ArticleFood science & nutrition2021
Inhibition of oxidative stress and apoptosis by camel milk mitigates cyclosporine-induced nephrotoxicity: Targeting Nrf2/HO-1 and AKT/eNOS/NO pathways.
Article in Food science & nutrition, 2021. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 16 papers.
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Who cites it
16 citing papers in PubMed, 27 citations in OpenAlex.
- NRF2/SLC7A11/GPX4 Antioxidant Axis Suppression by Camel Milk Whey Protein Sensitizes MCF-7 Breast Cancer Cells to Cisplatin.International journal of molecular sciences · 2026Article
- Camel Milk and Its Bioactive Components in Diseases Associated with Aging: A Narrative Review.Nutrients · 2026Review
- Amelioration of 5-Fluorouracil-Induced Hepatorenal Toxicity by Epigallocatechin Gallate-Functionalized Selenium Nanoparticles: A Multi-Targeted Protective Approach.International journal of molecular sciences · 2026Article
- From Cheese Whey to Functional Ingredients: Upcycling Whey Proteins for Cardiovascular and Immunomodulatory Health-Evidence Mapping and Perspectives from Portugal.Foods (Basel, Switzerland) · 2026Review
- Targeting lipocalin-2 in atherosclerosis: biological functions, pathogenic mechanisms, and therapeutic potential.Frontiers in cardiovascular medicine · 2026Review
- Non-Bovine Milk as Functional Foods with Focus on Their Antioxidant and Anti-Inflammatory Bioactivities.Antioxidants (Basel, Switzerland) · 2025Review
- The spatiotemporal and paradoxical roles of NRF2 in renal toxicity and kidney diseases.Redox biology · 2025Review
- A bibliometric analysis of six decades of camel research in North Africa: Trends, collaboration, and emerging themes.Open veterinary journal · 2024Article
- NOX1-mediated oxidative stress induces chondrocyte ferroptosis by inhibiting the Nrf2/HO-1 pathway.Scientific reports · 2024Article
- Targeting JAK2/STAT3, NLRP3/Caspase-1, and PK2/PKR2 Pathways with Arbutin Ameliorates Lead Acetate-Induced Testicular Injury in Rats.Pharmaceuticals (Basel, Switzerland) · 2024Article
- Cyclosporine-induced kidney damage was halted by sitagliptin and hesperidin via increasing Nrf2 and suppressing TNF-α, NF-κB, and Bax.Scientific reports · 2024Article
- Camel milk ameliorates diabetes in pigs by preventing oxidative stress, inflammation and enhancing beta cell function.Journal of diabetes and metabolic disorders · 2022Article
- Protective effect of quercetin on kidney diseases: From chemistry to herbal medicines.Frontiers in pharmacology · 2022Review
- Extracellular cyclophilins A and C induce dysfunction of pancreatic microendothelial cells.Frontiers in physiology · 2022Article
- Modulatory effect of camel milk on intestinal microbiota of mice with non-alcoholic fatty liver disease.Frontiers in nutrition · 2022Article
- Inhibition of oxidative stress and apoptosis by camel milk mitigates cyclosporine-induced nephrotoxicity: Targeting Nrf2/HO-1 and AKT/eNOS/NO pathways.Food science & nutrition · 2021Article
Corrections and comments
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Authors and funding
6 authors at 5 institutions in 2 countries.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Cyclosporine (CsA) is a widely used immunosuppressive agent that incurs marked nephrotoxicity in the clinical setting. Thus, there is a need for finding safe/effective agents that can attenuate CsA-induced kidney injury. Meanwhile, the underlying mechanisms for CsA-associated nephrotoxicity are inadequately investigated, in particular, the AKT/eNOS/NO pathway. Here, the present work aimed to explore the potential of camel milk, a natural product with distinguished antioxidant/anti-inflammatory actions, to ameliorate CsA-induced nephrotoxicity in rats. The molecular mechanisms related to renal oxidative aberrations and apoptosis were studied, including Nrf2/HO-1 and AKT/eNOS/NO pathways. The kidney tissues were inspected using histopathology, ELISA, Western blotting, and immunohistochemistry. The present findings demonstrated that camel milk (10 ml/kg) significantly lowered creatine, BUN, and NGAL nephrotoxicity markers and the aberrant histopathology, with similar efficacy to the reference quercetin. Moreover, camel milk suppressed the renal oxidative stress, as evidenced by significantly lowering NOX-1 and lipid peroxides and significantly augmenting the renal antioxidant moieties (GSH, GPx, and SOD), thereby, driving the restoration of Nrf2/HO-1 pathway. Meanwhile, camel milk counteracted the pro-apoptotic reactions by significantly lowering Bax protein expression, caspase-3 activity/cleavage, and PARP cleavage, alongside significantly increasing the expression of the proliferation signal PCNA. Regarding the anti-apoptotic AKT/eNOS/NO pathway, camel milk activated its signaling by significantly increasing the protein expression of PI3Kp110, p-AKT(Ser473)/total AKT, and p-eNOS (Ser1177)/total eNOS besides significantly boosting the renoprotective NO levels. In conclusion, these findings reveal that camel milk may be a promising candidate for the alleviation of CsA-induced nephrotoxicity.
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Read under generation 80e0d062 · epoch 390. Bibliography from PubMed, PubMed Central and OpenAlex; grants from NIH RePORTER; trial links from ClinicalTrials.gov; estimates, votes and beliefs from the OpenQuestion graph.