.

scholarly journals Immunohistochemical Analysis of 4-HNE, NGAL, and HO-1 Tissue Expression after Apocynin Treatment and HBO Preconditioning in Postischemic Acute Kidney Injury Induced in Spontaneously Hypertensive Rats

Antioxidants ◽  
2021 ◽  
Vol 10 (8) ◽  
pp. 1163
Author(s):  
Sanjin Kovacevic ◽  
Milan Ivanov ◽  
Maja Zivotic ◽  
Predrag Brkic ◽  
Zoran Miloradovic ◽  
...  
Keyword(s):  
Oxidative Stress ◽  
Acute Kidney Injury ◽  
Spontaneously Hypertensive Rats ◽  
Kidney Injury ◽  
Immunohistochemical Analysis ◽  
Tissue Expression ◽  
Pure Oxygen ◽  
Hypertensive Rats ◽  
Spontaneously Hypertensive ◽  
Renal Expression

Oxidative stress has been considered as a central aggravating factor in the development of postischemic acute kidney injury (AKI). The aim of this study was to perform the immunohistochemical analysis of 4-hydroxynonenal (4-HNE), neutrophil gelatinase-associated lipocalin (NGAL), and heme oxygenase-1 (HO-1) tissue expression after apocynin (APO) treatment and hyperbaric oxygenation (HBO) preconditioning, applied as single or combined protocol, in postischemic acute kidney injury induced in spontaneously hypertensive rats (SHR). Twenty-four hours before AKI induction, HBO preconditioning was carried out by exposing to pure oxygen (2.026 bar) twice a day, for 60 min in two consecutive days. Acute kidney injury was induced by removal of the right kidney while the left renal artery was occluded for 45 min by atraumatic clamp. Apocynin was applied in a dose of 40 mg/kg body weight, intravenously, 5 min before reperfusion. We showed increased 4-HNE renal expression in postischemic AKI compared to Sham-operated (SHAM) group. Apocynin treatment, with or without HBO preconditioning, improved creatinine and phosphate clearances, in postischemic AKI. This improvement in renal function was accompanied with decreased 4-HNE, while HO-1 kidney expression restored close to the control group level. NGAL renal expression was also decreased after apocynin treatment, and HBO preconditioning, with or without APO treatment. Considering our results, we can say that 4-HNE tissue expression can be used as a marker of oxidative stress in postischemic AKI. On the other hand, apocynin treatment and HBO preconditioning reduced oxidative damage, and this protective effect might be expected even in experimental hypertensive condition.

scholarly journals Protective Effects of Ulva lactuca Polysaccharide Extract on Oxidative Stress and Kidney Injury Induced by D-Galactose in Mice

Marine Drugs ◽  
2021 ◽  
Vol 19 (10) ◽  
pp. 539
Author(s):  
Qian Yang ◽  
Yanhui Jiang ◽  
Shan Fu ◽  
Zhaopeng Shen ◽  
Wenwen Zong ◽  
...  
Keyword(s):  
Oxidative Stress ◽  
Antioxidant Activity ◽  
Oxidative Damage ◽  
Renal Injury ◽  
Caspase 3 ◽  
Kidney Injury ◽  
Ulva Lactuca ◽  
Protective Mechanism ◽  
Serum Cystatin C ◽  
Apoptotic Protein

Reactive oxygen species (ROS) are the key factors that cause many diseases in the human body. Polysaccharides from seaweed have been shown to have significant antioxidant activity both in vivo and in vitro. The ameliorative effect of Ulva lactuca polysaccharide extract (UPE) on renal injury induced by oxidative stress was analyzed. As shown by hematoxylin–eosin staining results, UPE can significantly improve the kidney injury induced by D-galactose (D-gal). Additionally, the protective mechanism of UPE on the kidney was explored. The results showed that UPE could decrease the levels of serum creatinine (Scr), blood urea nitrogen (BUN), serum cystatin C (Cys-C), lipid peroxidation, protein carbonylation, and DNA oxidative damage (8-OHdG) and improve kidney glutathione content. Moreover, UPE significantly increased the activities of superoxide dismutase and glutathione peroxidase and total antioxidant activity in mice. UPE also decreased the levels of inflammatory cytokines TNF-α and IL-6. Further investigation into the expression of apoptotic protein caspase-3 showed that UPE decreased the expression of apoptotic protein caspase-3. These results indicate that UPE has a potential therapeutic effect on renal injury caused by oxidative stress, providing a new theoretical basis for the treatment of oxidative damage diseases in the future.

scholarly journals Angiotensin (1-7) Attenuates Sepsis-Induced Acute Kidney Injury by Regulating the NF-κB Pathway

2021 ◽  
Vol 12 ◽  
Author(s):  
Ying Zhu ◽  
Daliang Xu ◽  
Fang Deng ◽  
Yonglin Yan ◽  
Jian Li ◽  
...  
Keyword(s):  
Oxidative Stress ◽  
Acute Kidney Injury ◽  
Inflammatory Response ◽  
Cystatin C ◽  
Kidney Injury ◽  
Serum Levels ◽  
Control Group ◽  
Protective Mechanism ◽  
Ang Ii ◽  
Urea Nitrogen

This study explores the protective mechanism of angiotensin (1-7) [Ang-(1-7)] on kidneys by examining its effects on renal histomorphology, inflammatory response, oxidative stress, and NF-κB signaling in mice suffering from sepsis-induced acute kidney injury. A sepsis-induced acute kidney injury mouse model was established by intracervically injecting lipopolysaccharides (LPS group), followed by the administration of Ang-(1-7) [LPS + Ang-(1-7) group]. The serum levels of urea nitrogen, creatinine and cystatin. c were measured with an automatic biochemical analyzer, and changes in proinflammatory cytokines and angiotensin II (Ang II) in the serum and kidneys were quantified by enzyme-linked immunosorbent assays. Changes in oxidative stress indices in the renal cortex were detected by colorimetry. The localization of Ang II in kidneys was examined by immunohistochemistry. Western blotting was used to examine phosphorylated NF-κB-p65 and IκBα levels in kidneys. Compared with the control group, the serum levels of urea nitrogen, creatinine and cystatin. c were increased, whereas the levels of Ang II, TNFα, IL-1β, IL-6, and malondialdehyde (mda) were increased significantly. The levels of Ang II and phosphorylated NF-κB-p65 were elevated in kidneys, whereas the levels of superoxide dismutase (sod), Total antioxidative capacity (TAOC), and inhibitor of NF-κB (IκBα) were reduced in the LPS group (p &lt; 0.05). Pathological damage was also observed in kidneys of LPS-group mice. In Pearson correlation analysis, there was a positive correlation between Ang II and phosphorylated NF-κB-p65 levels, and a negative correlation between Ang II and IκBα levels (p &lt; 0.05). After the application of Ang-(1-7), the levels of urea nitrogen, creatinine, cystatin. c, Ang II, TNFα, IL-1β, IL-6, and mda, as well as the expression of Ang II and phosphorylated NF-κB-p65 in kidneys of LPS + Ang-(1-7)-group mice, were lower than those in kidneys of LPS-group mice, but the levels of sod, TAOC, and IκBα were higher than those of LPS-group mice (p &lt; 0.05). Pathological changes were less severe in mice of the LPS + Ang-(1-7) group. Overall, Ang-(1-7) can decrease the Ang II level, inhibit NF-κB signaling, reduce the inflammatory response, decrease oxidative stress, and mitigate sepsis-associated acute kidney injury.

Increased renal expression and urinary excretion of TLR4 in acute kidney injury associated with cirrhosis

2013 ◽  
Vol 33 (3) ◽  
pp. 398-409 ◽  
Author(s):  
Naina Shah ◽  
Fatma E. Mohamed ◽  
Maria Jover-Cobos ◽  
Jane Macnaughtan ◽  
Nathan Davies ◽  
...  
Keyword(s):  
Acute Kidney Injury ◽  
Urinary Excretion ◽  
Kidney Injury ◽  
Renal Expression

Abstract 29: An Orally Active Epoxyeicosatrienoic Acid (eet) Analog Attenuates Kidney Injury in Hypertensive Dahl Salt Sensitive Rat by Reducing Oxidative Stress, Inflammation and Endoplasmic Reticulum Stress

Hypertension ◽  
2012 ◽  
Vol 60 (suppl_1) ◽  
Author(s):  
Md Abdul H Khan ◽  
Praveena Narayanan ◽  
John R Falck ◽  
John D Imig
Keyword(s):  
Oxidative Stress ◽  
Blood Pressure ◽  
Er Stress ◽  
Renal Injury ◽  
Kidney Injury ◽  
Marker Genes ◽  
Kidney Protection ◽  
Salt Sensitive Hypertension ◽  
Orally Active ◽  
Renal Expression

Renal injury is associated with salt-sensitive hypertension. The Dahl salt-sensitive hypertensive rat (Dahl SS) is a model of salt-sensitive hypertension and the related kidney injury. The kidney injury in Dahl SS hypertension is associated with oxidative stress, inflammation and ER stress. We have recently developed orally active epoxyecosatrienoic acid (EET) analogs that provide organ protection in hypertension and other pathologies through multiple signaling pathways. We hypothesized that these EET analogs with their anti-inflammatory, anti-oxidant and anti-ER stress effects will protect the kidney in Dahl SS hypertension. Dahl SS rats received high salt diet and treated either with an EET analog (10 mg/kg/d) or vehicle (0.05% EtOH+0.1% PEG 400) in drinking water for 14 days. Blood pressure (SBP) was measured by tail-cuff plethysmography and urine, plasma and tissue samples were collected at the end of the treatment protocol. Urinary creatinine, albumin, nephrin, and renal tissue TBARS content were measured using ELISA or colorimetric assays. Renal expression of oxidative, inflammatory and ER stress marker genes were examined using RT-PCR. Histological analysis was done to assess renal injury. In Dahl SS rats, EET analog treatment did not affect the SBP compared to vehicle (183±6 vs. 185±12 mmHg). Interestingly, the EET analog treatment in Dahl SS reduced albumin-creatinine ratio (49±17 vs. 12±3) and nephrinuria (11±1 vs. 4±1 mg/d). EET analog treatment also reduced glomerular injury, intra-tubular cast formation and kidney fibrosis by 30-60% in Dahl SS rats compared to vehicle. In Dahl SS rats, EET analog treatment caused a 40% reduction in kidney TBARS content compared to vehicle. Moreover, the EET analog treatment in Dahl SS rats resulted 2-3 fold attenuation in the renal expression of oxidative ( p47PHOX ), inflammation ( IL-6, TGF-β ), and ER stress ( CHOP, GADD34 ) genes. These data, demonstrate that a novel orally active EET analog provides kidney protection in Dahl SS hypertension by reducing oxidative stress, inflammation and ER stress, and this kidney protection was independent of blood pressure reduction.

scholarly journals Hydrogen Sulfide Attenuates LPS-Induced Acute Kidney Injury by Inhibiting Inflammation and Oxidative Stress

2018 ◽  
Vol 2018 ◽  
pp. 1-10 ◽  
Author(s):  
Yuhong Chen ◽  
Sheng Jin ◽  
Xu Teng ◽  
Zhenjie Hu ◽  
Zhihong Zhang ◽  
...  
Keyword(s):  
Oxidative Stress ◽  
Acute Kidney Injury ◽  
Hydrogen Sulfide ◽  
Interleukin 1 ◽  
Kidney Injury ◽  
Protective Mechanism ◽  
Protective Effects ◽  
Caspase 1 ◽  
And Oxidative Stress

In order to investigate the protective mechanism of hydrogen sulfide (H2S) in sepsis-associated acute kidney injury (SA-AKI), ten AKI patients and ten healthy controls were enrolled. In AKI patients, levels of creatinine (Cre), urea nitrogen (BUN), tumor necrosis factor-α (TNF-α) and interleukin-1β (IL-1β), and myeloperoxidase (MPO) activity as well as concentrations of malondialdehyde (MDA) and hydrogen peroxide (H2O2) were significantly increased compared with those of controls. However, plasma level of H2S decreased and was linearly correlated with levels of Cre and BUN. After that, an AKI mouse model by intraperitoneal lipopolysaccharide (LPS) injection was constructed for in vivo study. In AKI mice, H2S levels decreased with the decline of 3-MST activity and expression; similar changes were observed in other indicators mentioned above. However, the protein expressions of TLR4, NLRP3, and caspase-1 in mice kidney tissues were significantly increased 6 h after LPS injection. NaHS could improve renal function and kidney histopathological changes, attenuate LPS-induced inflammation and oxidative stress, and inhibit expressions of TLR4, NLRP3, and caspase-1. Our study demonstrated that endogenous H2S is involved in the pathogenesis of SA-AKI, and exogenous H2S exerts protective effects against LPS-induced AKI by inhibiting inflammation and oxidative stress via the TLR4/NLRP3 signaling pathway.

scholarly journals N-acetyl-cysteine increases cellular dysfunction in progressive chronic kidney damage after acute kidney injury by dampening endogenous antioxidant responses

2018 ◽  
Vol 314 (5) ◽  
pp. F956-F968 ◽  
Author(s):  
David M. Small ◽  
Washington Y. Sanchez ◽  
Sandrine F. Roy ◽  
Christudas Morais ◽  
Heddwen L. Brooks ◽  
...  
Keyword(s):  
Oxidative Stress ◽  
Acute Kidney Injury ◽  
Mitochondrial Dysfunction ◽  
Transforming Growth Factor ◽  
Multiphoton Microscopy ◽  
Kidney Injury ◽  
Peroxisome Proliferator ◽  
Fluorescence Lifetime Imaging ◽  
Antioxidant Responses ◽  
Acetyl Cysteine

Oxidative stress and mitochondrial dysfunction exacerbate acute kidney injury (AKI), but their role in any associated progress to chronic kidney disease (CKD) remains unclear. Antioxidant therapies often benefit AKI, but their benefits in CKD are controversial since clinical and preclinical investigations often conflict. Here we examined the influence of the antioxidant N-acetyl-cysteine (NAC) on oxidative stress and mitochondrial function during AKI (20-min bilateral renal ischemia plus reperfusion/IR) and progression to chronic kidney pathologies in mice. NAC (5% in diet) was given to mice 7 days prior and up to 21 days post-IR (21d-IR). NAC treatment resulted in the following: prevented proximal tubular epithelial cell apoptosis at early IR (40-min postischemia), yet enhanced interstitial cell proliferation at 21d-IR; increased transforming growth factor-β1 expression independent of IR time; and significantly dampened nuclear factor-like 2-initiated cytoprotective signaling at early IR. In the long term, NAC enhanced cellular metabolic impairment demonstrated by increased peroxisome proliferator activator-γ serine-112 phosphorylation at 21d-IR. Intravital multiphoton microscopy revealed increased endogenous fluorescence of nicotinamide adenine dinucleotide (NADH) in cortical tubular epithelial cells during ischemia, and at 21d-IR that was not attenuated with NAC. Fluorescence lifetime imaging microscopy demonstrated persistent metabolic impairment by increased free/bound NADH in the cortex at 21d-IR that was enhanced by NAC. Increased mitochondrial dysfunction in remnant tubular cells was demonstrated at 21d-IR by tetramethylrhodamine methyl ester fluorimetry. In summary, NAC enhanced progression to CKD following AKI not only by dampening endogenous cellular antioxidant responses at time of injury but also by enhancing persistent kidney mitochondrial and metabolic dysfunction.

Propofol Attenuated Acute Kidney Injury after Orthotopic Liver Transplantation via Inhibiting Gap Junction Composed of Connexin 32

2015 ◽  
Vol 122 (1) ◽  
pp. 72-86 ◽  
Author(s):  
Chenfang Luo ◽  
Dongdong Yuan ◽  
Xiaoyun Li ◽  
Weifeng Yao ◽  
Gangjian Luo ◽  
...  
Keyword(s):  
Oxidative Stress ◽  
Liver Transplantation ◽  
Acute Kidney Injury ◽  
Gap Junction ◽  
Orthotopic Liver Transplantation ◽  
Critical Role ◽  
Kidney Injury ◽  
Cellular Injury ◽  
Knock Down ◽  
Hypoxia Reoxygenation

Abstract Background: Postliver transplantation acute kidney injury (AKI) severely affects patient survival, whereas the mechanism is unclear and effective therapy is lacking. The authors postulated that reperfusion induced enhancement of connexin32 (Cx32) gap junction plays a critical role in mediating postliver transplantation AKI and that pretreatment/precondition with the anesthetic propofol, known to inhibit gap junction, can confer effective protection. Methods: Male Sprague–Dawley rats underwent autologous orthotopic liver transplantation (AOLT) in the absence or presence of treatments with the selective Cx32 inhibitor, 2-aminoethoxydiphenyl borate or propofol (50 mg/kg) (n = 8 per group). Also, kidney tubular epithelial (NRK-52E) cells were subjected to hypoxia–reoxygenation and the function of Cx32 was manipulated by three distinct mechanisms: cell culture in different density; pretreatment with Cx32 inhibitors or enhancer; Cx32 gene knock-down (n = 4 to 5). Results: AOLT resulted in significant increases of renal Cx32 protein expression and gap junction, which were coincident with increases in oxidative stress and impairment in renal function and tissue injury as compared to sham group. Similarly, hypoxia–reoxygenation resulted in significant cellular injury manifested as reduced cell growth and increased lactate dehydrogenase release, which was significantly attenuated by Cx32 gene knock-down but exacerbated by Cx32 enhancement. Propofol inhibited Cx32 function and attenuated post-AOLT AKI. In NRK-52E cells, propofol reduced posthypoxic reactive oxygen species production and attenuated cellular injury, and the cellular protective effects of propofol were reinforced by Cx32 inhibition but cancelled by Cx32 enhancement. Conclusion: Cx32 plays a critical role in AOLT-induced AKI and that inhibition of Cx32 function may represent a new and major mechanism whereby propofol reduces oxidative stress and subsequently attenuates post-AOLT AKI.

scholarly journals Comparison of Effects of Different Statins on Contrast-Induced Acute Kidney Injury in Rats: Histopathological and Biochemical Findings

2017 ◽  
Vol 2017 ◽  
pp. 1-10 ◽  
Author(s):  
Xiao-lei Wang ◽  
Tuo Zhang ◽  
Liu-hua Hu ◽  
Shi-qun Sun ◽  
Wei-feng Zhang ◽  
...  
Keyword(s):  
Oxidative Stress ◽  
Acute Kidney Injury ◽  
Kidney Injury ◽  
Lipid Lowering ◽  
Control Group ◽  
Sprague Dawley ◽  
Atorvastatin Group ◽  
New Strategy ◽  
Ameliorative Effect ◽  
Markers Of Oxidative Stress

Statins are a promising new strategy to prevent contrast-induced acute kidney injury (CI-AKI). In this study we compared the ameliorative effect of different statins in a rat model of CI-AKI. Sprague-Dawley rats were divided into five groups: control group; CI-AKI group; CI-AKI + rosuvastatin group (10 mg/kg/day); CI-AKI + simvastatin group (80 mg/kg/day); and CI-AKI + atorvastatin group (20 mg/kg/day). CI-AKI was induced by dehydration for 72 hours, followed by furosemide intramuscular injection 20 minutes before low-osmolar contrast media (CM) intravenous injection. Statins were administered by oral gavage once daily for 3 consecutive days before CM injection and once 4 hours after CM injection. Rats were sacrificed 24 hours after CM injection, and renal function, kidney histopathology, nitric oxide (NO) metabolites, and markers of oxidative stress, inflammation, and apoptosis were evaluated. The results showed that atorvastatin and rosuvastatin but not simvastatin ameliorated CM-induced serum creatinine elevation and histopathological alterations. Atorvastatin and rosuvastatin showed similar effectiveness against CM-induced oxidative stress, but simvastatin was less effective. Atorvastatin was most effective against NO system dysfunction and cell apoptosis, whereas rosuvastatin was most effective against inflammation. Our findings indicate that statins exhibit differential effects in preventing CI-AKI when given at equivalent lipid-lowering doses.

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