Abstract Presently in order to excavate suitability of resources of lactic acid bacteria for fermentation of mandarin fish, a strain of lactic acid bacteria (LAB), which was cultivated from stinky mandarin fish via using traditional MRS medium (CMC 1-8), was firstly isolated and purified. Subsequently, it was discovered that the as-harvested LAB was recognized as Lactobacillus sakei subsp. sakei with assistance of technology of phenotypic identifying and 16S rRNA sequencing. Concurrently, relevant characteristics in aspects of growth curve, acid production capacity, temperature and salt tolerance of Lactobacillus sakei subsp. sakei were plainly investigated. Furthermore, the preliminary research on protease properties and biological properties was revealed. The results unfolded that the strain could grow and produce acid normally at 37 °C, and deliver a strong tolerance even under 3% NaCl at 12 °C, which could be significant sufficiently to satisfy the low-temperature and salty fermentation of mandarin fish. The best compatible temperature and pH value for protease production were at 70 °C and 9.0, respectively. Resultantly, the main metabolites, containing polyphenols, flavonoids and soluble polypeptides, performed a remarkable effect on scavenging abilities of 2,2'-azino-bis (3-ethylbenzothiazoline-6-sulfonic acid) (ABTS), 1,1-diphenyl-2-picrylhydrazine (DPPH) free radical and ferricyanide reducing ability, of which the IC50 were 1.05, 6.87, and 4.62 mg/mL, respectively. And, the metabolites displayed partial inhibitory effects on Escherichia coli, Staphylococcus aureus, Pseudomonas aeruginosa, and Bacillus subtilis. Therefore, CMC 1-8 can potentially serve as a functional microorganism to directionally ferment mandarin fish.

Abstract Danzhi Jiangtang capsule (DJC), a traditional medicinal formula composed of cortex moutan, heterophylly falsestarwort root, unprocessed rehmannia root, oriental waterplantain rhizome, dodder seed and leech, has been used to treat type 2 diabetes in clinic for almost 10 years. In addition, DJC was also confirmed that it could relieved oxidative stress of vascular endothelium in diabetic macroangiopathy. Based on the fact that the DJC could regulated the level of free fatty acids in diabetes patients and the constituents of DJC also possess potential anti-hyperlipidemic effect, thus, the present work aimed to evaluate the anti-hyperlipidemic effect of DJC and further investigated potential molecular mechanism of this action. As in vivo results revealed, DJC could reduced the levels of TC, TG, LDL, increased HDL level as well as decreased the level of ALT and AST of model rats. In addition, DJC also showed significant antioxidant effect by decreasing the level of MDA and increasing the level of SOD and GSH-Px. Furthermore, western blot analysis showed that DJC could up-regulated the expression of phosphorylated JAK2 and STAT3, and down-regulated the expression of SCOC3 protein, which indicated that DJC could regulate the metabolism of lipid via JAK2/STAT3 pathway.

The aim of this study was to investigate the influence of enhanced external counterpulsation (EECP) on the cardiac function of beagle dogs after prolonged ventricular fibrillation. Twenty-four adult male beagles were randomly divided into control and EECP groups. Ventricular fibrillation was induced in the animals for 12 min, followed by 2 min of cardiopulmonary resuscitation. They then received EECP therapy for 4 h (EECP group) or not (control group). The hemodynamics was monitored using the PiCCO2 system. Blood gas and hemorheology were assessed at baseline and at 1, 2, and 4 h after return of spontaneous circulation (ROSC). The myocardial blood flow (MBF) was quantified by 18F-flurpiridaz PET myocardial perfusion imaging at baseline and 4 h after ROSC. Survival time of the animals was recorded within 24 h. Ventricular fibrillation was successfully induced in all animals, and they achieved ROSC after cardiopulmonary resuscitation. Survival time of the control group was shorter than that of the EECP group [median of 8 h (min 8 h, max 21 h) vs median of 24 h (min 16 h, max 24 h) (Kaplan Meyer plot analysis, P=0.0152). EECP improved blood gas analysis findings and increased the coronary perfusion pressure and MBF value. EECP also improved the cardiac function of Beagles after ROSC in multiple aspects, significantly increased blood flow velocity, and decreased plasma viscosity, erythrocyte aggregation index, and hematocrit levels. EECP improved the hemodynamics of beagle dogs and increased MBF, subsequently improving cardiac function and ultimately improving the survival time of animals after ROSC.

OBJECTIVE: The role of Ulinastatin in neuronal injury after cardiopulmonary resuscitation has not been elucidated. We aim to evaluate the effects of Ulinastatin on inflammation, oxidation, and neuronal injury in the cerebral cortex after cardiopulmonary resuscitation. METHODS: Ventricular fibrillation was induced in 76 adult male Wistar rats for 6 min, after which cardiopulmonary resuscitation was initiated. After spontaneous circulation returned, the rats were split into two groups: the Ulinastatin 100,000 unit/kg group or the PBS-treated control group. Blood and cerebral cortex samples were obtained and compared at 2, 4, and 8 h after return of spontaneous circulation. The protein levels of tumor necrosis factor alpha (TNF-α) and interleukin 6 (IL-6) were assayed using an enzyme-linked immunosorbent assay, and mRNA levels were quantified via real-time polymerase chain reaction. Myeloperoxidase and Malondialdehyde were measured by spectrophotometry. The translocation of nuclear factor-κB p65 was assayed by Western blot. The viable and apoptotic neurons were detected by Nissl and terminal deoxynucleotidyl transferase dUTP nick end labeling (TUNEL). RESULTS: Ulinastatin treatment decreased plasma levels of TNF-α and IL-6, expression of mRNA, and Myeloperoxidase and Malondialdehyde in the cerebral cortex. In addition, Ulinastatin attenuated the translocation of nuclear factor-κB p65 at 2, 4, and 8 hours after the return of spontaneous circulation. Ulinastatin increased the number of living neurons and decreased TUNEL-positive neuron numbers in the cortex at 72 h after the return of spontaneous circulation. CONCLUSIONS: Ulinastatin preserved neuronal survival and inhibited neuron apoptosis after the return of spontaneous circulation in Wistar rats via attenuation of the oxidative stress response and translocation of nuclear factor-κB p65 in the cortex. In addition, Ulinastatin decreased the production of TNF-α, IL-6, Myeloperoxidase, and Malondialdehyde.