Currently, cage housing is regarded as a global mainstream production system for laying hens. However, limited living space and confinement of birds in cages cause welfare and health problems, such as feather pecking, osteoporosis, obesity, and premature aging. Many studies have been conducted to alleviate layer welfare problems by providing farm environmental enrichments such as litter, sand, alfalfa bales, chick papers, pecking stones, pecking strings, perches, slopes, elevated platforms, aviaries and outdoor access with a trend towards complex enrichments. The provision of appropriate enrichments continuously attracts layers towards pecking, foraging, dust bathing, and locomotion, thereby giving lifelong benefits to laying hens. Hence, raising chicks and pullets under such conditions may reduce feather and skin damage, as well as accumulation of abdominal fat, and improve several biological features such as health, productivity, quality products, and docility of laying hens. Therefore, providing enrichment during the first few days of the layer’s life without any interruption is crucial. In addition, due to different farm conditions, environmental enrichment should be managed by well-trained farm staff. For example, in preventing feather pecking among the birds, litter materials for foraging are superior to dust bath materials or new items. However, a limited supply of litter creates competition and challenges among birds. Therefore, providing farm environmental enrichment for layers requires proper handling, especially in commercial layer farms. Hence, improving the welfare of chicks and pullets through optimizing on-farm environmental enrichments is essential for production systems practicing cage housing.

Lipopolysaccharide (LPS) is an endotoxin that can cause an imbalance between the oxidation and antioxidant defense systems and then induces hepatic damages. Ferulic acid (FA) has multiple biological functions including antibacterial and antioxidant activities; however, the effect of FA on lipopolysaccharide-induced hepatic injury remains unknown. The purpose of this study was to investigate the mechanism of action of dietary Ferulic acid against Lipopolysaccharide-induced hepatic injuries in Tianfu broiler chickens. The results showed that supplementation of FA in daily feed increased body weight (BW) and decreased the feed conversion ratio (FCR) in LPS treatment broilers significantly (p < 0.05). Additionally, supplement of FA alleviated histological changes and apoptosis of hepatocytes in LPS treatment broilers. Supplement of FA significantly decreases the activities of ROS. Interestingly, the levels of antioxidant parameters including total superoxide dismutase (T-SOD), total antioxidant capacity (T-AOC), and glutathione (GSH) in LPS group were significantly increased by the FA supplementation (p < 0.05). Nevertheless, administration of LPS to broilers decreased the expressions of Nrf2, NQO1, SOD, GSH-Px, CAT and Bcl-2, whereas it increased the expressions of Bax and Caspase-3 (p < 0.05). Moreover, the expressions of Nrf2, NQO1, SOD, CAT, Bcl-2 were significantly upregulated and Caspase-3 were significantly downregulated in the FL group when compared to LPS group (p < 0.05). In conclusion, supplementation of FA in daily feed improves growth performance and alleviates LPS-induced oxidative stress, histopathologic changes, and apoptosis of hepatocytes in Tianfu broilers.

Aristolochic acid (AA) is a component of traditional Chinese herbs and commonly used for farm animals in China. Over-exposure of AA has been proven to be associated with hepatotoxicity; however, the mechanism of action of AA-I-induced hepatotoxicity remains unknown. In the current study, a subchronic toxicity test was conducted to evaluate the mechanism of AA-induced hepatotoxicity in Tianfu broilers. According to the results, AA-I-induced hepatotoxicity in Tianfu broilers was evidenced by the elevation of liver weight, levels of serum glutamic oxalacetic transaminase (GOT) and glutamic-pyruvic transaminase (GPT). Furthermore, hepatocyte swelling, vesicular degeneration and steatosis were observed. Additionally, AA-I elevated the production of reactive oxygen species (ROS) and induced oxidative stress, which further led to excessive apoptosis, characterized by mitochondrial depolarization, upregulation of Bax, and down-regulation of Bcl-2 expression. In conclusion, the mechanism of AA-I-induced hepatotoxicity was associated with oxidative-stress-mediated apoptosis and mitochondrial damage.