ArticlePharmaceuticals (Basel, Switzerland)2022
Candesartan Attenuates Cisplatin-Induced Lung Injury by Modulating Oxidative Stress, Inflammation, and TLR-4/NF-κB, JAK1/STAT3, and Nrf2/HO-1 Signaling.
Article in Pharmaceuticals (Basel, Switzerland), 2022. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 14 papers.
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Who cites it
14 citing papers in PubMed, 29 citations in OpenAlex.
- Obeticholic Acid and Edaravone Protect Against Cisplatin-Induced Hepatotoxicity Through Modulation of Keap1/Nrf2/ARE, TNF-α/NF-κB, and AKT/GSK-3β Pathways.Journal of biochemical and molecular toxicology · 2026Article
- The protective effects of naringin against cisplatin-induced pulmonary toxicity in rats: Insights into the modulation of ER stress and SIRT1/Nrf2 pathway.BMC complementary medicine and therapies · 2026Article
- Effects of candesartan on cellular redox status and bioenergetics of cardiac tissue in normal and chronically stressed rats.Frontiers in pharmacology · 2026Article
- Amelioration of cisplatin-induced myocardial injury by nanocurcumin through antioxidant, anti-inflammatory, and calcium regulatory mechanisms.Journal of molecular histology · 2025Article
- Candesartan preserves aortic structure and function in cisplatin-treated rats by upregulating SIRT1/Nrf2/HO-1 signaling and suppressing oxidative stress, TLR-4/NF-κB signaling, and necroptosis.Frontiers in pharmacology · 2025Article
- Article
- 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
- Rosmarinic acid protects against cyclophosphamide-induced hepatotoxicity via inhibition of oxidative stress, inflammation, and apoptosis and upregulation of Nrf2 in mice.Journal of molecular histology · 2024Article
- Trace elements and metal nanoparticles: mechanistic approaches to mitigating chemotherapy-induced toxicity-a review of literature evidence.Biometals : an international journal on the role of metal ions in biology, biochemistry, and medicine · 2024Review
- Exploring Candesartan, an angiotensin II receptor antagonist, as a novel inhibitor of NLRP3 inflammasome: alleviating inflammation in Neisseria gonorrhoeae infection.BMC infectious diseases · 2024Article
- High-throughput screening-based design of multifunctional natural polyphenol nano-vesicles to accelerate diabetic wound healing.Journal of nanobiotechnology · 2024Article
- Drug-Induced Pulmonary Fibrosis: National Database Analysis.Biomedicines · 2024Article
- Regulation of toll-like receptor (TLR) signaling pathways in atherosclerosis: from mechanisms to targeted therapeutics.Acta pharmacologica Sinica · 2023Review
- Azithromycin Mitigates Cisplatin-Induced Lung Oxidative Stress, Inflammation and Necroptosis by Upregulating SIRT1, PPARγ, and Nrf2/HO-1 Signaling.Pharmaceuticals (Basel, Switzerland) · 2022Article
Corrections and comments
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Authors and funding
9 authors at 7 institutions in 3 countries.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Cisplatin (CIS) is an effective chemotherapeutic agent against different cancers. The use of CIS is associated with acute lung injury (ALI) and other adverse effects, and oxidative stress and inflammation were implicated in its toxic effects. Candesartan (CAN), an angiotensin II (Ang II) receptor blocker, showed beneficial effects against oxidative stress and inflammation. Therefore, this study investigated the potential of CAN to prevent CIS-induced oxidative stress, inflammation, and lung injury in rats, pointing to the involvement of TLR4/NF-κB, JAK1/STAT3, PPARγ, and Nrf2/HO-1 signaling. The rats received CAN (5 mg/kg) for 10 days and were challenged with a single dose of CIS (7 mg/kg) on day 7. CIS caused injury to the alveoli and the bronchial tree, increased lipid peroxidation, nitric oxide, myeloperoxidase, TLR-4, NF-κB p65, iNOS, TNF-α, IL-6, IL-1β, and caspase-3, and decreased cellular antioxidants and IL-6 in the lungs of rats. CAN effectively prevented tissue injury, suppressed TLR-4/ NF-κB signaling, and ameliorated oxidative stress, inflammatory markers, and caspase-3 in CIS-administered rats. CAN enhanced antioxidants and IL-10, decreased Ang II, increased Ang (1-7), suppressed the phosphorylation of JAK1 and STAT3, and upregulated SOCS3 in CIS-administered rats. These effects were associated with the downregulation of Keap1 and enhanced Nrf2, GCLC, HO-1, and PPARγ. In conclusion, CAN prevented CIS-induced lung injury by attenuating oxidative stress, suppressing TLR-4/NF-κB and JAK1/STAT3 signaling, Ang II, and pro-inflammatory mediators, and upregulating PPARγ, and Nrf2/HO-1 signaling.
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