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Background
Porcine epidemic diarrhea virus (PEDV) is a highly contagious viral pathogen responsible for porcine epidemic diarrhea (PED), a severe enteric disease that affects pigs worldwide. The virus primarily infects epithelial cells in the small intestine, leading to severe diarrhea, dehydration, and high mortality rates, particularly in piglets. The global pig industry has experienced substantial economic losses due to PED outbreaks [1]. PEDV replication induces significant cellular stress, triggering inflammatory responses in epithelial cells and disrupting the integrity of the intestinal barrier [2]. Additionally, PEDV activates apoptotic pathways, leading to the loss of functional intestinal epithelial cells and further compromising intestinal integrity and function. The resulting villous atrophy impairs nutrient absorption and exacerbates fluid and electrolyte malabsorption, thereby worsening symptoms such as diarrhea and dehydration [3]. To mitigate the impact of PEDV, pig farms have adopted enhanced biosecurity measures and immunization strategies to bolster the resilience of pig populations against the virus [4]. However, PEDV’s high genetic variability and the limited duration of immune protection following vaccination present ongoing challenges for disease prevention and control.
Plant polysaccharides are large molecular compounds abundantly found in plants and are the principal water-soluble active constituents in traditional Chinese herbal decoctions. Poria cocos, commonly known as "Fuling" in China, is an edible medicinal mushroom derived from the dried sclerotium of polypore fungi. This fungus contains various bioactive compounds, including polysaccharides, triterpenoids, sterols, amino acids, choline, histidine, and potassium salts. Notably, Poria cocos polysaccharides (PCP), which constitute 70%–90% of the dry weight of Poria cocos, are recognized as its primary active ingredient [5]. PCP exhibits diverse biological activities, including immunomodulation, anti-inflammatory, antioxidant, and antiviral properties, suggesting potential therapeutic applications [5]. Previous research has indicated that PCP can modulate gastrointestinal function, strengthen the intestinal physical, immune, and microbial barriers [6], and alleviate cisplatin-induced intestinal damage and inflammation [7]. Moreover, PCP has been shown to facilitate intestinal mucosal repair by modulating the TLR and JNK signaling pathways, providing relief from clinical symptoms associated with functional dyspepsia [8]. Given these findings, we hypothesize that PCP may exert beneficial effects on intestinal damage caused by PEDV infection in piglets. Therefore, this study aimed to investigate this hypothesis and elucidate the underlying mechanisms.
Materials and methods
Animal experiments
Eighteen 7-day-old crossbred (Duroc ×...