This study assessed the possible protective role of green synthesized zinc oxide nanoparticles using Moringa olifera leaf extract (MO-ZNPs) in acrylamide (ACR)-induced reproductive dysfunctions in ...male rats. ACR (20 mg/kg b.wt/day) and/or MO-ZNPs (10 mg/kg b.wt/day) were given orally by gastric gavage for 60 days. Then, sperm parameters; testicular enzymes; oxidative stress markers; reproductive hormones including testosterone, luteinizing hormone (LH)-estradiol, and follicle-stimulating hormone (FSH) concentration; testis histology; steroidogenesis-related gene expression; and apoptotic markers were examined. The findings revealed that MO-ZNPs significantly ameliorated the ACR-induced decline in the gonadosomatic index and altered the pituitary-gonadal axis, reflected by decreased serum testosterone and FSH with increased estradiol and LH, and sperm analysis disruption. Furthermore, a notable restoration of the tissue content of antioxidants (catalase and reduced glutathione) but depletion of malondialdehyde was evident in MO-ZNPs+ACR-treated rats compared to ACR-exposed ones. In addition, MO-ZNPs oral dosing markedly rescued the histopathological changes and apoptotic caspase-3 reactions in the testis resulting from ACR exposure. Furthermore, in MO-ZNPs+ACR-treated rats, ACR-induced downregulation of testicular steroidogenesis genes and proliferating cell nuclear antigen (PCNA) immune-expression were reversed. Conclusively, MO-ZNPs protected male rats from ACR-induced reproductive toxicity by suppressing oxidative injury and apoptosis while boosting steroidogenesis and sex hormones.
Olive leaves are traditionally used in the Mediterranean basin in many medical conditions for its potent antioxidant activity. Cyclosporine A, a well-known immunosuppressant, can induce ...nephrotoxicity through oxidative stress. This study investigated the effect of olive leaf extract (OLE) on cyclosporine-induced nephrotoxicity in rats.
Thirty Wistar rats (180 g to 200 g) were classified into 5 groups, each containing 6 rats. The first group received normal saline and served as control. The second group was treated with cyclosporine, 25 mg/kg for 21 days for nephrotoxicity induction. Groups 3 to 5 were treated with cyclosporine, 25 mg/kg in addition to different doses of OLE (40 mg/kg, 80 mg/kg, and 120 mg/kg), respectively, for 21 days. After 21 days, the rats' body weights were recorded and the rats were sacrificed. Blood samples were collected and the animals were necropsied. Both kidneys were removed, one for histopathological and one for antioxidant activity evaluations.
Cyclosporine significantly reduced body weight and kidney weight; serum total protein, albumin, and sodium levels; and renal glutathione peroxidase, catalase, and superoxide dismutase. It also increased serum urea, creatinine, and calcium levels as compared to the control group. Groups 4 and 5 showed a significantly greater body weight and kidney weight; higher serum sodium, total protein, and albumin levels; greater glutathione peroxidase, catalase, and superoxide dismutase; and lower serum urea, creatinine, and calcium levels as compared to group 2.
Treatment with OLE can alleviate cyclosporine-induced nephrotoxicity when used in a proper dose.
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