NAFLD negatively affects the testicular redox system and HSP and TP expression, disrupting male fertility potential. In contrast, HP-treated rats showed a marked effect on NAFLD-induced damage by improving testicular anti-oxidant status and regulating the expression of HSPs and TP proteins. These findings suggest a potential therapeutic role for HP in safeguarding male fertility against the damaging effects of NAFLD.

The study divided rats into four groups: control, a group subjected to a high-fat diet (HFD) to induce NAFLD without supplementation, and two HFD-induced NAFLD groups receiving HP doses (20 and 300 mg/kg). After 70 days, the testicular total anti-oxidant capacity (TAC), malondialdehyde (MDA), glutathione (GSH), glutathione disulfide (GSSG), HSP70-2a, HSP90 expression, and TP mRNA levels were assessed.

The results showed that HFD-induced NAFLD significantly increased GSH and MDA levels and disrupted the GSH/GSSG ratio (P<0.05) while also reducing HSP70-2a, HSP90, TP1, and TP2 expression (P<0.05). However, HP administration effectively restored testicular redox balance, reduced oxidative stress, and enhanced these protective proteins' expression compared to HFD (P<0.05).