Veterinary journal (London, England : 1997) · 2026
Analysis of pathological histochemical characteristics of yak pancreas induced by Fasciola hepatica.
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Qie Xiaolong, Yuan Ligang, Chen Guojuan, Li Haijun, Zhou Yonghan
Аннотация
The purpose of this study was to identify the morphological features of Fasciola hepatica in yaks, compare the pancreatic pathological changes between normal and infected yaks, and analyze the distribution and expression patterns of insulin, glucagon, ERα, and ERβ, thereby providing basis for clinical diagnosis from pathological damage on pancreatic function. The types and characteristics of Fasciola hepatica were identified by using phalloidin staining and scanning electron microscopy (SEM). Transmission electron microscopy (TEM), hematoxylin-eosin (H&E) and periodic acid-Schiff (PAS) staining were performed to compare tissue structural differences and glycogen distribution between the normal group (NG) and the infection group (IG). Blood glucose concentrations were measured and compared in yaks from both groups. Furthermore, the distribution, localization, and protein expression levels of insulin, glucagon, ERα, and ERβ were analyzed by immunohistochemical staining, double immunofluorescence labeling and Western blotting. The results showed that the parasite was confirmed as Fasciola hepatica based on morphological features. Compared with the NG, the IG exhibited pancreatic tissue inflammatory necrosis, islet atrophy, interstitial hyperplasia, reduced glycogen storage, and elevated blood glucose concentration. The protein expression levels of insulin, glucagon, ERα, and ERβ in the IG were extremely significant difference (P < 0.01). Our results indicate that the Fasciola hepatica infection in yaks induces pancreatic inflammation and damage, leading to decreased glycogen synthesis and increased blood glucose concentration; the insulin and glucagon exert antagonistic effects with increased secretions; and the insulin stimulation causing the expression of ERα/ERβ enhanced which further promotes insulin release and induces metabolic insulin resistance (IR).