Preparation of Liposomal Nanoparticles Containing Ziziphora tenuir Essential Oil and Evaluation of its Antimicrobial Effects

Background and Objectives  Natural preservatives extracted from herbs are important sources for bioactive compounds that can be used in protection of food products. Essential oils are aromatic oily liquids, obtained from plant material like flowers, buds, seeds, leaves, and roots. Unfortunately, most natural compounds are biologically instable, poorly soluble in water and they distribute poorly to target sites. Currently, some novel methods have been introduced in order to improve their stability and their bioavailability, among which is the use of liposomal encapsulation. Microencapsulation reduces reactivity with the environment (water, oxygen, light), decreases the evaporation or the transfer rate to the outside environment, promotes handling ability, masks taste and enhances dilution to achieve a uniform distribution in the final product when used in very small amounts. Essential oils, as natural extracted compounds extracted from plants, are unstable compounds with low water solubility and unable to achieve target cells. Essential oils encapsulation by nanoliposomes is a novel method for increasing their biological activity and protecting them from destructive factors. The aim of this study was production and optimization of nanoliposomes containing Z. teniur essential oil and investigating their antibacterial effects against pathogens (Staphylococcus aureus and Escherichia coli).   Materials and Methods  Lipid film hydration method was used to produce nanoliposomes containing Z. teniur essential oil. Soy phosphatidylcholine and cholesterol were the main wall materials and chloroform was used as the mixing solvent . The particle size of nanoliposomes and their zeta-potential were investigated using laser diffraction method. In order to determine the minimum inhibitory concentration and the minimum bactericidal concentration of Z. teniur essential oil against examined bacteria, serial dilution method was used. Also, antioxidant activity of free and nano-encapsulated essential oil of Z. teniur was determined by DPPH method.   Results  According to the results, highest encapsulation efficiency achieved by using 80:20 ratio of soy phosphatidylcholine to cholesterol in nanoliposomes’ wall structures. In general, by increasing the ratio of phosphatidylcholine to cholesterol, encapsulation efficiency was improved. Zeta-potential of nanoliposomes was equal to -5.3 mv and mean particle sizes were in the range of 94.7-119.9 nm. Results indicated that essential oil ejection from nanoliposomes has direct relation to the time of storage and after 30 hours, ejection rate will increase considerably. Ejection rate was higher in phosphate buffer pH=7.4 in comparison with phosphate buffer pH=5.4. Minimum inhibitory concentration and minimum bactericidal concentration of free essential oil against Escherichia coli was 100 and 175 (µl/ml) respectively. Although, Minimum inhibitory concentration and minimum bactericidal concentration of nanoliposomes containing Z. teniur essential oil were equal to 75 and 150 (µl/ml) respectively. Also, results shown that , minimum inhibitory concentration and minimum bactericidal concentration of encapsulated Z. teniur essential oil against Staphylococcus aureus were lower in comparison with free form of Z. teniur essential oil. Staphylococcus aureus (as Gram-positive bacteria) was more susceptible than Escherichia coli (as Gram-negative bacteria).   Conclusion  Encapsulation of Z. teniur essential oil by nanoliposomes led to improve antibacterial effects of essential oil against Staphylococcus aureus and Escherichia coli. Also, investigating of antioxidant activity showed that encapsulated Z. teniur essential oil in nanoliposomes was more effective than free form of Z. teniur essential oil in scavenging of DPPH free radicals. Using nanoliposome encapsulation technology can be an effective way for increasing the efficiency of natural antibacterial compounds and essential oils encapsulated in nanoliposomes are suitable alternatives for synthetic preservatives used in food industry nowadays. The use of liposomes containing Z. teniur essential oil can provide the necessary protection against growth of spoilage and pathogenic microorganisms such as Staphylococcus aureus and Escherichia coli in food products

Neurophysiological consequences of synapse loss in progressive supranuclear palsy

Synaptic loss occurs early in many neurodegenerative diseases and contributes to cognitive impairment even in the absence of gross atrophy. Currently, for human disease there are few formal models to explain how cortical networks underlying cognition are affected by synaptic loss. We advocate that biophysical models of neurophysiology offer both a bridge from clinical to preclinical models of pathology, and quantitative assays for experimental medicine. Such biophysical models can also disclose hidden neuronal dynamics generating neurophysiological observations like electro- and magneto-encephalography. Here, we augment a biophysically informed mesoscale model of human cortical function by inclusion of synaptic density estimates as captured by [11C]UCB-J positron emission tomography, and provide insights into how regional synapse loss affects neurophysiology. We use the primary tauopathy of progressive supranuclear palsy (Richardson's syndrome) as an exemplar condition, with high clinicopathological correlations. Progressive supranuclear palsy causes a marked change in cortical neurophysiology in the presence of mild cortical atrophy and is associated with a decline in cognitive functions associated with the frontal lobe. Using parametric empirical Bayesian inversion of a conductance-based canonical microcircuit model of magnetoencephalography data, we show that the inclusion of regional synaptic density-as a subject-specific prior on laminar specific neuronal populations-markedly increases model evidence. Specifically, model comparison suggests that a reduction in synaptic density in inferior frontal cortex affects superficial and granular layer glutamatergic excitation. This predicted individual differences in behaviour, demonstrating the link between synaptic loss, neurophysiology, and cognitive deficits. The method we demonstrate is not restricted to progressive supranuclear palsy or the effects of synaptic loss: such pathology-enriched dynamic causal models can be used to assess the mechanisms of other neurological disorders, with diverse non-invasive measures of pathology, and is suitable to test the effects of experimental pharmacology

Neurophysiological consequences of synapse loss in progressive supranuclear palsy

AbstractSynaptic loss occurs early in many neurodegenerative diseases and contributes to cognitive impairment even in the absence of gross atrophy. Currently, for human disease there are few formal models to explain how cortical networks underlying cognition are affected by synaptic loss. We advocate that biophysical models of neurophysiology offer both a bridge from clinical to preclinical models of pathology, and quantitative assays for experimental medicine. Such biophysical models can also disclose hidden neuronal dynamics generating neurophysiological observations like electro- and magneto-encephalography (MEG). Here, we augment a biophysically informed mesoscale model of human cortical function by inclusion of synaptic density estimates as captured by [11C]UCB-J positron emission tomography, and provide insights into how regional synapse loss affects neurophysiology. We use the primary tauopathy of progressive supranuclear palsy (Richardson’s syndrome) as an exemplar condition, with high clinicopathological correlations. Progressive supranuclear palsy causes a marked change in cortical neurophysiology in the presence of mild atrophy and is associated with a decline in cognitive functions associated with the frontal lobe. Using (parametric empirical) Bayesian inversion of a conductance-based canonical microcircuit model of MEG data, we show that the inclusion of regional synaptic density—as a subject-specific prior on laminar specific neuronal populations—markedly increases model evidence. Specifically, model comparison suggests that a reduction in synaptic density in inferior frontal cortex affects superficial and granular layer glutamatergic excitation. This predicted individual differences in behaviour, demonstrating the link between synaptic loss, neurophysiology, and cognitive deficits. The method we demonstrate is not restricted to progressive supranuclear palsy or the effects of synaptic loss: such pathology-enriched dynamic causal models can be used to assess the mechanisms of other neurological disorders, with diverse non-invasive measures of pathology, and is suitable to test the effects of experimental pharmacology.</jats:p