Abstract
Coccidiosis, caused by Eimeria tenella, leads to severe intestinal damage, growth retardation, and significant economic losses in poultry. Drug resistance in conventional anticoccidial treatments has prompted exploration of herbal extracts, with S. flavescens showing promise due to its anti-inflammatory and antiparasitic properties. This study assessed the anticoccidial efficacy of S. flavescens aqueous extract (SFAE) and its modulation of the MAPK signaling pathway in MDBK cells and white-feathered broilers, using four groups: negative control (NC), E. tenella infection (PC), infection + SFAE (PC+SF), and infection + diclazuril (PC+DC). In vivo, compared to the NC group, PC group broilers exhibited significant bloody diarrhea, cecal lesions, and reduced survival (83 %; p < 0.01). The PC+SF group achieved an anticoccidial index of 162.8, with reduced lesions (p < 0.01) and normalized weight gain by day 6 (p > 0.05). HE staining revealed significant villus shedding and inflammation in the PC group (p < 0.01), while the PC+SF group showed intact villi and reduced inflammation (p < 0.01). In vitro, SFAE (10 mg/mL) had no significant effect on MDBK cell viability (p > 0.05). Compared to the NC group, PC group MDBK cells displayed increased p38 and MEK phosphorylation (p < 0.01), which was significantly reduced in the PC+SF group (p < 0.01), with no difference from NC by day 10 (p > 0.05). Serum ELISA showed significantly elevated IL-1β, IL-6, and TNF-α and reduced IL-10 in the PC group (p < 0.01), while the PC+SF group demonstrated highly significant downregulation of pro-inflammatory cytokines and upregulated IL-10 (p < 0.01), with levels comparable to NC by days 6 and 10 (p > 0.05). In vivo qPCR and Western blot analyses confirmed that MAPK pathway components (ERK, MEK, JNK, Raf1, p38) were highly significantly upregulated in the PC group (p < 0.01), which were significantly reduced in the PC+SF group (p < 0.01), ultimately showing no significant difference from the NC group by day 10 (p > 0.05). SFAE effectively mitigates E. tenella-induced damage by suppressing MAPK signaling and inflammation, suggesting its potential as an anticoccidial agent.