Gallic acid attenuates torsion/detorsion-induced testicular injury in rats through suppressing of HMGB1/NF-κB axis and endoplasmic reticulum stress.
Selim DemirIlke Onur KazazGokcen KerimogluNihal Turkmen AlemdarFatih ColakTugba AriciAhmet MenteseYuksel AliyaziciogluPublished in: Revista internacional de andrologia (2024)
It was aimed to evaluate whether gallic acid (GA) have a beneficial effect in the testicular ischemia/reperfusion injury (IRI) model in rats for the first time. Testicular malondialdehyde, 8-hydroxy-2'-deoxyguanosine, superoxide dismutase, catalase, high mobility group box 1 protein, nuclear factor kappa B, tumor necrosis factoralpha, interleukin-6, myeloperoxidase, 78-kDa glucose-regulated protein, activating transcription factor 6, CCAAT-enhancer-binding protein homologous protein and caspase-3 levels were determined using colorimetric methods. The oxidative stress, inflammation, endoplasmic reticulum stress and apoptosis levels increased statistically significantly in the IRI group compared with the sham operated group ( p < 0.05). GA application improved these damage significantly ( p < 0.05). Moreover, it was found that the results of histological examinations supported the biochemical results to a statistically significant extent. Our findings suggested that GA may be evaluated as a protective agent against testicular IRI.
Keyphrases
- metabolic syndrome
- endoplasmic reticulum stress
- induced apoptosis
- oxidative stress
- binding protein
- nuclear factor
- transcription factor
- ischemia reperfusion injury
- pet ct
- diabetic rats
- signaling pathway
- germ cell
- toll like receptor
- dna damage
- gold nanoparticles
- hydrogen peroxide
- cell death
- adipose tissue
- clinical trial
- high glucose
- dna binding
- heat shock protein
- nitric oxide
- sensitive detection
- inflammatory response
- dna repair
- double blind
- stress induced
- skeletal muscle
- immune response