ArticlePharmaceuticals (Basel, Switzerland)2023
TLR4/Inflammasomes Cross-Talk and Pyroptosis Contribute to N-Acetyl Cysteine and Chlorogenic Acid Protection against Cisplatin-Induced Nephrotoxicity.
Article in Pharmaceuticals (Basel, Switzerland), 2023. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 17 papers.
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Who cites it
17 citing papers in PubMed, 27 citations in OpenAlex.
- HMGB1/NF-κB Axis, IL-8, and Cuproptosis Contribute to Cisplatin-Induced Testicular Injury: Protective Potential Effect of Thymol.Biomolecules · 2025Article
- Cuproptosis Contributes to Cisplatin-Induced Nephrotoxicity: Insights into Thymol's Potential Inhibitory and Protective Effects.Pharmaceuticals (Basel, Switzerland) · 2025Article
- Article
- Sitagliptin Mitigates Diabetic Cardiomyopathy Through Oxidative Stress Reduction and Suppression of VEGF and FLT-1 Expression in Rats.Biomolecules · 2025Article
- Morin hydrate protects against cisplatin-induced testicular toxicity by modulating ferroptosis and steroidogenesis genes' expression and upregulating Nrf2/Heme oxygenase-1.Scientific reports · 2025Article
- Dibenzazepine, a γ-Secretase Enzyme Inhibitor, Protects Against Doxorubicin-Induced Cardiotoxicity by Suppressing NF-κB, iNOS, and Hes1/Hey1 Expression.Inflammation · 2025Article
- Ameliorative Effect of N-Acetylcysteine Against 5-Fluorouracil-Induced Cardiotoxicity via Targeting TLR4/NF-κB and Nrf2/HO-1 Pathways.Medicina (Kaunas, Lithuania) · 2025Article
- Cardamom extract alleviates tamoxifen-induced liver damage by suppressing inflammation and pyroptosis pathway.Scientific reports · 2025Article
- Tamarix honey phenolics attenuate cisplatin-induced kidney toxicity by inhibition of inflammation mediated IL-6/STAT3/TNF-α and oxidative stress-dependent Nrf2/caspase-3 apoptotic signaling pathways.Frontiers in pharmacology · 2025Article
- Pharmacological advances of the chlorogenic acids family: current insights and future research directions.Frontiers in pharmacology · 2025Review
- Advances in ginsenoside treatment for common kidney diseases: pharmacological evaluation and potential mechanisms.Frontiers in pharmacology · 2025Review
- Imidacloprid exposure in rats induces cardiac inflammatory response through activating TLR4/NF-κB/NLRP3 and JAK/STAT signaling pathways: focus on the berberine-loaded nanoliposomes.Frontiers in toxicology · 2025Article
- Thymol Protects against 5-Fluorouracil-Induced Hepatotoxicity via the Regulation of the Akt/GSK-3β Pathway in In Vivo and In Silico Experimental Models.Pharmaceuticals (Basel, Switzerland) · 2024Article
- Effect of N-Acetylcysteine on Cisplatin Toxicity: A Review of the Literature.Biologics : targets & therapy · 2024Review
- Alcohol-induced liver injury in signalling pathways and curcumin's therapeutic potential.Toxicology reports · 2023Review
- The Protective Effect ofMolecules (Basel, Switzerland) · 2023Article
- Protective effects of N-acetyl-l-cysteine against penconazole-triggered hepatorenal toxicity in adult rats.Journal of veterinary research · 2023Article
Corrections and comments
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Authors and funding
7 authors at 3 institutions in 2 countries.
Funding
Abstract
backgroundCisplatin (Cp) is an antineoplastic agent with a dose-limiting nephrotoxicity. Cp-induced nephrotoxicity is characterized by the interplay of oxidative stress, inflammation, and apoptosis. Toll-4 receptors (TLR4) and NLPR3 inflammasome are pattern-recognition receptors responsible for activating inflammatory responses and are assigned to play a significant role with gasdermin (GSDMD) in acute kidney injuries. N-acetylcysteine (NAC) and chlorogenic acid (CGA) have documented nephroprotective effects by suppressing oxidative and inflammatory pathways. Therefore, the current study aimed to investigate the contribution of the upregulation of TLR4/inflammasomes/gasdermin signaling to Cp-induced nephrotoxicity and their modulation by NAC or CGA.
methodsA single injection of Cp (7 mg/kg, i.p.) was given to Wistar rats. Rats received either NAC (250 mg/kg, p.o.) and/or CGA (20 mg/kg, p.o.) one week before and after the Cp injection.
resultsCp-induced acute nephrotoxicity was evident by the increased blood urea nitrogen and serum creatinine and histopathological insults. Additionally, nephrotoxicity was associated with increased lipid peroxidation, reduced antioxidants, and elevated levels of inflammatory markers (NF-κB and TNF-α) in the kidney tissues. Moreover, Cp upregulated both TLR4/NLPR3/interleukin-1beta (IL-1β) and caspase-1/GSDMD-signaling pathways, accompanied by an increased Bax/BCL-2 ratio, indicating an inflammatory-mediated apoptosis. Both NAC and/or CGA significantly corrected these changes.
conclusionsThis study emphasizes that inhibition of TLR4/NLPR3/IL-1β/GSDMD might be a novel mechanism of the nephroprotective effects of NAC or CGA against Cp-induced nephrotoxicity in rats.
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