ArticleCurrent research in pharmacology and drug discovery2020
Suppression of cirrhosis-related renal injury by N-acetyl cysteine.
Article in Current research in pharmacology and drug discovery, 2020. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 12 papers.
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Who cites it
12 citing papers in PubMed, 23 citations in OpenAlex.
- Sitagliptin protects against bile duct ligation-induced cholemic nephropathy in male rats through modulation of inflammation, sestrin2, and the Nrf2/SOD pathway.Research in pharmaceutical sciences · 2026Article
- Sildenafil blunts cholestasis-associated cholemic nephropathy in a rat model of bile duct ligation.Clinical and experimental hepatology · 2025Article
- Bile cast nephropathy: A systematic review of case reports and case series.World journal of hepatology · 2025Article
- Potential of oligonucleotide- and protein/peptide-based therapeutics in the management of toxicant/stressor-induced diseases.Naunyn-Schmiedeberg's archives of pharmacology · 2024Review
- Cirrhosis-induced oxidative stress in erythrocytes: The therapeutic potential of taurine.Clinical and experimental hepatology · 2023Article
- The effects of N-acetylcysteine on hepatic, hematologic, and renal parameters in cirrhotic patients: a randomized controlled trial.Gastroenterology and hepatology from bed to bench · 2023Article
- Cellular and mitochondrial taurine depletion in bile duct ligated rats: a justification for taurine supplementation in cholestasis/cirrhosis.Clinical and experimental hepatology · 2022Article
- Pentoxifylline mitigates cholestasis-related cholemic nephropathy.Clinical and experimental hepatology · 2021Article
- The activation of nuclear factor-E2-related factor 2 (Nrf2)/heme oxygenase-1 (HO-1) signaling blunts cholestasis-induced liver and kidney injury.Toxicology research · 2021Article
- Taurine mitigates bile duct obstruction-associated cholemic nephropathy: effect on oxidative stress and mitochondrial parameters.Clinical and experimental hepatology · 2021Article
- Mitochondrial dysfunction and oxidative stress are involved in the mechanism of tramadol-induced renal injury.Current research in pharmacology and drug discovery · 2021Article
- The Role of Mitochondrial Impairment and Oxidative Stress in the Pathogenesis of Lithium-Induced Reproductive Toxicity in Male Mice.Frontiers in veterinary science · 2021Article
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Authors and funding
6 authors at 3 institutions in 2 countries.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Cirrhosis-induced renal injury or cholemic nephropathy (CN) is a serious clinical complication with poor prognosis. CN could finally lead to renal failure and the need for organ transplantation. Unfortunately, there is no specific pharmacological intervention against CN to date. On the other hand, various studies mentioned the role of oxidative stress and mitochondrial impairment in the pathogenesis of CN. The current study aimed to evaluate the potential protective effects of NAC as a thiol-reducing agent and antioxidant in CN. Bile duct ligation (BDL) was used as a reliable animal model of cholestasis. BDL animals received NAC (0.25% and 1% w: v) in drinking water for 28 consecutive days. Finally, urine, blood, and kidney samples were collected and analyzed. Significant elevation in serum biomarkers of renal injury, along with urine markers of kidney damage, was evident in the BDL group. Moreover, markers of oxidative stress, including reactive oxygen species (ROS) formation, lipid peroxidation, protein carbonylation, and increased oxidized glutathione (GSSG) were evident detected in the kidney of cholestatic rats. Renal tissue antioxidant capacity and reduced glutathione (GSH) were also significantly depleted in the BDL group. Significant mitochondrial depolarization, depleted ATP content, and mitochondrial permeabilization was also detected in mitochondria isolated from the kidney of cholestatic animals. Renal histopathological alterations consisted of significant tissue fibrosis, interstitial inflammation, and tubular atrophy. It was found that NAC (0.25 and 1% in drinking water for 28 consecutive days) blunted histopathological changes, decreased markers of oxidative stress, and improved mitochondrial indices in the kidney of cirrhotic rats. Moreover, serum and urine biomarkers of renal injury were also mitigated in upon NAC treatment. These data indicate a potential renoprotective role for NAC in cholestasis. The effects of NAC on cellular redox state and mitochondrial function seem to play a fundamental role in its renoprotective effects during CN.
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