In this study, endoplasmic reticulum (ER) stress inducer tunicamycin (TM) and inhibitor 4-phenylbutyric acid (4-PBA) were used to treat postmortem chicken breast muscle to investigate changes in tenderness and effects on apoptosis and autophagy during 5 days ageing. TM-induced ER stress reduced shear force, enhanced myofibril fragmentation index (MFI), disrupted myofibril structure, increased desmin degradation, and activated μ-calpain and caspase-12. In addition, TM-induced ER stress increased the expression of Bax, Bim, and cytochrome c, and decreased the expression of Bcl-xL. Furthermore, TM-induced ER stress improved the conversion of LC3I to LC3II, raised the expression of Beclin-1, and decreased the expression of p62, PI3K, and mTOR. The opposite results were observed after 4-PBA treatment. These results suggested that ER stress could improve chicken tenderness, promote apoptosis and autophagy during chicken postmortem ageing.

Quercetin compounds have antioxidant, anti-inflammatory and anticancer pharmacological functions. Longterm exposure to acrylamide (AA) can cause liver injury and endanger human health. However, whether quercetin compounds can attenuate AA-induced liver injury and the specific mechanism are not clear. Here, we studied the mechanism and structure-activity relationship of quercetin compounds in reducing AA-induced hepatotoxicity in vivo and in vitro. In vivo studies found that quercetin-like compounds protect against AA-induced liver injury by reducing oxidative stress levels, activating the Akt/mTOR signaling pathway to attenuate autophagy, and improving mitochondrial apoptosis and endoplasmic reticulum stress-mediated apoptosis. In vitro studies found that quercetin compounds protected HepG2 cells from AA by attenuating the activation of AA-induced autophagy, lowering reactive oxygen species (ROS) levels by exerting antioxidant effects and thus attenuating oxidative stress, increasing mitochondrial membrane potential (MMP), and improving apoptosis-related proteins, thus attenuating AA-induced apoptosis. Furthermore, the conformational differences between quercetin compounds correlated with their protective capacity against AA-induced hepatotoxicity, with quercetin showing the best protective capacity due to its strongest antioxidant activity. In conclusion, quercetin compounds can protect against AA-induced liver injury through multiple pathways of oxidative stress, autophagy and apoptosis, and their protective capacity correlates with antioxidant activity.