Astragalus polysaccharide mitigates transport stress-induced hepatic metabolic stress via improving hepatic glucolipid metabolism in chicks.

In the modern poultry industry, newly hatched chicks are unavoidably transported from the hatching to the rearing foster. Stress caused by multiple physical and psychological stressors during transportation is particularly harmful to the liver. Astragalus polysaccharide (APS) possesses multiple benefits against hepatic metabolic disorders. Given that transport stress could disturb hepatic glucolipid metabolism and the role of APS in metabolic regulation, we speculated that APS could antagonize transport stress-induced disorder of hepatic glucolipid metabolism. Firstly, newly hatched chicks were transported for 0, 2, 4, and 8 h, respectively. Subsequently, to further investigate the effects of APS on transport stress-induced hepatic glucolipid metabolism disturbance, chicks were pretreated with water or APS and then subjected to transport treatment. Our study suggested that APS could relieve transport stress-induced lipid deposition in liver. Meanwhile, transport stress also induced disturbances in glucose metabolism, reflected by augmented mRNA expression of key molecules in gluconeogenesis and glycogenolysis. Surprisingly, APS could simultaneously alleviate these alterations via peroxisome proliferator-activated receptor gamma coactivator 1 alpha (PGC-1α)/Sirtuin 1 (SIRT1)/AMP-activated protein kinase (AMPK) pathway. Moreover, APS treatment regulated the level of peroxisome proliferator-activated receptor alpha (PPARα) and peroxisome proliferator-activated receptor gamma (PPARγ), thereby alleviating transport stress-induced alterations of VLDL synthesis, cholesterol metabolism, lipid oxidation, synthesis, and transport-related molecules. These findings indicated that APS could prevent the potential against transport stress-induced hepatic glucolipid metabolism disorders via PGC-1α/SIRT1/AMPK/PPARα/PPARγ signaling system.

In the modern poultry industry, newly hatched chicks are unavoidably transported from the hatching to the rearing foster. During transportation, chicks are frequently subjected to various physical and psychological stressors, which can lead to alterations in blood composition, hormones, metabolites, enzymes, and behavior. These alterations adversely affect animal health and welfare. Stress caused by transportation is especially harmful to liver, which can cause significant effects on liver function, and disturb hepatic lipid metabolism and glucose metabolic. The current study demonstrated that Astragalus polysaccharide (APS) possesses multiple benefits against hepatic metabolic disorders. Administration of APS to chicks before transport could prevent transport-induced stress and hepatic glucolipid metabolism disorders.

Astragalus polysaccharide alleviates transport stress-induced heart injury in newly hatched chicks via ERS-UPR-autophagy dependent pathway.

Transport stress (TS) not only affects animal welfare but also eventually leads to higher morbidity and mortality. Moreover, TS could induce heart injury in animals, but the possible mechanism has yet to be fully explored. Astragalus polysaccharide (APS) is a main active component of Radix Astragali, which has an extensive anti-stress effect. However, the effect of APS on TS-induced heart injury has not yet been elucidated. In this study, a chick model of simulated TS was used. 240 newly hatched chicks were arranged into 4 groups: Control (Con), Transport group (T), Transport + water group (TW), and Transport + APS group (TA). Before transport, the chicks of the TW and TA groups were treated with deionized water and APS (0.25 mg/mL, 100 µL) by oral drops respectively. The histopathological analysis of myocardial tissue was assessed by hematoxylin and eosin staining. qRT-PCR and Western Blotting assays were employed to measure the expression of genes and proteins. Semiquantitative PCR was performed for the X box-binding protein-1 (XBP-1) mRNA splicing assay. The results indicated that APS significantly reduced TS-induced myocardial histopathological changes. Meanwhile, TS induced endoplasmic reticulum stress (ERS), evidenced by an activation of the unfolded protein response (UPR) signaling pathway and up-regulation of ERS-markers (P < 0.05). Moreover, TS markedly triggered autophagy induction by activating AMP-activated protein kinase (AMPK), reflected by augmented LC3-II/LC3-I, AMPK phosphorylation and autophagy-related genes (ATGs) expression (P < 0.05). Importantly, our study manifested that treatment of APS could reduce TS-induced ERS and AMPK-activated autophagy, accordingly alleviating heart injury of transported chicks. In summary, these findings indicate that TS induces heart injury in chicks via an ERS-UPR-autophagy-dependent pathway, and APS as an effective therapeutic method to alleviate it.

Transport Stress Induced Cardiac NO-NOS Disorder Is Mitigated by Activating Nrf2/HO-1/NQO1 Antioxidant Defense Response in Newly Hatched Chicks.

With the development of the intensive poultry industry, the health problems of chickens caused by transportation have attracted more and more attention. Transport stress reduces performance, immune function, and meat quality in chicks, which has become one of the most important factors that endanger the development of the poultry industry. Currently, studies on the effects of transport stress have mainly focused on the performance of livestock and poultry to be slaughtered. However, the effects of transport stress on heart damage and oxidative stress in newborn chicks have not been reported. In this study, we selected newborn chicks as the object. This study was intended to explore the effects of transport stress on the heart damage of newly hatched chicks. The findings suggested that transport stress could cause oxidative stress in the hearts of newly hatched chicks by increasing the levels of malondialdehyde (MDA), hydrogen peroxide (H2O2) and decreasing the contents of Total antioxidant capacity (T-AOC), and the activities of antioxidant enzymes (SOD), together with increasing the activities of antioxidant enzymes (Catalase (CAT) and Glutathione S-transferase (GST)). Transport stress disrupted the balance between oxidation and antioxidant systems. The Nrf2 signaling pathway was activated by transport stress and triggered the transcription of antioxidant signaling. In short, transport stress-induced nitric oxide (NO)-nitric oxide synthases (NOS) system metabolic disorders and cardiac oxidative stress are mitigated by activating the nuclear factor-erythroid 2-related factor 2 (Nrf2)/heme oxygenase-1 (HO-1)/NAD(P)H quinone oxidoreductase-1 (NQO1) antioxidant defense response in newly hatched chicks.