Introduction: One of the most common aetiology of opportunistic fungal infections in humans is Candida species. The virulence of Candida species is due to repertoire of factors, specifically, the ability to form biofilms. Medical devices such as intravenous catheters, prosthetic heart valves and surgical interventions provide pathogenic microorganisms with a surface to adhere to form biofilm. Fungi present as biofilms are often resistant to antifungal treatment because these biofilms offer a protective barrier that prohibits the drugs to get to the active site of the fungi. The objective of this study is to investigate the biofilm architecture of Candida rugosa (C.rugosa) at different developmental phases and to identify Sessile Minimum Inhibition Concentrations (SMICs) of amphotericin B, caspofungin, fluconazole, and voriconazole for the biofilm of C. rugosa. Methods: Confocal scanning laser microscopy (CSLM) and scanning electron microscopy (SEM) were used to visualize C. rugosa biofilms at different developmental phases. The antifungal susceptibility test was performed using serial doubling dilution. The growth kinetics of Candida biofilms was quantified using XTT reduction assay and crystal violet assay. Results: From the antifungal susceptibility test, the biofilms had SMIC of >16μg/mL for amphotericin B, 6µg/mL for caspofungin, >64μg/mL for fluconazole and >16μg/ mL for voriconazole. From the SEM micrographs, C. rugosa biofilm have a structure composed of an adherent yeast cells and blastopores with hyphal elements. There were significant alterations in the morphology after exposure to antifungal agents. The quantitative measurement of the matrix thickness of embedded yeast cells were obtained from CLSM micrographs. Conclusion: In conclusion, the ability of C. rugosa to form biofilms may attribute to one of the virulence factors that causes reduced susceptibility to antifungal agents.
Introduction: Amyloid-β (Aβ) peptides play a key role in the pathogenesis of Alzheimer disease and exert various toxic effects on neurons. Dietary phytochemicals are currently used as an adjuvant therapy to accelerate their therapeutic efficacy. Therefore, the present study was designed to investigate the effect of curcumin and its co-administration with piperine against Aβ42 induced cytotoxicity, fibril aggregation and oxidative damage in SH-SY5Y cells. Methods: The neuroblastoma SH-SY5Y cells were cultured with different treatments of Aβ42, individual curcumin and piperine and combination of curcumin and piperine. Cell viability, Aβ fibril aggregation and oxidative damage such as lipid peroxidation, catalase and glutathione were assessed. The abilities of curcumin and its combination, piperine to scavenge free radicals and to inhibit Aβ aggregation and β-sheeted formation were further assessed. Results: Curcumin and piperine preserves cell viability, which is decreased by Aβ, indicate that curcumin protects Aβ-induced neuronal damage. Under aggregating conditions in vitro, curcumin and piperine inhibited aggregation as well as disaggregated fibrillar Aβ42, indicating favorable stoichiometry for inhibition. Results also showed that curcumin and piperine as a combination was a better Aβ42 aggregation inhibitor than the individual compounds. Curcumin and piperine depresses Aβ-induced up-regulation of neuronal oxidative stress. The ability of these compounds to scavenge free radicals and inhibit the formation of Aβ aggregation are implicated from the results of this study. Conclusion: This combination of curcumin and piperine shows a more protective effect on neuronal oxidative damage when they was added into cultured neurons not later than Aβ, especially prior to Aβ. The curcumin and piperine combination prevents neurons from Aβ-induced oxidative stress, indicating a promising therapeutic in preventive medicine for Alzheimer disease.
Introduction: Alzheimer disease (AD) is the most widely recognised neurodegenerative disorder in the ageing population, characterised by progressive neuronal loss. The enhanced level of acetylcholine (ACh) in the human brain is another measure of identifying the progression of the disease. Increased acetylcholinesterase (AChE) level plays a fundamental role in the hydrolysis of Ach which worsens the cognitive function. Though there are several medications or drugs currently used in treating AD, their clinical implications remains debatable due to its adverse effects. Methods: In this study, the combined nutraceutical effect of natural plant compounds, piperine and curcumin were evaluated for acetylcholinesterase inhibitory assay using Ellman colourimetric method. Results: Results obtained from the study revealed that combined effects of natural plant compounds showed promising acetylcholinesterase inhibition activity with an IC50 of 104.1 ± 0.08 µg/mL compared to individually treated compounds, i.e., IC50 of curcumin = 134.5 ± 0.05 µg/mL and IC50 of piperine = 62.81 ± 0.00 µg/mL. Conclusion: The results suggest that the natural plant compounds taken in combination act as natural acetylcholinesterase inhibitors, and could be beneficial in the treatment of AD.