Evaluation of Volatile Compounds during the Fermentation Process of Yogurts by Streptococcus thermophilus Based on Odor Activity Value and Heat Map Analysis.

The volatile composition of yogurt produced by Streptococcus thermophilus fermentation at different time points was investigated by gas chromatography-mass spectrometry combined with simultaneous distillation and extraction. A total of 53 volatile compounds including 11 aldehydes, 10 ketones, 8 acids, 7 benzene derivatives, 13 hydrocarbons, and 4 other compounds were identified in all of the samples. Ketones and hydrocarbons were the predominant volatile components in the early stage, whereas acids were the predominant volatiles in the late stage. The importance of each volatile was evaluated based on odor, threshold, and odor activity values (OAVs). Twenty-nine volatiles were found to be odor-active compounds (OAV > 1), among which (E, E)-2,4-decadienal had the highest OAV (14623-22278). Other aldehydes and ketones such as octanal, dodecanal, 2-nonen-4-one, and 2-undecanone also showed high odor intensity during fermentation. Heat map analysis was employed to evaluate the differences during fermentation. The results demonstrated that the volatile profile based on the content and OAVs of volatile compounds enables the good differentiation of yogurt during fermentation.

Neuroprotective effects of a Smoothened receptor agonist against postoperative cognitive dysfunction by promoting autophagy in the dentate gyrus of aged rats.

Objectives: To investigate the effect of purmorphamine (PUR), a Shh co-receptor Smoothened (Smo) agonist, on postoperative cognitive dysfunction (POCD) rat models. Methods: Eighteen-month-old male Sprague-Dawley rats were subjected to intramedullary fixation of a tibial fracture with 7% chloral hydrate anesthesia to mimic human clinical surgery. PUR was administered via an intraperitoneal injection at a dose of 15mg/kg/day for 3 consecutive days at 6 h after surgery. The aged rats were sacrificed after performing a Morris water maze test 1, 3, and 7 days postoperatively to evaluate the expression of related proteins at the appointed time. Results: Compared to the POCD + vehicle group and sham + PUR group, the POCD + PUR group restored neurological deficit (P = 0.01). PUR administration induced upregulation of Shh expression on postoperative day 1 (P = 0.02), which continued on the third day (P = 0.008) but dropped by the 7th day (P = 0.03). Immunofluorescent analysis, similar to western blot analysis, showed a significant increase in the autophagy-marker LC3 (P = 0.006) as well as p62 degradation (P = 0.000) in the dentate gyrus of the aged rats (P = 0.000) after PUR treatment. Importantly, LC3 was mainly found in the presynaptic and postsynaptic membranes of the hippocampus. Conclusions: These results indicate a link between Shh and autophagy in the rat model of POCD, providing new insights into Shh signaling pathway-mediated mechanisms of neuroprotection and cognitive repair after POCD. It also provides a potential entry point for the development of clinical drugs.

[APPL1-mediated effects of leptin on activity of GSK-3ß in C2C12 cell].

OBJECTIVE: To observe the effects of leptin on activity of GSK-3ß and explore its mechanism. METHODS: C2C12 myoblasts differentiated for 3 days into myotubes in differentiation medium. Myotubes were stimulated by leptin (100 nmol/L) for 0, 5, 15 or 30 min respectively. Western blot was used to detect the expression levels of GSK-3ß and phospho-GSK-3ß (ser-9). Co-immunoprecipitation (CO-IP) was performed to determine the relationship among APPL1, leptin receptor and GSK-3ß in the presence or absence of leptin. The expression level of GSK-3ß at phospho-GSK-3ß (ser-9) was detected in APPL1-suppressed C2C12 myotube while that of APPL1 at phospho-APPL1 (ser-401) determined in GSK-3ß overexpressed/inhibited C2C12 cell. RESULTS: Leptin time-dependently increased the phosphorylation level of GSK-3ß at ser-9 in C2C12 cell, and the pGSK-3ß level in cells incubated by leptin for 30 min was as 4.08 times as which in control cells (P < 0.01). The triple complex of APPL1, leptin receptor and GSK-3ß, in the presence of leptin, the binding capacity between APPL1 and GSK-3ß was stronger. The level of phospho-GSK-3ß was significantly lower in APPL1-suppressed C2C12 cell compared with that in control cells. And the phosphorylation of APPL1 at ser-401 could be induced by GSK-3ß. CONCLUSION: Leptin promotes muscle glycogen synthesis by inducing phosphorylation of GSK-3ß in C2C12 cell. Such a function may be mediated by the triple complex of APPL1, leptin receptor and GSK-3ß. Meanwhile, GSK-3ß can also increase the phosphorylation of APPL1 at ser-401.