&lt;p&gt;Curcumin Supplementation Alleviates Polymyxin E-Induced Nephrotoxicity&lt;/p&gt;

Vazin, Afsaneh; Heidari, Reza; Khodami, Zahra

doi:10.2147/jep.s255861

Cited by 12 publications

(5 citation statements)

References 47 publications

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“…Several antioxidants with renoprotective background have been tested against renal disease or xenobiotics-induced kidney injury ( Farombi and Ekor, 2006 ; Ommati et al., 2021a ; Vazin et al., 2020 ). As oxidative stress and its related complications play a role in TMDL-induced renal injury, the use of clinically applicable molecules ( e.g.…”

Section: Discussionmentioning

confidence: 99%

Mitochondrial dysfunction and oxidative stress are involved in the mechanism of tramadol-induced renal injury

Mousavi

Manthari

Najibi

et al. 2021

Current Research in Pharmacology and Drug Discovery

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Tramadol (TMDL) is an opioid analgesic widely administered for the management of moderate to severe pain. On the other hand, TMDL is commonly abused in many countries because of its availability and cheap cost. Renal injury is related to high dose or chronic administration of TMDL. No precise mechanism for TMDL-induced renal damage has been identified so far. The current study aimed to evaluate the potential role of oxidative stress and mitochondrial impairment in the pathogenesis of TMDL-induced renal injury. For this purpose, rats were treated with TMDL (40 and 80 mg/kg, i.p, 28 consecutive days). A significant increase in serum Cr and BUN was detected in TMDL groups. On the other hand, TMDL (80 mg/kg) caused a substantial increase in urine glucose, ALP, protein, and γ-GT levels. Moreover, urine Cr was significantly decreased in TMDL-treated rats (40 and 80 mg/kg). Renal histopathological alterations included inflammation, necrosis, and tubular degeneration in the kidney of TMDL-treated animals. Reactive oxygen species (ROS) formation, increased oxidized glutathione (GSSG), lipid peroxidation, and protein carbonylation was increased, whereas total antioxidant capacity and reduced glutathione levels were considerably decreased in TMDL groups. Significant mitochondrial impairment was also detected in the form of mitochondrial depolarization, adenosine-tri-phosphate (ATP) depletion, mitochondrial permeabilization, lipid peroxidation, and decreased mitochondrial dehydrogenase activity in the kidney of TMDL (80 mg/kg)-treated animals. These data suggest mitochondrial impairment and oxidative stress as mechanisms involved in the pathogenesis of TMDL-induced renal injury.

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Section: Discussionmentioning

confidence: 99%

Mitochondrial dysfunction and oxidative stress are involved in the mechanism of tramadol-induced renal injury

Mousavi

Manthari

Najibi

et al. 2021

Current Research in Pharmacology and Drug Discovery

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“…The mixture was incubated in the dark (5 min, 37°C). Finally, the absorbance was measured at λ = 595 nm using an EPOCH Plate reader (BioTek, USA) [ 15 , 59 ].…”

Section: Methodsmentioning

confidence: 99%

Pentoxifylline mitigates cholestasis-related cholemic nephropathy

Ommati¹,

Hojatnezhad²,

Abdoli³

et al. 2021

ceh

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Aim of the study Cholestasis is the stoppage of bile flow that primarily affects liver function. On the other hand, kidneys are also severely influenced during cholestasis. Cholestasis-induced kidney injury is known as cholemic nephropathy (CN). There is no precise pharmacological option in CN. Previous studies revealed that oxidative stress plays a crucial role in the pathogenesis of CN. On the other hand, the positive effects of pentoxifylline (PTX) against renal injury with different etiologies have been frequently reported. In the current study, the potential nephroprotective role of PTX in cholestasis-induced renal injury is investigated. Material and methods Bile duct ligated (BDL) rats were treated with PTX (10, 50, and 100 mg/kg), and renal markers of oxidative stress, urine level of inflammatory cytokines, as well as renal histopathological alterations were monitored. Results Significant changes in oxidative stress markers were detected in the BDL group. On the other hand, it was found that PTX (10, 50, and 100 mg/kg) significantly ameliorated cholestasis-induced oxidative stress in renal tissue. Renal histopathological changes, including interstitial inflammation, tubular atrophy, fibrosis, and cast formation, were detected in the BDL rats. Moreover, urine pro-inflammatory cytokines [interleukin (IL)-1, IL-9, IL-18, tumor necrosis factor α (TNF-α), and interferon γ (INF-γ)] were significantly increased in the cholestatic animals. PTX (10, 50, and 100 mg/kg, 14 days) significantly ameliorated renal histopathological alterations and urine levels of inflammatory cytokines. Conclusions These data indicate a potential nephroprotective role for PTX in cholestasis. The effects of PTX on oxidative stress parameters and the inflammatory response could play a primary role in its renoprotective mechanisms.

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“…This represents mitochondrial function as a key mechanism in the pathogenesis of this complication (Figure 7). Recently, we tested different safe and clinically applicable agents with antioxidant and mitochondrial protecting agents in various experimental models or patients with renal disorders (5,42,91,(137)(138)(139). Some of these compounds even underwent clinical trials for different types of renal injury and nephropathy.…”

Section: Treatments Glomerular Damage Tubular Damage Inflammationmentioning

confidence: 99%

Mitochondrial Impairment and Oxidative Stress Are Essential Mechanisms Involved in the Pathogenesis of Acute Kidney Injury

Rezaei,

Honarpishefard,

Ghaderi

et al. 2023

jrenhep

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Acute kidney injury (AKI) is an emergency condition that requires restrictive and appropriate clinical interventions. Identifying mechanisms of organ injury is a critical step in developing clinical interventions. Unilateral ureter obstruction (UUO) is widely used as an animal model for investigating AKI. The current study was designed to evaluate the role of mitochondrial impairment and oxidative stress in the pathogenesis of renal injury in UUO model. Mice underwent UUO surgery. Then, kidney tissue histopathological changes, plasma biomarkers of renal injury, oxidative stress, and different renal mitochondrial indices were evaluated at scheduled time intervals (3, 7, 14, and 21 days after UUO surgical procedure). Significant increase in plasma creatinine and blood urea nitrogen levels was evident in UUO mice. The UUO surgery induced severe kidney tissue histopathological alterations, including necrosis, severe tubular atrophy, and interstitial inflammation. Moreover, kidney biomarkers of oxidative stress included reactive oxygen species formation, lipid peroxidation, protein carbonylation, decreased glutathione reservoirs (GSH), and increased oxidized glutathione (GSSG) observed in UUO mice. On the other hand, significant mitochondrial depolarization, decreased mitochondrial dehydrogenases activity, mitochondrial permeabilization, and decreased adenosine triphosphate and GSH/GSSG levels were discovered in mitochondria isolated from the kidneys of UUO mice. The data obtained from the current study demonstrated a pivotal and interconnected role for oxidative stress and mitochondrial dysfunction in the pathogenesis of renal injury in UUO model. Therefore, these directions could serve as therapeutic targets in animal models or patients of acute renal failure.

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<p>Curcumin Supplementation Alleviates Polymyxin E-Induced Nephrotoxicity</p>

Cited by 12 publications

References 47 publications

Mitochondrial dysfunction and oxidative stress are involved in the mechanism of tramadol-induced renal injury

Mitochondrial dysfunction and oxidative stress are involved in the mechanism of tramadol-induced renal injury

Pentoxifylline mitigates cholestasis-related cholemic nephropathy

Mitochondrial Impairment and Oxidative Stress Are Essential Mechanisms Involved in the Pathogenesis of Acute Kidney Injury

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