Transport stress affects the animal's metabolism and psychological state. As a pro-survival pathway, the heat shock response (HSR) protects healthy cells from stressors. However, it is unclear whether the HSR plays a role in transport stress-induced heart damage. To evaluate the effects of transport stress on heart damage and HSR protection, newly hatched chicks were treated with transport stress for 2 h, 4 h and 8 h. Transport stress caused decreases in body weight and increases in serum creatine kinase (CK) activity, nitric oxide (NO) content in heart tissue, cardiac nitric oxide syntheses (NOS) activity and NOS isoforms transcription. The mRNA expression of heat shock factors (HSFs, including HSF1-3) and heat shock proteins (HSPs, including HSP25, HSP40, HSP47, HSP60, HSP70, HSP90 and HSP110) in the heart of 2 h transport-treated chicks was upregulated. After 8 h of transport stress in chicks, the transcription levels of the same HSPs and HSF2 were reduced in the heart. It was also found that the changes in the HSP60, HSP70 and HSP90 protein levels had similar tendencies. These results suggested that transport stress augmented NO generation through enhancing the activity of NOS and the transcription of NOS isoforms. Therefore, this study provides new evidence that transport stress induces heart damage in the newly hatched chicks by blocking the cytoprotective HSR and augmenting NO production.
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.
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, 8 h, respectively. Subsequently, to further investigated 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 PGC1α/SIRT1/AMPK pathway. Moreover, APS treatment regulated the level of PPARα and 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 PGC1α/ SIRT1/ AMPK/ PPARα/ PPARγ signaling system.
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