Abstract Aflatoxin B1 (AFB1) is a carcinogenic mycotoxin present in many foods, posing a serious human health problem. Oriental high-salt fermented foods are highly susceptible to AFB1 contamination due to their production process and condition. Therefore, it is necessary to isolate microbial resources that can remove AFB1 in a high-salt condition. In the current study, forty-nine salt-tolerant microorganisms with the ability to remove AFB1 were isolated from Doubanjiang, a Chinese typical high-salt red pepper paste. Among them, Bacillus velezensis AD8 had the highest removal rate of AFB1. The AFB1 removal activity of B. velezensis AD8 was mainly attributed to culture supernatant, and it was sensitive to sodium dodecyl sulfate (SDS) or/and proteinase-K treatment, which indicated that extracellular enzyme contributed to the degradation of AFB1. The optimal incubation time, pH value and NaCl concentration of the initial medium for degradation of AFB1 by the B. velezensis AD8 were investigated. In addition, the AFB1 concentration had no significant effect on degradation activity. The addition of nitrogen source, Mg2+ and Mn2+ stimulated degradation rate, whereas addition of carbon source, Zn2+ and Fe2+ inhibited degradation. Thus, B. velezensis AD8 might be a potential candidate to degrade AFB1 in high-salt food matrices.

Abstract To investigated the role of HIF-1α in myocardial inflammatory injury in rats induced by CME and its possible mechanism. Forty SD rats were separated randomly and equally into four groups, i.e. CME+HIF-1α stabilizer dimethyloxalyl glycine (CME+DMOG) group, CME+HIF-1α inhibitor YC-1 (CME+YC-1) group, CME group, and Sham group. HBFP staining, myocardial enzyme assessment, and cardiac ultrasound were used to measure microinfarct, serum c-troponin I (cTnI) level, and Cardiac function. ELISA and western blot were applied for detecting NLRP3 inflammasome pathway and TLR4/MyD88/NF-κB signaling level.Pro-inflammatory factors of IL-18, IL-1β and TNF-α increased their expression levels after CME, which indicated inflammatory responses in the myocardium. Additionally, in the inflammatory process, NLRP3 inflammasome and TLR4/MyD88/NF-κB signaling were involved. DMOG reverses these effects of CME, whereas YC-1 aggravates these effects. HIF-1α may attenuate myocardial inflammatory injury induced by CME and improve cardiac function, which can perhaps be explained by the fact that TLR4/MyD88/NF-κB signaling pathway activation is inhibited.

Se ha demostrado que la ketamina, una anestésico general, produce una respuesta de choque térmico (HSR) en algunos animales experimentales. Examinamos si la ketamina mejora la supervivencia en lesión por quemadura severa en ratas, a través de la expresión de la proteína de choque 70. Un total de 124 ratas Wistar machos se dividieron aleatoriamente en 3 grupos: un grupo de control (grupo C, n = 20), un grupo quemado (grupo B, n = 52) y un grupo quemado + ketamina (grupo K, n = 52). Las ratas de los grupos B y K presentaban quemaduras de espesor completo en el 30% del total de su superficie corporal. Las ratas del grupo K se trataron con ketamina (40mg/kg, i.m.) a los 15min después de la lesión y las del grupo B se inyectaron con igual volumen de solución salina. Luego de practicar la eutanasia a las ratas, se examinó la expresión de HSP70 en muestras del miocardio y del cerebro con análisis Western blot. En las ratas que no se sacrificaron se evaluó el estado de supervivencia. Luego de 10 días, la tasa de supervivencia en las ratas del grupo K era superior a las del grupo B (70% versus 30%). Los análisis Western blot mostraron que la expresión de proteína HSP70 en el miocardio en respuesta a la administración de ketamina es más fuerte que en respuesta a la administración de solución salina a las 3 h (158% versus 65%) y a las 6h (165% versus 68%). En comparación con el grupo B, la ketamina aumentó marcadamente el nivel de expresión de la proteína HSP70 en tejido cerebral a las 3h y a las 6 h (79% versus 51% a las 3 h; 123% versus 98% a las 6 h). Concluimos que el tratamiento con ketamina mejora la supervivencia en lesión por quemadura severa, mediante la expresión de la proteína de choque 70 en los tejidos del miocardio y del cerebro.

Ketamine, a general anesthetic, has been shown to elicit the heat-shock response (HSR) in some of the animal models. We examined whether ketamine improves survival in severe burn injury in rats via the expression of heat shock protein 70. 124 male Wistar rats were randomly divided into three groups: a control group (group C, n = 20), burned group (group B, n = 52), and burned + ketamine group (group K, n = 52). The rats in groups B and K had full-thickness burns of 30% of their total body surface. The rats in group K were treated with ketamine (40 mg/kg, i.m.) 15 min after injury, and those in group B were injected with saline at the same volume. After the rats were euthanized, HSP70 expression in myocardium and brain samples was examined by Western blot analysis. Survival status was evaluated for the rats not euthanized. After 10 days, survival rate of rats in group K was higher than that of group B (70% versus 30%). Western blot analyses revealed that HSP70 protein expression in myocardium in response to ketamine administration is stronger than that in response to saline administration at 3 h (158% versus 65%) and 6 h (165% versus 68%). Compared with that in group B, ketamine strongly increased HSP70 protein expression level in cerebral tissue at 3 h and 6 h (79% versus 51%, at 3 h; 123% versus 98%, at 6 h). We concluded that ketamine therapy improves survival in severe burn injury via the expression of heat shock protein 70 in myocardial and cerebral tissues.