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Simple Summary: Weaning is a challenging stage for piglets, involving sudden changes in diet, environment, and social interactions, which place stress on their digestive and immune systems. In commercial pig farming, early weaning often leads to immature gut development, making piglets more vulnerable to health issues like post-weaning diarrhoea. This review discusses natural dietary nutrient strategies to help piglets transition smoothly through weaning without relying on antimicrobials. Lowering crude protein in piglet diets can reduce undigested proteins in the gut, which helps prevent harmful bacteria from causing digestive problems. Adding organic acids to the diet helps maintain a healthy stomach pH, improves digestion, and supports a balanced gut microbiome. Another approach is to boost gut health with butyrate, a beneficial compound that reduces inflammation and protects the gut lining. Butyrate can be provided directly or encouraged naturally by promoting beneficial gut bacteria. These strategies present promising approaches to enhancing piglet health during weaning, although further research is necessary to achieve consistent outcomes. Combining these strategies may provide an effective solution to improving growth, gut health, and the overall sustainability of post-weaned pig production. Weaning in piglets presents significant physiological and immunological challenges, including gut dysbiosis and increased susceptibility to post-weaning diarrhoea (PWD). Abrupt dietary, environmental, and social changes during this period disrupt the intestinal barrier and microbiota, often necessitating antimicrobial use. Sustainable dietary strategies are critical to addressing these issues while reducing reliance on antimicrobials. Reducing dietary crude protein mitigates the availability of undigested proteins for pathogenic bacteria, lowering harmful by-products like ammonia and branched-chain fatty acids, which exacerbate dysbiosis. Organic acid supplementation improves gastric acidification, nutrient absorption, and microbial balance, while also serving as an energy-efficient alternative to traditional grain preservation methods. Increasing intestinal butyrate, a key short-chain fatty acid with anti-inflammatory and gut-protective properties, is particularly promising. Butyrate strengthens intestinal barrier integrity by upregulating tight junction proteins, reduces inflammation by modulating cytokine responses, and promotes anaerobic microbial stability. Exogenous butyrate supplementation via salts provides immediate benefits, while endogenous stimulation through prebiotics (e.g., resistant starch) and probiotics promotes sustained butyrate production. These interventions selectively enhance butyrate-producing bacteria such as Roseburia and Faecalibacterium prausnitzii, further stabilising the gut microbiota. Integrating these strategies can enhance gut integrity, microbial resilience, and immune responses in weaned piglets. Their combination offers a sustainable, antimicrobial-free approach to improving health and productivity in modern pig production systems. [ABSTRACT FROM AUTHOR]

Magnolia officinalis Rehder & E.H. Wilson is traditionally used in the treatment of gastrointestinal disorders, diarrhea, and cough. Its main active ingredient, magnolol, exhibits protective effects on the lungs and gastrointestinal tract, including the inhibition of inflammation in these organs. This work aims to explore the molecular mechanism by which magnolol suppressed Chronic obstructive pulmonary disease (COPD) intestinal damage by improving the intestinal epithelial barrier. The study focused on investigating the mitigation effect of magnolol on intestinal injury and epithelial barrier in a COPD rat. Caco-2 cells were induced with TNF-α or IL-1β to establish the barrier injury model in order to explore the direct protective effect of magnolol on the intestinal barrier and elucidate the molecular mechanism by which it activates peroxisome proliferators-activated receptors-γ (PPARγ). Magnolol significantly improves pulmonary function and tissue damage in COPD rats by inhibiting inflammation, protease imbalance, and oxidative stress. It also suppresses colon tissue damage and inflammation, and protects colon epithelial barrier function by suppressing the decline of tight junction proteins, reducing colon epithelial permeability. In Caco-2 cells, magnolol directly reduces monolayer permeability, increases TEER, and upregulates tight junction protein expression induced by TNF-α or IL-1β. Drug Affinity Responsive Target Stability (DARTS) and thermal shift assays show that magnolol effectively binds to SRC, activating PPARγ signaling in Caco-2 cells and colon tissues of COPD rats. Furthermore, magnolol enhances the binding of PPARγ and RXRα, promoting their activation and entry into the nucleus. The PPARγ inhibitor GW9662 can reverse the effects of magnolol on PPARγ activation and tight junction protein upregulation in IL-1β or TNF-α induced Caco-2 cells. This work demonstrates that magnolol enhances lung and intestinal functions in COPD rats, and elucidates its mechanism of action in protecting the intestinal epithelial barrier by activating PPARγ. [Display omitted] [ABSTRACT FROM AUTHOR]