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Objective: The effect of frozen temperature on the storage characteristics of ready-to-eat snakehead sausages were investigated. Methods: In this study, The freezing temperature dehydration technique was used to control the moisture content of snakehead sausage at about 50%, and then the temperature was lowered to-5.6 ℃. Subsequently, the sausage was stored at -4 ℃, and those stored at 4 ℃ were set as the control. The changes in the quality and microstructure of the snakehead sausages were analyzed, by measuring the physicochemical indexes such as total bacterial colony, color, water holding capacity, textural properties, biogenic amines and scanning electron microscopy during storage. Results: The logarithmic values of TVC were （5.37±0.06）; TVB-N were （17±0.03） mg/100 g; the total amine mass fraction were （324.93±1.89） mg/kg at 42 d. The results of colony count and TVB-N analysis showed that, compared to those stored at 4 ℃, frozen storage could extend the shelf life of snakehead sausage by 1-fold. The low-field NMR results showed that the moisture distribution of snakehead sausage during frozen storage was better than that of the control. Scanning electron microscopy showed that the gel network of the frozen-storage group had a higher degree of binding to fat particles. The frozen storage of snakehead sausage was superior to the refrigerated storage. Conclusion: The preservation effect of snakehead sausage stored at freezing temperature is better than that of refrigerated storage.

The amyloid-beta peptide (Aβ) is the neurotoxic component in senile plaques of Alzheimer's disease (AD) brains. Previously we have reported that Aβ toxicity is mediated by the induction of sonic hedgehog (SHH) to trigger cell cycle re-entry (CCR) and apoptosis in post-mitotic neurons. Basella alba is a vegetable whose polysaccharides carry immunomodulatory and anti-cancer actions, but their protective effects against neurodegeneration have never been reported. Herein, we tested whether polysaccharides derived from Basella alba (PPV-6) may inhibit Aβ toxicity and explored its underlying mechanisms. In differentiated rat cortical neurons, Aβ25-35 reduced cell viability, damaged neuronal structure, and compromised mitochondrial bioenergetic functions, all of which were recovered by PPV-6. Immunocytochemistry and western blotting revealed that Aβ25-35-mediated induction of cell cycle markers including cyclin D1, proliferating cell nuclear antigen (PCNA), and histone H3 phosphorylated at Ser-10 (p-Histone H3) in differentiated neurons was all suppressed by PPV-6, along with mitigation of caspase-3 cleavage. Further studies revealed that PPV-6 inhibited Aβ25-35 induction of SHH; indeed, PPV-6 was capable of suppressing neuronal CCR and apoptosis triggered by the exogenous N-terminal fragment of sonic hedgehog (SHH-N). Our findings demonstrated that, in the fully differentiated neurons, PPV-6 exerts protective actions against Aβ neurotoxicity via the downregulation of SHH to suppress neuronal CCR and apoptosis. [ABSTRACT FROM AUTHOR]