Ameliorative effects of myricetin nanoparticles on carbon tetrachloride-induced spermatogenic dysfunction in mice.
TL;DR
It is suggested that myricetin nanoparticles confer partial amelioration on testicular tissue under systemic stress conditions, probably by preserving gene expression critical for spermatogenesis.
Abstract
Environmental toxins like carbon tetrachloride (CCl4) induce systemic oxidative stress, which can severely impair testicular function and spermatogenesis. Myricetin is a potent antioxidant, although its bioavailability is limited. Nanoformulation may enhance its absorption and effectiveness. This study evaluated the therapeutic potential of myricetin nanoparticles on CCl4-induced testicular damage. Twenty-four adult male C57BL/6 mice were divided into four groups: Sham, CCl4-induced liver injury model, empty nanoparticle, and myricetin nanoparticle treatment (25 mg/kg). Testicular histology was assessed using Johnsen's scoring, and the gene expression of TDRD5, CLCN2, and MORC1 was measured via Real-Time PCR. CCl4 treatment significantly reduced seminiferous tubule diameter (115 ± 18 vs. 188.3 ± 17.1 µm), Johnsen's score (5 ± 0 vs. 8.3 ± 1.2), and expression of spermatogenesis-related genes compared to the Sham group. Myricetin nanoparticle treatment partially ameliorated these effects, with preserved TDRD5 expression relative to sham and a less pronounced reduction in CLCN2 and MORC1 levels (p < 0.05). These findings suggest that myricetin nanoparticles confer partial amelioration on testicular tissue under systemic stress conditions, probably by preserving gene expression critical for spermatogenesis.