The intensive broiler farming model has accelerated the development of the poultry farming industry. However, it has also inevitably brought about many stressors that lead to oxidative stress in the organism. The intestine is the leading site of nutrient digestion, absorption, and metabolism, as well as a secretory and immune organ. Oxidative stress in animal production can harm the intestine, potentially leading to significant losses for the farming industry. Under conditions of oxidative stress, many free radicals are produced in the animal’s body, attacking the intestinal mucosal tissues and destroying the barrier integrity of the intestinal tract, leading to disease. Recently, herbs have been shown to have a favorable safety profile and promising application in improving intestinal oxidative stress in poultry. Therefore, future in-depth studies on the specific mechanisms of herbs and their extracts for treating intestinal oxidative stress can provide a theoretical basis for the clinical application of herbs and new therapeutic options for intestinal oxidative stress injury during poultry farming. This review focuses on the causes and hazards of oxidative stress in the intestinal tract of poultry, and on herbs and their extracts with therapeutic potential, to provide a reference for developing and applying new antioxidants.

Bisphenol A (BPA), extensively utilized in the manufacture of epoxy resins and polycarbonate plastics, is prevalent in the environment. Its exposure has been associated with an increased risk of hepatic lesions; however, the underlying mechanisms and the spectrum of its effects remain poorly understood. This study investigates the role of the Keap1-Nrf2 signaling pathway in regulating BPA-induced hepatotoxicity in vivo using a rat model. Over a 30-day period, rats were orally administered either corn oil or BPA (0.5, 5, and 50 mg/kg). Changes in hepatic and kidney histology were assessed via transmission electron microscopy and HE staining. Oxidative stress levels in the liver tissue and serum were quantified, while the mRNA expression of Nrf2, Keap1, GPX2, HO-1, and caspase-3 was evaluated using qRT-PCR. Additionally, the expression of Nrf2 and cleaved caspase-3 in the liver tissue was measured through immunohistochemistry and Western blotting. Results indicated that BPA exposure significantly reduced the liver and adrenal coefficients in the treated rats compared to controls. Notable histomorphological alterations were observed in the liver and kidney tissues of the BPA-treated rats. The serum levels of GOT and TNF-α were significantly elevated in the BPA group relative to the controls. Evidence of oxidative stress was supported by increased malondialdehyde levels and decreased total superoxide dismutase activity in the liver and kidney, alongside a reduction in glutathione peroxidase activity in the liver tissue. Furthermore, BPA exposure enhanced the mRNA expression levels of Nrf2, Keap1, GPX2, HO-1, and caspase-3 in the liver tissue. Concurrently, Nrf2 and cleaved caspase-3 expression levels were elevated in the BPA-treated group compared to the controls. These findings suggest that BPA may contribute to metabolic disorders of liver function and poses a hepatotoxicity risk. Moreover, the activation of the Keap1-Nrf2 pathway may offer protective effects against hepatotoxicity, with potential implications for human liver disease.

Bisphenol A (BPA), a widespread environmental contaminant used in plastics and resins, poses significant health risks due to its endocrine-disrupting properties and potential for inducing intestinal toxicity. This study explored the toxicological effects of BPA on the small intestine of rats, focusing on the duodenum, jejunum, and ileum. Histopathological evaluation revealed that the duodenum experienced the most severe structural damage, including villous atrophy, epithelial shedding, and mitochondrial degeneration. BPA exposure disrupted oxidative stress homeostasis by reducing superoxide dismutase activity and increasing malondialdehyde levels, along with upregulating antioxidant-related genes like GPX2 and HO-1 upregulated, indicating lipid peroxidation and oxidative damage. Inflammatory markers such as IL-1 and NFκB were significantly upregulated, highlighting an active inflammatory response and epithelial cell apoptosis. BPA also altered lipid metabolism, with increased expression of lipogenic genes such as SREBP-1c and FAS, indicating metabolic dysregulation. Fecal microbiota analysis revealed reduced α-diversity, enrichment of pathogenic taxa like Escherichia-Shigella, and depletion of beneficial genera such as Lachnospiraceae NK4A136 group, exacerbating gut inflammation and barrier dysfunction. These findings suggest that BPA-induced small intestinal damage is driven by oxidative stress, inflammation, and gut dysbiosis, with the duodenum and jejunum being the more vulnerable segments.

The study investigated the effects of microencapsulated essential oils (MEO) on the growth performance, diarrhea, and intestinal microenvironment of weaned piglets. The 120 thirty-day-old weaned piglets (Duroc × Landrace × Yorkshire, 8.15 ± 0.07 kg) were randomly divided into four groups and were fed with a basal diet (CON) or CON diet containing 300 (L-MEO), 500 (M-MEO), and 700 (H-MEO) mg/kg MEO, respectively, and data related to performance were measured. The results revealed that MEO supplementation increased the ADG and ADFI in weaned piglets (p < 0.05) compared with CON, and reduced diarrhea rates in nursery pigs (p < 0.05). MEO supplementation significantly increased the duodenum’s V:C ratio and the jejunal villi height of weaned piglets (p < 0.05). The addition of MEO significantly increased the T-AOC activity in the jejunum of piglets (p < 0.05), but only L-MEO decreased the MDA concentration (p < 0.01). H-MEO group significantly increases the content of isobutyric acid (p < 0.05) in the piglet colon, but it does not affect the content of other acids. In addition, MEO supplementation improved appetite in the nursery and increased the diversity and abundance of beneficial bacteria in the intestinal microbiome. In conclusion, these findings indicated that MEO supplementation improves growth and intestinal health in weaned piglets.

This investigation evaluates the impact of the EOB on chicken growth performance, meat quality, and lipid metabolism. Two hundred and fifty-six one-day-old, white-feathered broilers were randomly allocated to four groups. Each group was subdivided into eight replicates, each with eight unsexed chicks, including the control group (CON), EOB₁₅₀, EOB₂₅₀, and EOB₃₅₀, with 0, 150, 250, and 350 mg/L of the EOB added to the drinking water, respectively. The expression levels of genes associated with antioxidants and lipid metabolism were analyzed using real-time polymerase chain reaction (RT-PCR). Additionally, the FA profile of the breast muscle was determined using gas chromatography. The data displayed that those birds in the EOB₂₅₀ group had a higher breast muscle index compared to the CON group. The breast meat in the EOB groups showed that there is increased yellowness, water holding capacity (WHC), and polyunsaturated fatty acids (PUFAs), while cooking losses, drip losses, and saturated fatty acids (SFAs) were reduced compared to the CON. The application of supplements for the EOB₂₅₀ and EOB₃₅₀ groups increased antioxidant indices as well as the expression of antioxidant-related genes in the liver and muscles. However, these groups decreased the concentrations of triglycerides (TG), total cholesterol (TC), and low-density lipoprotein (LDL-C) in serum and liver compared to the EOB₁₅₀ and CON groups. These EOB groups downregulated expression of some genes linked to liver FA synthesis and elevated the expressions of lipid β-oxidation-related genes compared to the CON. It can be concluded that the supplementation with 250 mg/L of the EOB has the potential as an alternative water additive in the broiler industry.

The high concentration of particulate matter (PM) in broiler houses seriously endangers the biological safety of broilers and causes low growth performance, deserving more attention. This study aimed to investigate the effects of PM collected from a broiler house on the lung and systemic inflammatory responses and liver lipid anabolic process in broilers. Broilers were systemically exposed to fresh air (control) and 4 mg·m⁻³ and 8 mg·m⁻³ total suspended particles (TSP). Lung, liver, and serum were sampled after 7 (E7) and 14 (E14) days of PM exposure and 7 days after self-recovery (R 7). Corresponding kits were used to assay the inflammatory cytokines and serum biochemical indicators. The expression levels of genes related to lipid metabolism were detected by real-time polymerase chain reaction (RT-PCR) assay. The results showed a significant decrease in the average daily gain in broilers for 7 days of PM exposure (p < 0.05) and clear lung and liver inflammations in PM groups. In addition, upregulation of lung interleukin (IL)-1β and IL-8 and serum low-density lipoprotein cholesterol (LDL-C) and triglyceride (TG) occurred after 7 days of PM exposure (p < 0.05), and upregulation of lung serum tumor necrosis factor (TNF)-α and cholesterol (CHOL) occurred after 14 days of PM exposure (p < 0.05). A decrease in serum total antioxidant capacity (T-AOC) and glutathione peroxidase (GSH-px) levels was found after 14 days of PM exposure (p < 0.05), and the GSH-px level was maintained until 7 days after cessation of exposure (p < 0.05). Seven days after cessation of exposure, the expression levels of 3-hydroxy-3-methylglutaryl-CoA synthase 2 (Hmgcs2) and fatty acid synthase (Fas) genes significantly increased (p < 0.05) and decreased (p < 0.05), respectively. These results demonstrate that exposure to PM in broiler houses can induce systemic inflammation and dyslipidemia through local pulmonary inflammation and also exert toxic effects on the liver by disturbing the expression of genes involved in the hepatic lipid anabolic process.