Bee Venom Activates the Nrf2/HO-1 and TrkB/CREB/BDNF Pathways in Neuronal Cell Responses against Oxidative Stress Induced by Aß1-42.

Honeybee venom has recently been considered an anti-neurodegenerative agent, primarily due to its anti-inflammatory effects. The natural accumulation of amyloid-beta (Aß) in the brain is reported to be the natural cause of aging neural ability downfall, and oxidative stress is the main route by which Aß ignites its neural toxicity. Anti-neural oxidative stress is considered an effective approach for neurodegenerative therapy. To date, it is unclear how bee venom ameliorates neuronal cells in oxidative stress induced by Aß. Here, we evaluated the neuroprotective effect of bee venom on Aß-induced neural oxidative stress in both HT22 cells and an animal model. Our results indicate that bee venom protected HT22 cells against apoptosis induced by Aß1-42. This protective effect was explained by the increased nuclear translocation of nuclear factor erythroid 2-like 2 (Nrf2), consequently upregulating the production of heme oxygenase-1 (HO-1), a critical cellular instinct antioxidant enzyme that neutralizes excessive oxidative stress. Furthermore, bee venom treatment activated the tropomyosin-related kinase receptor B (TrkB)/cAMP response element-binding (CREB)/brain-derived neurotrophic factor (BDNF), which is closely related to the promotion of cellular antioxidant defense and neuronal functions. A mouse model with cognitive deficits induced by Aß1-42 intracerebroventricular (ICV) injections was also used. Bee venom enhanced animal cognitive ability and enhanced neural cell genesis in the hippocampal dentate gyrus region in a dose-dependent manner. Further analysis of animal brain tissue and serum confirmed that bee venom reduced oxidative stress, cholinergic system activity, and intercellular neurotrophic factor regulation, which were all adversely affected by Aß1-42. Our study demonstrates that bee venom exerts antioxidant and neuroprotective actions against neural oxidative stress caused by Aß1-42, thereby promoting its use as a therapeutic agent for neurodegenerative disorders.

A study of bactericidal effect and optimization of pathogenic bacteria using TiO2 photocatalyst.

The photocatalytic degradation of Salmonella choleraesuis subsp. and Vibrio parahaemolyticus in water by TiO2 catalysts was investigated in a batch reactor. After 30 min of irradiation with UV light in the presence of 1 mg/ml of TiO2, death ratio of S. choleraesuis subsp. and V. parahaemolyticus was 60% and 83%, respectively. And complete killing of the cells was achieved after 3 h of illumination in the presence of TiO2. We established the response surface methodology to investigate the effect of principal parameters on the pathogenic bacteria sterilization such as TiO2 concentration, pH and temperature. By applying response surface analysis to the bactericidal effect of S. almonella choleraesuis subsp. and V. parahaemolyticus, we found that the cell death ratio was influenced significantly by the first order term of TiO2 concentration.

Bactericidal effect of TiO2 on the selected Vibrio parahaemolyticus and optimization using response surface methodology.

In this work, the bactericidal effect of TiO2 on selected typical food pathogenic bacteria, Vibrio parahaemolyticus was studied. V parahaemolyticus is an important pathogen of humans and aqua-cultured animals. We established the response surface methodology (Box-Behnken Design) to investigate the effect of principal parameters on the cell sterilization such as TiO2 concentration, UV illumination time, temperature, and pH. The sterilization rate reached maximum value at the TiO2 concentration of 1.0 mg/ml. During irradiation under the time of 30 min with UV light with the 1g-TiO2/l, the sterilization rate was greater than 85%, and 99% or more cell lost their viability with 3 hours of irradiation. Sterilization rate of the cell increased with decrease in the pH and temperature.