Deoxynivalenol (DON), also known as vomitoxin, is a mycotoxin that can cause antifeeding and vomiting in animals. However, the mechanism of DON inducing anorexia is complicated. Studies have shown that intestinal hormones play a significant part in the anorexia caused by DON. We adopted the “modeling of acute antifeeding in mice” as the basic experimental model, and used two methods of gavage and intraperitoneal injection to explore the effect of intestinal hormones on the antifeedant response induced by DON in mice. We found that 1 and 2.5 mg/kg·bw of DON can acutely induce anorexia and increase the plasma intestinal hormones CCK, PYY, GIP, and GLP-1 in mice within 3 h. Direct injection of exogenous intestinal hormones CCK, PYY, GIP, and GLP-1 can trigger anorexia behavior in mice. Furthermore, the PYY receptor antagonist JNJ-31020028, GLP-1 receptor antagonist Exendin(9-39), CCK receptor antagonist Proglumide, GIP receptor antagonist GIP(3-30)NH₂ attenuated both intestinal hormone and DON-induced anorectic responses. These results indicate that intestinal hormones play a critical role in the anorexia response induced by DON.

Cd34+Pdgfra+Telocytes (CPTCs) are interstitial stromal cells implicated in long-distance intercellular communication, yet their role in bridging the distin

Fascia serves as both a mechanical scaffold and a progenitor cell reservoir critical for wound healing and tissue regeneration. This study developed an In Situ Induced Fascial Analogue (iFA) via low-growth-factor Matrigel injection into mouse subcutaneous fascia, using silicone as a control. At 14 days, histological and ultrastructural analyses showed that the iFA possessed an organized collagen architecture comparable to native fascia, distinct from the dense fibrous capsules in controls. qPCR and immunofluorescence revealed a pro-reparative macrophage-associated microenvironment characterized by increased CD206 expression and demonstrated the enrichment of CD34⁺/PDGFRα⁺ co-expressing telocytes (TCs) within the iFA, consistent with their characteristic molecular and ultrastructural features. Ex vivo assays demonstrated cell migratory activity, and in vivo wound healing assays showed that iFA-derived cells significantly accelerated wound closure and re-epithelialization. This study established a structurally biomimetic fascial analogue enriched with CD34⁺/PDGFRα⁺ TCs that avoids pathological fibrosis, providing a novel in situ engineering strategy for generating fascia-like tissues and a platform for future regenerative research.