Decrease In Cholinesterase Activity Research Articles

Effects of polymethylmethacrylate nanoplastics on the polychaete Hediste diversicolor: Behavioural, regenerative, and biochemical responses

Plastics, particularly microplastics (MPs) and nanoplastics (NPs), have been regarded as pollutants of emerging concern due to their effects on organisms and ecosystems, especially considering marine environments. However, in terms of NPs, there is still a knowledge gap regarding the effects of size and polymer on marine invertebrates, such as benthic organisms. Therefore, this study aimed to understand, regarding behavioural, physiological, and biochemical endpoints (neurotransmission, energy metabolism, antioxidant status, and oxidative damage), the effects of 50 nm waterborne polymethylmethacrylate (PMMA) NPs (0.5 to 500 µg/L) on the marine benthic polychaete Hediste diversicolor, a key species in estuarine and coastal ecosystems. Results demonstrated that worms exposed to PMMA NPs had a shorter burrowing time than control organisms. Nevertheless, worms exposed to PMMA NPs (0.5 and 500 µg/L) decreased cholinesterase activity. Energy metabolism was decreased at 50 and 500 µg/L, and glycogen content decreased at all concentrations of PMMA NPs. Enzymes related to the antioxidant defence system (superoxide dismutase and glutathione peroxidase) displayed increased activities in H. diversicolor specimens exposed to concentrations between 0.5 and 500 µg/L, which led to no damage at the cell membrane and protein levels. In this study, polychaetes also displayed a lower regenerative capacity when exposed to PMMA NPs. Overall, the data obtained in this study emphasize the potential consequences of PMMA NPs to benthic worms, particularly between 0.5 and 50 µg/L, with polychaetes exposed to 50 µg/L being the most impacted by the analysed NPs. However, since sediments are considered to be sinks and sources of plastics, further studies are needed to better understand the impacts of different sizes and polymers on marine organisms, particularly benthic species.

Evaluation of neuroprotective and anti-amnesic effects of the chloroform fraction of Nigella sativa L. on scopolamine-induced memory impairment in rats

The aim of this study was to investigate the neuroprotective and anti-amnesic effects of total extract (NTE) and chloroform fraction of Nigella sativa (NCE) on scopolamine (SCO)-induced memory impairment in the rat. After plant extraction and fractionation, the rats were treated with different doses of NTE (200, 400, and 800 mg/kg) and NCE (50, 100 or 200 mg/kg) before scopolamine administration for 7 successive days compared to donepezil (DON). Learning power and memory capacity of the treated animals were evaluated and the rat brain samples were further assessed for in vivo acetylcholinesterase (AChE) activity, lipid peroxidation, and finally validated by histopathological examination. Pretreatment with NTE and NCE effectively increased antioxidant activity, decreased cholinesterase activity and malondialdehyde (MDA) content in the hippocampal and cortical tissues as well as mitigated scopolamine-induced behavioral, and histological changes in a manner comparable to DON. Based on the pathology results, the most toxicity of NCE was observed at 200 mg/kg. The observed neuroprotective and anti-amnesic effects of NCE indicate that this fraction could be a promising candidate both for further studies to isolate the active components and for use in clinical trials in patients with cognitive impairment.

Evaluation of Toxic Effects Induced by Sub-Acute Exposure to Low Doses of α-Cypermethrin in Adult Male Rats.

To contribute new information to the pyrethroid pesticide α-cypermethrin toxicity profile, we evaluated its effects after oral administration to Wistar rats at daily doses of 2.186, 0.015, 0.157, and 0.786 mg/kg bw for 28 days. Evaluations were performed using markers of oxidative stress, cholinesterase (ChE) activities, and levels of primary DNA damage in plasma/whole blood and liver, kidney, and brain tissue. Consecutive exposure to α-cypermethrin affected the kidney, liver, and brain weight of rats. A significant increase in concentration of the thiobarbituric acid reactive species was observed in the brain, accompanied by a significant increase in glutathione peroxidase (GPx) activity. An increase in GPx activity was also observed in the liver of all α-cypermethrin-treated groups, while GPx activity in the blood was significantly lower than in controls. A decrease in ChE activities was observed in the kidney and liver. Treatment with α-cypermethrin induced DNA damage in the studied cell types at almost all of the applied doses, indicating the highest susceptibility in the brain. The present study showed that, even at very low doses, exposure to α-cypermethrin exerts genotoxic effects and sets in motion the antioxidative mechanisms of cell defense, indicating the potential hazards posed by this insecticide.

Review of the clinical management of current organophosphate poisoning treatments in humans

Although they have several uses, organophosphates (OPs) are mostly employed in agriculture as insecticides. Every year, OPs are too accountable for the deaths of hundreds of thousands of individuals. Acute toxicity is caused by overstimulating the central and autonomic nervous systems with nicotinic and muscarinic receptors, as well as the neuromuscular junction, as a result of acetylcholinesterase (AChE) enzyme suppression. Based on the poisoning history, the odor of pesticides, the distinctive clinical symptoms, and decreased cholinesterase activity are used to make the diagnosis of OP poisoning. The keys to successful outcomes are appropriate supportive care, decontamination, intensive anti-muscarinic therapy, early seizure management, and the administration of antidotal oxime medication.

Protective effect of huperzine A on phenytoin induced cognition impairment: Behavioral and biochemical study

Phenytoin, a drug of choice for Epilepsy is also known for its adverse effects. The most common adverse effect due to phenytoin is cognition impairment. Cognition impairment is a serious problem in society as it debars the person's social life. Thus to overcome such a problem demand for a solution arises. Huperzine, sesquiterpene alkaloids having immense neuroprotective properties. Thus in this study, it was aimed to evaluate the effectiveness of huperzine on Phenytoin- induced Cognition Impairment. The protective effect of huperzine on phenytoin-induced cognition impairment was evaluated in rats. The effect of Huperzine on phenytoin-induced cognitive impairment was evaluated by behavioral, biochemical, and histopathological studies. The co-administration of huperzine with phenytoin showed significant results. The treatment of Huperzine with phenytoin resulted in significant improvement in learning and memory. The oxidative stress induced by Phenytoin was reversed by huperzine. A significant decrease in cholinesterase activity was also observed. The histopathology showed damaged neuronal cells in periventricular regions and cortex due to phenytoin which was altered by Huperzine. Thus, the present study demonstrates the protective effect of huperzine on phenytoin-induced cognition impairment.

Plasma cholinesterase activity is influenced by interactive effect between omethoate exposure and CYP2E1 polymorphisms

The aim of this study was to explore the association between metabolizing enzyme gene polymorphisms and the decrease in cholinesterase activity induced by omethoate exposure. A total of 180 workers exposed to omethoate over an extended period were recruited along with 115 healthy controls. Cholinesterase activity in whole blood, erythrocyte, and plasma was detected using acetylthiocholine and the dithio-bis-(nitrobenzoic acid) method. Six polymorphic loci of GSTT1(+/-), GSTM1(+/-), GSTP1 rs1695, CYP2E1 rs6413432, CYP2E1 rs3813867, and PON2 rs12026 were detected by polymerase chain reaction and restriction fragment length polymorphism (PCR-RFLP). The gene-environment interactions were analyzed using the generalized linear model method. The cholinesterase activity of erythrocyte and plasma in the exposure group was significantly lower than that in the control group (P < 0.001) in general. The plasma cholinesterase activity in the TT + AT genotype in CYP2E1 rs6413432 was lower than that in the AA genotype in the exposure group (P = 0.016). Interaction between the AA genotype in CYP2E1 rs6413432 and omethoate exposure had a significant effect on plasma cholinesterase activity (P = 0.079). The decrease in plasma cholinesterase activity was associated with interaction between the AA genotypes in rs6413432 and omethoate exposure.

Токсикодинаміка за сумісної дії хлорпірифосу та івіну при тривалому надходженні до організму

The combined action of pesticides is one of the problems of toxicology, because in comparison to individual active substances, their mixtures can increase toxicity and delayed action effects, which is a risk to human health. It is known that plant growth regulators (PGR) when applied together with pesticides help to reduce the quantitative rates of pesticides applied, the accumulation of pesticides and heavy metals in plants, reduce the acute toxicity of xenobiotics. The combined effect of the prolonged admission of PGRs and pesticides is an unexplored area, and it is an important issue in preventive toxicology. The Aim of the Research. Determination of the nature of toxic effects of Chlorpyrifos and “Ivin” combined action at subchronic oral admission. Materials and Methods. Chlorpyrifos and PGR “Ivin” (2.6-dimethyl-N-pyridine oxide) combined action was studied on male Wistar Han rats. Substances were administered orally, via a feeding tube for 13 weeks; Chlorpyrifos was administered in the form of an aqueous emulsion with an auxiliary material OP-10 at a dose of 5 mg/kg (1/15 LD50), “Ivin” — in the form of an aqueous solution at a dose of 13 mg/kg and 0.013 mg/kg (1/100 and 1/100000 LD50 respectively), the control group of rats was given water with an auxiliary material OP-10. Signs of intoxication were recorded, body weight was measured in 4, 9 and 13 weeks, biochemical indicators of blood serum were determined (the activity of ALT and AST enzymes and alkaline phosphatase; the content of crude protein, urea, cholesterol, triglycerides and glucose were determined using kits of reagents by BioSystems (Spain); cholinesterase (ChE) activity in serum, red blood cells and brain tissue was determined with the use of methodology by Hesrtin S. using a kit of reagents produced by LLC NPP Filisit-Diagnostics (Ukraine). Results. No clinical signs of intoxication were detected in the experimental groups of rats. Under the isolated use of Chlorpyrifos a significant decrease in body weight, ChE inhibition activity in all bio substrates, with the greatest effect in the brain (by 48.8%); increase (after 9 and 13 weeks) in the activity of ALT and AST by 26.7–32.6%, 12.5–12.0%; a slight but a significant increase in the level of urea and glucose in blood serum to 17.3% and 17.6 %, respectively was detected. Under the combined action of Chlorpyrifos and “Ivin” in specified doses the body weight of rats was at control level, decrease of ChE activity was observed in all biological substrates and was at nearly the same level with the isolated use of Chlorpyrifos. There was a tendency towards the decline in ChE inhibition activity in brain tissue, and under the combined action of Chlorpyrifos with “Ivin” at higher doses after 4 weeks this effect was a significant (22.15%, p &lt; 0.05). Conclusions. Chlorpyrifos under the isolated oral admission for 13 weeks has a weak hepatotoxic effect, as evidenced by the increase in cytolysis enzymes and urea levels in serum and causes a moderate anticholinesterase effect. “Ivin” under combined with Chlorpyrifos admission to the organism eliminates the hepatotoxic effects of Chlorpyrifos and reduces its anticholinergic effects in brain, which contributes to a less severe intoxication. Key Words: Chlorpyrifos, Ivin, hepatotoxic effect, anticholinesterase effect.

Rutin restores neurobehavioral deficits via alterations in cadmium bioavailability in the brain of rats exposed to cadmium

Many plant foods are rich sources of rutin, a flavonoid with many biological activities and health benefits. Exposure to cadmium has been implicated in neurotoxicity and cognitive dysfunction in animal models. However, there is a dearth of information on the effect of rutin on the cadmium bioavailability in the brain of rats exposed to cadmium. Thus, the present study investigated the therapeutic efficacy of rutin in an animal model of cognitive impairment via alterations of cadmium bioavailability in cadmium-exposed rats. Animals were divided into six groups (n = 6): group 1 served as control, groups 2 and 3 are normal rats received 25 and 50 mg/kg of rutin respectively, group 4 received cadmium (5 mg/kg), while groups 5 and 6 are cadmium-exposed rats treated with 25 and 50 mg/kg rutin respectively via oral administration for 21 days. Rutin was administered 30 min after cadmium administration each day. The spatial working memory of the exposed and treated rats was assessed using Morris water maze and Y-Maze tasks. Furthermore, the residual level of cadmium ion in the brain of the rats was estimated. The cholinesterase (AChE and BChE) activities and nitric oxide level were determined. Besides, the level of oxidative stress markers (ROS and MDA) was assessed. Results revealed that rutin significantly reduced cadmium bioavailability in the brain of cadmium-exposed rats. Moreso, cadmium increased cholinesterase (AChE and BChE) activities and level of oxidative stress markers in the brain, with a concomitant decrease in nitric oxide level. However, treatment with rutin decreased cholinesterase activities and the level of oxidative stress markers in cadmium-exposed rats. Also, rutin improved spatial working memory and learning processes as revealed by Morris water maze and Y-Maze tasks. Conclusively, rutin could be considered to possess cognitive-enhancing properties possibly through alterations of cadmium bioavailability in the brain of cadmium-exposed rats.

Comparison of the Respiratory Toxicity and Total Cholinesterase Activities in Dimethyl Versus Diethyl Paraoxon-Poisoned Rats.

The chemical structure of organophosphate compounds (OPs) is a well-known factor which modifies the acute toxicity of these compounds. We compared ventilation at rest and cholinesterase activities in male Sprague-Dawley rats poisoned with dimethyl paraoxon (DMPO) and diethyl paraoxon (DEPO) at a subcutaneous dose corresponding to 50% of the median lethal dose (MLD). Ventilation at rest was recorded by whole body plethysmography. Total cholinesterase activities were determined by radiometric assay. Both organophosphates decreased significantly the respiratory rate, resulting from an increase in expiratory time. Dimethyl-induced respiratory toxicity spontaneously reversed within 120 min post-injection. Diethyl-induced respiratory toxicity was long-lasting, more than 180 min post-injection. Both organophosphates decreased cholinesterase activities from 10 to 180 min post-injection with the same degree of inhibition of total cholinesterase within an onset at the same times after injection. There were no significant differences in residual cholinesterase activities between dimethyl and diethyl paraoxon groups at any time. The structure of the alkoxy-group is a determinant factor of the late phase of poisoning, conditioning duration of toxicity without significant effects on the magnitude of alteration of respiratory parameters. For same duration and magnitude of cholinesterase inhibition, there was a strong discrepancy in the time-course of effects between the two compounds.

Changes in murine anorectum signaling across the life course.

BackgroundIncreasing age is associated with an increase in the incidence of chronic constipation and fecal impaction. The contribution of the natural aging process to these conditions is not fully understood. This study examined the effects of increasing age on the function of the murine anorectum.MethodsThe effects of increasing age on cholinergic, nitrergic, and purinergic signaling pathways in the murine anorectum were examined using classical organ bath assays to examine tissue function and electrochemical sensing to determine age‐related changes in nitric oxide and acetylcholine release.Key ResultsNitrergic relaxation increased between 3 and 6 months, peaked at 12 months and declined in the 18 and 24 months groups. These changes were in part explained by an age‐related decrease in nitric oxide (NO) release. Cholinergic signaling was maintained with age by an increase in acetylcholine (ACh) release and a compensatory decrease in cholinesterase activity. Age‐related changes in purinergic relaxation were qualitatively similar to nitrergic relaxation although the relaxations were much smaller. Increasing age did not alter the response of the anorectum smooth muscle to exogenously applied ACh, ATP, sodium nitroprusside or KCl. Similarly, there was no change in basal tension developed by the anorectum.Conclusions and InferencesThe decrease in nitrergic signaling with increasing age may contribute to the age‐related fecal impaction and constipation previously described in this model by partially obstructing defecation.

Association of genetic polymorphisms of telomere binding proteins with cholinesterase activity in omethoate-exposed workers

Omethoate, an organophosphorous pesticide, can cause a variety of health effects, especially the decrease of cholinesterase activity. The aim of this study is to explore the association of genetic polymorphisms of telomere binding proteins with cholinesterase activity in omethoate-exposed population. Cholinesterase activities in whole blood, red blood cell and plasma were detected using acetylthiocholine and dithio-bis-(nitrobenzoic acid) method; Genetic Genotyping of POT1 rs1034794, POT1 rs10250202, TERF1 rs3863242 and TERT rs2736098 were performed with PCR-RFLP. The cholinesterase activities of whole blood, red blood cells and plasma in exposure group are significantly lower than that of the control group (P < 0.001). Multivariate analysis indicates that exposure group (b = − 1.016, P < 0.001), agender (b = 0.365, P < 0.001), drinking (b = 0.271, P = 0.004) and TERF1rs3863242 (b = − 0.368, P = 0.016) had an impact on cholinesterase activities. The results suggest that individual carrying AG+GG genotypes in TERF1 gene rs3863242 polymorphism were susceptible to damage in cholinesterase induced by omethoate.

Determining a threshold sub-acute dose leading to minimal physiological alterations following prolonged exposure to the nerve agent VX in rats.

VX, a potent inhibitor of cholinesterase (ChE), is considered as one of the most toxic, persistent and least volatile nerve agents. VX is absorbed in various environmental surfaces and is gradually released long after its initial dispersal. Its toxicity is mainly caused by disrupting central and peripheral cholinergic nervous system activity, leading to potential long-term detrimental effects on health. The primary objective of the present study was to assess the threshold VX dose leading to minimal physiological alterations following prolonged VX exposure. Characterization of such a threshold is crucial for dealing with unresolved operative dilemmas such as when it is safe enough to resettle a population that has been evacuated from a VX-contaminated area. Rats, continuously exposed to various doses of VX (0.225-45µg/kg/day) for 4weeks via implanted mini-osmotic pumps, showed a dose-dependent and continuous decrease in ChE activity in whole blood, brain and muscles, ranging between 20 and 100%. Exposure to 13.5µg/kg/day led to a stable low ChE activity level (~20%), accompanied by transient and negligible electrocorticogram spectral power transformations, especially in the theta and alpha brain wave frequencies, and a significant decrease in total brain M2 receptor density. These changes were neither accompanied by observable signs of intoxication nor by changes in motor function, circadian rhythm or TSPO level (a reliable marker of brain damage). Following exposure to lower doses of 2.25 and 0.225µg/kg/day, the only change measured was a reduction in ChE activity of 60 and 20%, respectively. Based on these results, we delineate ChE inhibition as the physiological measure most susceptible to alterations following prolonged VX exposure, and determine for the first time the threshold sub-acute VX dose for minimal physiological effects (up to 20% reduction in ChE activity) in the rat as 0.225µg/kg/day.

Effect of pomegranate extracts on brain antioxidant markers and cholinesterase activity in high fat-high fructose diet induced obesity in rat model

BackgroundTo investigate beneficial effects of Pomegranate seeds oil (PSO), leaves (PL), juice (PJ) and (PP) on brain cholinesterase activity, brain oxidative stress and lipid profile in high-fat-high fructose diet (HFD) induced-obese rat.MethodsIn vitro and in vivo cholinesterase activity, brain oxidative status, body and brain weight and plasma lipid profile were measured in control rats, HFD-fed rats and HFD-fed rats treated by PSO, PL, PJ and PP.ResultsIn vitro study showed that PSO, PL, PP, PJ inhibited cholinesterase activity in dose dependant manner. PL extract displayed the highest inhibitory activity by IC50 of 151.85 mg/ml. For in vivo study, HFD regime induced a significant increase of cholinesterase activity in brain by 17.4% as compared to normal rats. However, the administration of PSO, PL, PJ and PP to HDF-rats decreased cholinesterase activity in brain respectively by 15.48%, 6.4%, 20% and 18.7% as compared to untreated HFD-rats. Moreover, HFD regime caused significant increase in brain stress, brain and body weight, and lipid profile disorders in blood. Furthermore, PSO, PL, PJ and PP modulated lipid profile in blood and prevented accumulation of lipid in brain and body evidenced by the decrease of their weights as compared to untreated HFD-rats. In addition administration of these extract protected brain from stress oxidant, evidenced by the decrease of malondialdehyde (MDA) and Protein carbonylation (PC) levels and the increase in superoxide dismutase (SOD) and glutathione peroxidase (GPx) levels.ConclusionThese findings highlight the neuroprotective effects of pomegranate extracts and one of mechanisms is the inhibition of cholinesterase and the stimulation of antioxidant capacity.

Evaluation of chronic intoxication by organophosphate insecticides among hygiene workers in the city of Fez, Morocco

Summary Context of the study The use of pesticides in the field of public health involves a risk for both humans and the environment. Objective The purpose of this study, carried out for the first time in the center of Morocco, was to evaluate chronic intoxication by organophosphate insecticides. This was done through the evaluation of cholinesterase activity as a biomarker of pesticide intoxication among a population of hygiene workers who daily handled these products, in six districts of the city of Fez. Method This study is a descriptive cross-sectional study including 30 consenting hygiene workers carried out during a period of 4 months (February-May 2015). The study included a physical examination and biotoxicological measurements: plasma and erythrocyte acetylcholinesterase activity. Erythrocyte acetylcholinesterase activity was determined by spectrophotometric method at ambient laboratory temperature (25 °C) using the kit “Test Mat - model 400”. Results Twenty-nine subjects of the studied population were of male gender with an average age of 48 ± 8 years and a body mass index of 25.67 ± 2.09 kg/m 2 ; and only one subject was of female gender aged 56, and a body mass index of 26.25 kg/m 2 . The somatic clinical examination of the participants in this study revealed neither serious clinical history nor cases of pesticide poisoning. The mode value of erythrocyte cholinesterase activity was 54, and that of plasmatic cholinesterase activity was 65. The measured cholinesterase activity is not correlated with age but it is correlated with the body mass index. Three cases showed a decrease in cholinesterase activity of the order of (35%, 36%, and 25%) compared to 30% as recommended by the World Health Organization. Conclusion These results relating to the determination of cholinesterase activity, although preliminary, should reassure the exposed persons and the authorities concerned without neglecting the systematic control of the three cases detected. The use of organophosphates in the field of public health requires regular checking, precautions, and training of the hygiene workers to avoid any serious health risk.

Impact of Exposure to Fenitrothion on Vital Organs in Rats.

This study was designed to investigate the impact of oral administration of fenitrothion (10 mg/kg) on liver, kidney, brain, and lung function in rats. The effect was studied on days 7, 14, 21, 28, and 42. Our results have shown deterioration in liver function as evidenced by the elevation in serum ALT, AST, ALP, and bilirubin and reduction in albumin and hepatic glycogen. This was associated with a state of hyperglycemia and hyperlipidemia and increased prothrombin time, while hemoglobin content was reduced. In addition, the kidney function was reduced as indicated by the elevation in serum creatinine, uric acid, and BUN, while the serum levels of magnesium, potassium, and sodium were reduced. This study also showed an impairment in brain neurotransmitter (elevated 5-HT, glutamate, GABA, and reduced dopamine and norepinephrine level). This was associated with a reduction in the barrier capacity in brain and lung. Fenitrothion also caused a decrease in cholinesterase activity in serum, lung, and brain activity associated with a state of oxidative stress in all tested organs and hyperammonemia. These results support the hazards of pesticide use and shows the importance of minimizing pesticide use or discovering new safe pesticides.

Comparative study of the cholinesterase activities in tissues of the round goby Neogobius melanostomus (Gobiidae) from different locations of the Black and Azov seas

Cholinesterase activity has been assayed in the liver, muscles, and blood serum of the round goby Neogobius melanostomus caught in the coastal waters of the Black and Azov seas differing in the degree of anthropogenic impact. The highest enzyme activity in the fish individuals from both seas is observed in the liver and the lowest is observed in the blood serum. The fish caught in the most polluted (by municipal and agricultural wastewaters) sites of both seas display a decrease in cholinesterase activity. The utility of cholinesterase activity as a biomarker in monitoring of the marine areas affected by anthropogenic pollution is discussed.

Effects of a lyophilized aqueous extract of Feretia apodanthera Del. (Rubiaceae) on pentylenetetrazole-induced kindling, oxidative stress, and cognitive impairment in mice

Feretia apodanthera Del. (Rubiaceae) is extensively used in ethnomedicine in Cameroon and Nigeria for epilepsy, febrile convulsions, and rheumatic pains and for enhancing cognitive performance. The aim of the present study was to examine the effects of a lyophilized aqueous extract of F. apodanthera on the course of kindling development, kindling-induced learning deficit, oxidative stress markers, and cholinesterase activity in pentylenetetrazole (PTZ)-kindled mice. Pentylenetetrazole, 30mg/kg, induced kindling in mice after 30.00±1.67days. The aqueous extract of F. apodanthera showed dose-dependent antiseizure effects. Feretia apodanthera (150–200mg/kg) significantly increased the latency to myoclonic jerks, clonic seizures, and generalized tonic–clonic seizures. The extract also improved the seizure score and decreased the number of myoclonic jerks. Pentylenetetrazole kindling induced significant oxidative stress and cognitive impairment which were reversed by pretreatment with F. apodanthera in a dose-dependent manner. The significant decrease in cholinesterase activity observed in the PTZ-kindled mice was reversed by pretreatment with the F. apodanthera extract. The results indicated that pretreatment with the aqueous extract of F. apodanthera antagonizes seizures, oxidative stress, and cognitive impairment in PTZ-kindled mice. The aqueous extract of F. apodanthera also showed anxiolytic activities, but the inhibition of memory impairment was not attributed to the anxiolytic activities of the plant. These results thus suggest the potential of F. apodanthera as an adjuvant in epilepsy both to prevent seizures as well as to protect against seizure-induced oxidative stress and memory impairment.

Activity of the liver enzymes in children’s serum in case of chronic and exacerbative granulating apical periodontitis in permanent teeth

The study involved 63 children with granulating periodontitis of permanent teeth, aged 12-1 and determined the activity of liver enzymes: arginase, cholinesterase, aspartate aminotransferase (AST) and alanine aminotransferase (ALT) of serum. A marked increased activity of arginase and decrease in cholinesterase activity in case of chronic granulating apical periodontitis of permanent teeth and in case of the exacerbation of this pathological process have been revealed. It was also found a significant increase of ALT and AST parameters in case of the exacerbation of disease. The results obtained suggest that periodontal pathology affects the functional activity of the liver cells.

Protective effect of madecassoside against cognitive impairment induced by d-galactose in mice

This study was designed to investigate the protective effect of madecassoside from Hydrocotyle sibthorpioides against cognitive impairment induced by d-galactose (d-gal) in mice. The result revealed that treatment with madecassoside significantly reversed d-gal-induced learning and memory impairments, as measured by the Morris water-maze test. Studies on the potential mechanisms of this action showed that madecassoside significantly reduced oxidative stress and suppress inflammatory responses via blocking NF-κB and ERK/p38 MAPK pathways. Moreover, madecassoside markedly attenuated the content and deposition of β-amyloid peptide by inducing a decrease in the expression of amyloid protein precursor, β-site amyloid cleaving enzyme-1 and cathepsin B and an increase in the levels of neprilysin and insulin-degrading enzyme. Madecassoside significantly increased the expression of synapse plasticity-related proteins in the hippocampus, such as postsynaptic density 95, long-term potentiation, N-methyl-d-aspartic acid receptors, Ca2+/calmodulin-dependent protein kinase II, NMDA receptor subunit 1, protein kinase C, protein kinase A, cAMP-response element binding protein, and brain-derived neurotrophic factor. In addition, madecassoside significantly increased the levels of acetylcholine but decreased cholinesterase activity. In conclusion, the protective effect of madecassoside against d-gal-induced cognitive impairment was mainly due to its ability to reduce oxidative damage, improve synaptic plasticity and restore cholinergic function. These findings suggest that madecassoside can be considered as a potential agent for preventing cognitive impairment.

Protective effect of Millettia pulchra polysaccharide on cognitive impairment induced by d-galactose in mice

A polysaccharide (PMP) was isolated from Millettia pulchra and purified by DEAE-cellulose and Sephadex G-75 chromatography. The results showed that PMP was composed of d-glucose and d-arabinose in a molar ratio of 90.79% and 9.21%, with an average molecular weight of about 14,301Da. Furthermore, the effect of PMP on cognitive impairment induced by d-galactose in mice was evaluated. Treatment with PMP significantly reversed d-galactose-induced learning and memory impairments, as measured by behavioral tests. One of the potential mechanisms of this action was to reduce oxidative stress and suppress inflammatory responses. Furthermore, our results also showed that PMP markedly reduced the content and deposition of β-amyloid peptide, improved the dysfunction of synaptic plasticity, increased the levels of acetylcholine, but decreased cholinesterase activity. These results suggest that PMP exerts an effective protection against d-galactose-induced cognitive impairment, and PMP may be a major bioactive ingredient in M. pulchra.