Dual‐Pathway Defense: Ultramicro‐Pulverised Powder of <i>Polygonum chinense</i> L. and <i>Atractylodes rhizome</i> (PAUP) Rescues Broilers From <i>E. coli</i> ‐Triggered Liver Injury Through Modulation of Oxidative Stress and Inflammation

This study characterizes the composition and blood components of ultramicro-pulverized <i>Polygonum chinense</i> <i>L</i>. and <i>Atractylodes rhizome</i> powder (PAUP) and investigates its protective mechanisms against <i>Escherichia coli</i> (<i>E. coli</i>)-induced liver injury in broilers. PAUP constituents and serum metabolites were profiled by ultra-high-performance liquid chromatography-mass spectrometry (UPLC-MS). Fourteen-day-old broilers were randomly divided into 6 groups: control, <i>E. coli</i> model, gentamicin, and PAUP high/medium/low-dose groups. Broilers were infected with 10¹⁰ CFU/mL <i>E. coli</i> O157:H7 via intraperitoneal injection. PAUP was administered 4 h post-<i>E. coli</i> infection for 7 days by gavage. Then, serum and liver samples from half of the chicks in each group were collected for further analysis. Recovery groups were analyzed after 7 additional days. UPLC-MS identified 718 PAUP components, predominantly lipid, flavonoids, acids, and oxides. Serum metabolomics revealed 130 significantly elevated metabolites in PAUP groups, including atractylenolide I, linoleic acid, araliadiol, baicalin, gallocatechin, atractylodin, etc. PAUP normalized weight gain, reduced feed conversion ratio (FCR), and liver index in <i>E. coli</i> <i>-</i>infected broilers. It significantly decreased bacterial load, suppressed serum AST and TBA levels, and relieved liver histopathological damage. Furthermore, PAUP restored redox balance (increased GSH activity, decreased MDA and ROS levels) via Nrf2-HO-1 pathway actvation (increased protein levels of Nrf2, Keap1, NQO1 and HO-1). PAUP obviously attenuated inflammation (decreased IL-6 and TNF-α) through TLR4/NF-κB inhibition. PAUP mitigates <i>E. coli</i>-induced liver injury through Nrf2/HO-1-mediated antioxidant activation and TLR4/NF-κB inflammatory suppression.