Ellagic acid inhibits proinflammatory intermediary manufacture by suppressing NF-κB/Akt, VEGF and activating Nrf-2/Caspase-3 signaling pathways in rat testicular damage: a new way for testicular damage cure and in silico approach.
Abdullah AslanOzlem GokSeda BeyazHarun UsluFazilet ErmanOrhan ErmanSerpil BaspinarPublished in: Toxicology mechanisms and methods (2022)
Ellagic acid (EA) has protective effect on testicular damage and this natural compound decreases oxidative damage. The present study aims to examine the preventive effect of ellagic acid (EA) against carbon tetrachloride (CCl 4 )-induced testicular tissue damage in rats. In testicular tissue, tumor necrosis factor-α (TNF-α), Nuclear factor erythroid-2 related factor 2 (Nrf-2), B-cell lymphoma-2 (Bcl-2), vascular endothelial growth factor (VEGF), Nuclear factor-kappa B (NF-κB), cysteine aspartic proteases (caspase-3) and protein kinase B (Akt) synthesis levels were analyzed by western blot method, reactive oxygen species (ROS) was measured by malondialdehyde (MDA) levels, Glutathione (GSH) level and catalase (CAT) by spectrophotometer. As a result, in comparison with the CCl 4 group, caspase-3 and Nrf-2 protein synthesis levels increased in EA + CCl 4 group, however, VEGF, Bcl-2, NF-κB, TNF-α and Akt protein synthesis levels decreased, EA application raised GSH levels and CAT activity, reduced MDA levels. In this study, in silico tools were applied to confirm the activity of EA against the cancer with macromolecules such as the above mentioned transcription factors. EA, turned out to show significant activity similarly to some cocrystal ligands, particularly against cancer. These results points out that EA can be used as a testicular damage cure drug in future.
Keyphrases
- nuclear factor
- oxidative stress
- signaling pathway
- vascular endothelial growth factor
- toll like receptor
- induced apoptosis
- germ cell
- liver injury
- reactive oxygen species
- endothelial cells
- diabetic rats
- cell death
- pi k akt
- rheumatoid arthritis
- drug induced
- cell proliferation
- transcription factor
- emergency department
- epithelial mesenchymal transition
- protein kinase
- fluorescent probe
- lps induced
- squamous cell carcinoma
- breast cancer cells
- molecular dynamics simulations
- single molecule
- south africa
- dna binding
- squamous cell
- adverse drug