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Graphical abstract Highlights • Sub-chronic treatment of EBN has no observable toxic effect on mice. • EBN improves motor function, locomotor activity and balancing in PD mice. • EBN prevents loss of dopaminergic neurons in substantia nigra of PD mice. • Antioxidant and microglia markers are regulated by EBN in substantia nigra of PD mice. • NO production and lipid peroxidation are attenuated by EBN in in vitro PD model. Abstract Parkinson's disease (PD) is a neurological disorder originated from the death of dopaminergic neurons in the midbrain. Evidences showed that oxidative and nitrosative stress play a central role in neurodegeneration. In this study, we examine the neuroprotective effects of EBN (20 mg/kg and 100 mg/kg) in 6-hydroxydopamine (6-OHDA)-treated C57BL/6J mice. Twenty eight days of EBN oral administration greatly improved locomotor activity of PD mice in terms of travel distance and balancing. EBN also protected dopaminergic neuron against 6-OHDA in the substantia nigra. EBN reversed the reduction in the expression of antioxidant enzyme glutathione peroxidase 1 and the increased microglia activation in PD mice. Our results also showed that EBN effectively reduced 6-OHDA-induced nitric oxide formation and lipid peroxidation in SH-SY5Y cells. The data altogether indicates that EBN exerted neuroprotection through enhancement of antioxidant enzyme activity and the inhibition of microglia activation, nitric oxide formation and lipid peroxidation in PD model. [ABSTRACT FROM AUTHOR]

Neural stem cells (NSC) are multipotent precursor cells in the neurogenic regions of the brain which respond to trophic factors to achieve functional recovery from neurodegenerative diseases. Edible bird's nest (EBN) is a salivary product of Aerodramus swiftlets and may contain potent neurotrophic compounds. Crude and water extracts of EBN were shown to have neurotrophic properties by promoting proliferation and migration of the NSC model, embryonic mouse neuroectodermal cells (NE-4C). Neuronal differentiation of retinoic acid-primed NE-4C was also increased after being treated with EBN extracts. Using de novo peptide sequencing with tandem mass spectrometry, a total of 29 proteins were identified from EBN extracts. It is suggested that the repulsive guidance molecule domain family member B, which has been shown to promote neurite extension and axonal growth, as well as proteins involved in the process of cell proliferation and migration such as protein lin-9 and hyaluronan mediated motility receptor might be involved in the neurotrophic effects of EBN extracts. Other proteins found in EBN extracts were known to have potential roles in immunity, extracellular matrix formation, cell survival and apoptosis, antioxidation, and common cellular processes, which may be implicated in other EBN studies. Seven hypothetical proteins suggested using the PEAKS Studio 7.0 software did not have a match in the Swiss-Prot database, which may need to be further characterized in the future. In conclusion, this study described the neurotrophic properties of EBN extracts and supports the use of EBN as a potential functional food against neurodegenerative diseases. • EBN increased NE-4C proliferation and migration rate. • Neurogenesis was promoted in retinoic acid-primed NE-4C cell after EBN treatment. • Protein in raw and water extracts of EBN was studied using de novo peptide sequencing. • EBN may act as a nutraceutical food in the treatment of neurodegenerative diseases. [ABSTRACT FROM AUTHOR]

Abstract: para-Phenylenediamine (p-PD) is a major aromatic amine that is a widely used commercial oxidative-type hair dye. Some epidemiologic studies have suggested that the use of p-PD-based hair dyes might be related to increased risk of human malignant tumors including bladder cancer. However, the effects of p-PD on autophagy in human uroepithelial cells (SV-HUC-1) is still unclear. In this study, we demonstrate that p-PD can activate the extracellular signaling-regulated protein kinase 1/2 (ERK1/2) signaling pathway in SV-HUC-1 cells. In addition, we observed that autophagosomes increased in p-PD-treated SV-HUC-1 cells as shown by electron microscopy. Our results showed incremental increase of the concentrations, Beclin-1 and microtubule-associated protein light chain 3B (LC3B), which are important regulators of autophagosomes. In contrast, the MEK inhibitor (U0126) was suppressed autophagy and the effect of p-PD on ERK1/2, Beclin-1 and LC3B proteins expression, except for mutant p53. In this study, we demonstrated that inactivation of p53 induces a potent autophagy response. Finally, our results suggest that p-PD can activate the ERK1/2 signaling pathway and mutant p53, leading to the stimulation of autophagy in SV-HUC-1 cells. These results provide us with new insights for the understanding of the mechanism of p-PD-induced cell death in urothelial cells. [Copyright &y& Elsevier]

Abstract: Sevoflurane is an inhalation anesthetic used for general anesthesia. Several studies have demonstrated that reactive oxygen species (ROS) exist in cardioprotection when preconditioned with sevoflurane. Moreover, sevoflurane can also directly trigger the formation of peroxynitrite. Up to now, information pertinent to the effect of sevoflurane on cellular injuries in human polymorphonuclear neutrophils (PMN) is scant. In this study, we demonstrated that sevoflurane significantly increases intracellular H2O2 and/or peroxide, superoxide, and nitric oxide (NO) in PMN within 1h treatment. Intensification of intracellular glutathione (GSH) depletion in PMN has been demonstrated with the presence of sevoflurane. Inhibition of sevoflurane-mediated intracellular H2O2 and/or peroxide in PMN by catalase, mannitol, dexamethasone, N-acetylcysteine (NAC) and trolox, but not superoxide dismutase (SOD) pretreatment, was observed. Among them, catalase has the best effect scavenging intracellular H2O2 and/or peroxide, suggesting that H2O2 is the major ROS during sevoflurane treatment. Two apoptotic critical factors—lowering of the mitochondrial transmembrane potential (ΔΨ m) and activation of caspase 3/7—were significantly increased after 1h of sevoflurane treatment. Apoptosis of PMN were determined by comet assay and flow cytometric analysis of annexin V-FITV protein binding to the cell surface. Exposure of PMN to sevoflurane markedly increased apoptosis in a dose-dependent manner. In summary, these results are important for demonstrating the oxidative stress and cellular injury on sevoflurane-treated human PMN. [Copyright &y& Elsevier]

Algae and its metabolites have been a popular subject of research in numerous fields over the years. Various reviews have been written on algal bioactive components, but a specific focus on Antarctic-derived algae is seldom reviewed. Due to the extreme climate conditions of Antarctica, it is hypothesized that the acclimatized algae may have given rise to a new set of bioactive compounds as a result of adaptation. Although most studies done on Antarctic algae are based on ecological and physiological studies, as well as in the field of nanomaterial synthesis, some studies point out the potential therapeutic properties of these compounds. As an effort to shed light on a different application of Antarctic algae, this review focuses on evaluating its different medicinal properties, including antimicrobial, anticancer, antioxidative, anti-inflammatory, and skin protective effects. [Display omitted] [ABSTRACT FROM AUTHOR]

Abstract: The mechanism of toxicity p-phenylenediamine (p-PD), a component of human permanent hair dye and a suspected carcinogen, on the growth of Mardin–Darby canine kidney cells (MDCK) was investigated. With the analysis of flow cytometry, a dose-dependent accumulation of the sub-G1 peak and the G0/G1-phase arrested in cell cycle, and time-dependent induction of apoptosis after staining with Annexin V-Fluorescein and propidium iodide were observed. After the treatment of cells with p-PD, dose dependent DNA fragmentation shown by gel electrophoresis, the reduction of membrane potential (ΔΨ m) by mitochondria membrane depolarization and the increase of the expression of p53 protein in cells, suggested that the effect of p-PD on overall viability and cell numbers is mediated by an increase in apoptosis. [Copyright &y& Elsevier]