Article detail · 2024
Magnolin alleviates cyclophosphamide-induced oxidative stress, inflammation, and apoptosis via Nrf2/HO-1 signaling pathway
- Year
- 2024
- Type
- article
Data source split
- YÖKSİS YÖKSİS article record
- YÖKSİS venue Toxicology Research
- Catalog match (ISSN) Toxicology Research
- OpenAlex OpenAlex enrichment (abstract, citations, topics)
Abstract
OpenAlex · English
Abstract In the present study, we investigated the protective effect of magnolin (MAG) against oxidative stress induced by cyclophosphamide (CP) and its role in the Nrf2/HO-1 signaling pathway. Rats were administered MAG (1 mg/kg, i.p.) for 14 days and CP (75 mg/kg, i.p.) on the 14th day. CP administration increased tissue damage, as evidenced by elevated levels of transaminases (aspartate and alanine), alkaline phosphatase, and renal parameters (blood urea nitrogen and creatinine). Additionally, 8-hydroxy-2′-deoxyguanosine and malondialdehyde levels were increased, whereas glutathione levels, along with catalase and superoxide dismutase activities, decreased in CP-treated rats. CP also down-regulated the expression of Bcl-2, HO-1, Nrf2, and NQO-1, while up-regulating Bax, Cas-3, TNF-α, Cox-2, iNOS, IL-6, IL-1β, and NFκB in liver and kidney tissues. In addition, CP treatment caused histopathological changes in heart, lung, liver, kidney, brain, and testis tissues. Treatment with MAG improved biochemical and oxidative stress parameters and prevented histopathological changes in CP-treated rats. Moreover, MAG suppressed the expression of inflammatory cytokines and apoptosis markers. In conclusion, MAG effectively prevented CP-induced toxicity by reducing oxidative stress, inflammation, and apoptosis, with its protective efficacy associated with the up-regulation of Nrf2/HO-1 signaling.
Topics
Citations
OpenAlex cited_by_count. Not a WoS or Scopus citation count; those sources have no separate column here.
23 citations
OpenAlex cited_by_count (cache / database)
20 publications in the local catalog that cite this work (OpenAlex reference match; not the full global list).
- Syringaldehyde Mitigates Cyclophosphamide‐Induced Liver and Kidney Toxicity in Mice by Inhibiting Oxidative Stress, Inflammation, and Apoptosis Through Modulation of the Nrf2/HO‐1/NFκB Pathway 2025
- Syringaldehyde Mitigates Cyclophosphamide‐Induced Liver and Kidney Toxicity in Mice by Inhibiting Oxidative Stress, Inflammation, and Apoptosis Through Modulation of the Nrf2/HO‐1/NFκB Pathway 2025
- Syringaldehyde Mitigates Cyclophosphamide‐Induced Liver and Kidney Toxicity in Mice by Inhibiting Oxidative Stress, Inflammation, and Apoptosis Through Modulation of the Nrf2/HO‐1/NFκB Pathway 2025
- Iristectorin A Ameliorates Cisplatin‐Induced Hepatorenal Injury in Mice Through Modulation of the Nrf2/HO‐1 Signaling Pathway 2025
- Spinosin Alleviates Cyclophosphamide‐Induced Oxidative Stress, Inflammation, and Apoptosis in Liver and Kidney Injury in Mice 2025
- Spinosin Alleviates Cyclophosphamide‐Induced Oxidative Stress, Inflammation, and Apoptosis in Liver and Kidney Injury in Mice 2025
- Iristectorin A Ameliorates Cisplatin‐Induced Hepatorenal Injury in Mice Through Modulation of the Nrf2/HO‐1 Signaling Pathway 2025
- Spinosin Alleviates Cyclophosphamide‐Induced Oxidative Stress, Inflammation, and Apoptosis in Liver and Kidney Injury in Mice 2025
- Iristectorin A Ameliorates Cisplatin‐Induced Hepatorenal Injury in Mice Through Modulation of the Nrf2/HO‐1 Signaling Pathway 2025
- Obtusifolin improves cisplatin-induced hepatonephrotoxicity via the Nrf2/HO-1 signaling pathway 2025