The antioxidant and anti-apoptotic potential of Pleurotus eryngii extract and its chitosan-loaded nanoparticles against doxorubicin-induced testicular toxicity in male rats.
Elif Erdem GüzelNalan Kaya TektemurAhmet TektemurHilal AcayAyfer YildirimPublished in: Andrologia (2021)
This study was conducted to evaluate the protective role of Pleurotus eryngii extract (PE) and Pleurotus eryngii extract-loaded chitosan nanoparticles (PE-CSNP) against doxorubicin (DOX)-induced testicular toxicity in rats. Male rats were divided into six groups: control (DMSO/ethanol), PE (200 mg/kg PE), PE-CSNP (30 mg/kg PE-CSNP), DOX (10 mg/kg DOX, a single dose, i.p), DOX+PE (10 mg/kg DOX+200 mg/kg PE) and DOX+PE-CSNP (10 mg/kg DOX+30 mg/kg PE-CSNP). PE and PE-CSNP were administered by oral gavage every other day for 21 days. DOX-treated rats showed histopathological impairment compared with the control group. There was an increase in the apoptotic index, caspase 3 (CASP3), BCL2-associated X apoptosis regulator (BAX), dynamin-related protein 1 (DRP1) expression and total oxidative status (TOS) in the DOX group, while mitofusin-2 (MFN2), total antioxidative status (TAS) and serum testosterone levels of the DOX group reduced when compared with the other groups. PE and PE-CSNP treatments provided significant protection against DOX-induced oxidative stress by reducing TOS levels and increasing TAS levels. CASP3, BAX, apoptotic index and DRP1-MFN2 expressions were restored by PE and PE-CSNP. However, the PE-CSNP showed higher antioxidant and anti-apoptotic efficacy compared with PE. Thus, our results provide evidence that CSNP and PE could synergistically have a potent antioxidant and anti-apoptotic therapy against DOX-induced testicular damage in male rats.
Keyphrases
- oxidative stress
- anti inflammatory
- cell death
- drug delivery
- diabetic rats
- mesenchymal stem cells
- cancer therapy
- cell proliferation
- risk assessment
- wound healing
- endoplasmic reticulum stress
- endothelial cells
- nitric oxide
- signaling pathway
- long non coding rna
- cell therapy
- cell cycle arrest
- replacement therapy
- binding protein