Search

Objective: To identify potential salivary biomarkers for the diagnosis and monitoring of disease progression in oral squamous cell carcinoma and oral leukoplakia. Materials and Methods: An advance search from PubMed and Hindawi was performed with keywords; oral leukoplakia/oral squamous cell carcinoma, salivary biomarker and diagnosis/prognosis. An additional search of articles was done through a manual search from the Google Scholar database. Results: Twenty studies involving salivary biomarkers as diagnostic tools for oral squamous cell carcinoma and/or oral leukoplakia were identified. A narrative review was carried out. Conclusion: Single or multiple salivary biomarkers reported by most studies have shown great potential as diagnostic tools for oral squamous cell carcinoma and oral leukoplakia. However, the validation of sensitivity and specificity should be carried out to ensure the accuracy of the biomarkers. Furthermore, a standardised method for saliva collection should be established to prevent variability in the expression of biomarkers. [ABSTRACT FROM AUTHOR]

According to previous studies, oxidative stress is a leading cause of dopaminergic neuron death and may contribute to the pathogenesis of Parkinson's disease (PD). In the current study, we used chromatography of gel filtration to identify a novel peptide (Lignosus rhinocerotis peptide [LRP]) from the sclerotium of Lignosus rhinocerotis (Cooke) Ryvarden. Its neuroprotective effect was evaluated using an in vitro PD model constructed by 6‐hydroxydopamine (6‐OHDA)‐stimulated to apoptosis in PC12 cells. The molecular weight of LRP is determined as 1532 Da and the secondary structure is irregular. The simple amino acid sequence of LRP is Thr‐Leu‐Ala‐Pro‐Thr‐Phe‐Leu‐Ser‐Ser‐Leu‐Gly‐Pro‐Cys‐Leu‐Leu. Notably, LRP has the ability to significantly boost the viability of PC12 cells after exposure to 6‐OHDA, as well as enhance the cellular activity of antioxidative enzymes like superoxide dismutase (SOD), catalase (CAT), and glutathione peroxidase (GSH‐Px). LRP also lowers the level of malondialdehyde (MDA), decreases the activation performance of Caspase‐3, and reduces 6‐OHDA‐induced apoptosis via inhibition of nuclear factor‐kappa B (NF‐κB) activation. These data indicate that LRP may have the potential to act as a neuroprotective agent. [ABSTRACT FROM AUTHOR]

Negletein has been shown to have therapeutic potential for inflammation-associated diseases, but its effect on neurite outgrowth is still unknown. The present study showed that negletein alone did not trigger PC12 cells to differentiate and extend neurites. When compared with the cells in the untreated control, a significant ( P < 0.05) induction and a higher neurite outgrowth activity was observed when the cells were cotreated with negletein (10 µM) and a low dose of nerve growth factor (NGF; 5 ng/mL). The neurite outgrowth process was blocked by the tyrosine kinase receptor (Trk) inhibitor, K252a, suggesting that the neuritogenic effect was NGF-dependent. Negletein (10 µM) together with NGF (5 ng/mL) enhanced the phosphorylation of extracellular signal-regulated kinases (ERKs), protein kinase B (Akt), and cAMP response element-binding protein (CREB). The growth associated protein-43 (GAP-43) and the NGF level were also upregulated by negletein (10 µM) and a low dose of NGF (5 ng/mL). Negletein at nanomolar concentration also was found to be sufficient to mediate the survival of serum-deprived PC12 cells up to 72 h. Taken together, negletein might be useful as an efficient bioactive compound to protect neurons from cell death and promote neuritogenesis. © 2016 BioFactors, 42(6):591-599, 2016 [ABSTRACT FROM AUTHOR]