Folia morphologica · 2026
Effects of asprosin on high-fat diet-induced liver injury in rats: a histopathological, immunohistochemical, and molecular study.
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Karadeniz Saygili Suna, Akcilar Raziye
Аннотация
BACKGROUND: Asprosin, a fasting-induced hormone, regulates glucose metabolism. Recent studies suggest that it modulates cellular stress, but its role in high-fat diet (HF)-induced liver damage is unknown. This study examined the histological, immunohistochemical, and molecular effects of asprosin on HF-induced liver injury in rats, focusing on oxidative stress and apoptosis.
MATERIALS AND METHODS: Twenty-eight male Sprague-Dawley rats were randomly assigned to four groups: control (Group C), asprosin-treated (Group A), high-fat diet group (Group HF), and high-fat diet with asprosin treatment group (Group HF+A). A high-fat emulsion was administered orally for 8 weeks to establish the HF model, followed by intraperitoneal administration of recombinant asprosin (1 μg/kg/day) during the final 10 days. Liver tissues were collected for histological analysis using hematoxylin-eosin (H&E), Masson's trichrome (MT), and periodic acid-Schiff (PAS) staining. Immunohistochemical expression of Nrf2, HO-1, and caspase-3 was assessed using the H-score method, and gene expression was evaluated by quantitative real-time PCR. Statistical analysis was performed using one-way analysis of variance (one-way ANOVA) followed by Tukey's post hoc test.
RESULTS: Rats in Group HF showed marked hepatic steatosis, increased collagen deposition, and reduced glycogen content. In Group HF+A, asprosin treatment reduced steatosis and collagen accumulation. Compared with Group HF, Group HF+A exhibited significantly increased hepatic Nrf2 and HO-1 expression and decreased caspase-3 expression (p < 0.05).
CONCLUSIONS: Asprosin attenuates oxidative stress and apoptosis in HF-induced liver injury, as supported by morphological, immunohistochemical, and molecular findings, suggesting a potential protective role against diet-related metabolic stress.
MATERIALS AND METHODS: Twenty-eight male Sprague-Dawley rats were randomly assigned to four groups: control (Group C), asprosin-treated (Group A), high-fat diet group (Group HF), and high-fat diet with asprosin treatment group (Group HF+A). A high-fat emulsion was administered orally for 8 weeks to establish the HF model, followed by intraperitoneal administration of recombinant asprosin (1 μg/kg/day) during the final 10 days. Liver tissues were collected for histological analysis using hematoxylin-eosin (H&E), Masson's trichrome (MT), and periodic acid-Schiff (PAS) staining. Immunohistochemical expression of Nrf2, HO-1, and caspase-3 was assessed using the H-score method, and gene expression was evaluated by quantitative real-time PCR. Statistical analysis was performed using one-way analysis of variance (one-way ANOVA) followed by Tukey's post hoc test.
RESULTS: Rats in Group HF showed marked hepatic steatosis, increased collagen deposition, and reduced glycogen content. In Group HF+A, asprosin treatment reduced steatosis and collagen accumulation. Compared with Group HF, Group HF+A exhibited significantly increased hepatic Nrf2 and HO-1 expression and decreased caspase-3 expression (p < 0.05).
CONCLUSIONS: Asprosin attenuates oxidative stress and apoptosis in HF-induced liver injury, as supported by morphological, immunohistochemical, and molecular findings, suggesting a potential protective role against diet-related metabolic stress.