Correlation Analysis between Microbial Communities and Flavor Compounds during the Post-Ripening Fermentation of Traditional Chili Bean Paste.

Chili bean paste is a traditional flavor sauce, and its flavor compounds are closely related to its microflora. This study focused on investigating the content of bioactive compounds, flavor compounds, and microbial communities during the post-ripening fermentation of chili bean paste, aiming to provide a reference for improving the flavor of chili bean paste by regulating microorganisms. Compared to no post-ripening fermentation, the content of organic acids increased significantly (p < 0.05), especially that of citric acid (1.51 times). Glutamic acid (Glu) was the most abundant of the 17 free amino acids at 4.0 mg/g. The aroma profiles of the samples were significantly influenced by fifteen of the analyzed volatile compounds, especially methyl salicylate, methyl caproate, and 2-octanol (ROAV > 1). Latilactobacillus (27.45%) and Pseudomonas (9.01%) were the dominant bacterial genera, and Starmerella (32.95%) and Pichia (17.01%) were the dominant fungal genera. Weissella, Lacticaseibacillus, Pichia, and Kazachstania had positive effects on volatile flavoring compounds, which enriched the texture and flavor of the chili bean paste. Therefore, the microbial-community activity during the post-ripening fermentation is the key to enhance the flavor quality of the product.

Acute and subchronic toxicity of Ag+-laden liposomes on Daphnia magna: the effect of encapsulation.

The toxic effects of various substances on Daphnia magna (D. magna) observed through traditional waterborne uptake may involve alterations to the nutritional quality of the contaminated algae and culture media. It is essential to find an alternative delivery method that will not affect the nutritional quality of D. magna's diet in order to elucidate the mechanisms of dietary metal toxicity. Therefore, this study examined the application of liposome encapsulation on the dietary toxicity of D. magna. Ag+-laden liposomes were prepared and the Ag encapsulation efficiency and inhibition effect on algae growth were examined. Then, acute and 14-day subchronic studies were performed to examine the effect of Ag+-laden liposomes on D. magna. The EC50 for the 24 h immobilization test was 10.59 µg/L for Ag+-laden liposomes and 3.07 µg/L for Ag+. In terms of subchronic effects, the estimated ECx values under the Ag+-laden liposome condition were always higher than the direct exposure condition. Furthermore, the bioaccumulation of Ag+-laden liposomes was about 1.68 times lower than direct exposure. Generally, Ag+-laden liposomes produced less efficient toxicity than direct exposure, e.g., lower D. magna mortality, production of more neonates, higher intrinsic rate of natural increase (rm), earlier time to first brood, and higher enzyme activities.

FGF21 attenuates hypoxia­induced dysfunction and apoptosis in HPAECs through alleviating endoplasmic reticulum stress.

Vascular endothelial apoptosis and dysfunction have a crucial role in triggering pathological vascular remodeling of hypoxia­induced pulmonary arterial hypertension (PAH). Fibroblast growth factor (FGF)21, an endocrine regulator, has recently been reported to protect cardiac endothelial cells from damage and suppress inflammatory responses. In addition, FGF21 is reported to be involved in endoplasmic reticulum stress (ERS). Previous studies have suggested that ERS participates in the development of PAH, and attenuation of ERS could be an effective therapeutic strategy for the protection of pulmonary arteries. However, whether FGF21 has a protective function via suppression of ERS in pulmonary arterial endothelial cells in hypoxia remains unclear. The present study aimed to explore whether FGF21 could reduce the hypoxia­induced apoptosis of human pulmonary arterial endothelial cells (HPAECs) and prevent endothelial dysfunction via the inhibition of ERS. HPAECs were divided into six groups: Normoxia, hypoxia, hypoxia plus FGF21, hypoxia plus salubrinal (an ERS inhibitor), hypoxia plus tunicamycin (an ERS agonist), and hypoxia plus tunicamycin plus FGF21. The endoplasmic reticulum ultrastructure in HPAECs was assessed by transmission electron microscopy, and proliferation and apoptosis were examined by cell counting kit­8 and terminal deoxyribonucleotide transferase­mediated dUTP nick end­labelling assays, respectively. The expression levels of ERS­related proteins, including binding immunoglobulin protein (BiP), protein kinase R­like endoplasmic reticulum kinase (PERK), phosphorylated (p­) PERK, transcription factor C/EBP homologous protein (CHOP), B­cell lymphoma-2 (Bcl­2) and caspase­4 were detected by western blotting. Transwell migration chamber assays were performed, and the concentration of nitric oxide (NO)/endothelin­1 (ET­1) in the culture medium was determined to examine endothelial function. The results revealed that hypoxia increased the % of apoptotic cells and diminished the viability of HPAECs, accompanied by an upregulation of ERS­dependent apoptosis by increasing the expression of the proapoptotic caspase­4 and decreasing the antiapoptotic Bcl­2. Additionally, hypoxia upregulated the expression of representative proteins in the PERK branch of ERS, including BiP, p­PERK and CHOP, while it downregulated the expression of PERK. Furthermore, the secretion of NO/ET­1 and the migration rate of HPAECs were downregulated under conditions of hypoxia. FGF21 significantly attenuated the hypoxia­induced apoptosis and dysfunction of HPAECs through alleviating the aforementioned changes in ERS­dependent signaling pathways. In conclusion, ERS may be a crucial mechanism in the hypoxia­induced apoptosis and endothelial dysfunction of HPAECs. FGF21 may attenuate the hypoxia­induced apoptosis and dysfunction of HPAECs through alleviating ERS, via the PERK/CHOP signaling pathway and inhibition of caspase­4 expression.