Impact of the ABO and RhD Blood Groups on the Evaluation of the Erythroprotective Potential of Fucoxanthin, ß-Carotene, Gallic Acid, Quercetin and Ascorbic Acid as Therapeutic Agents against Oxidative Stress.

Previous studies detail that different blood groups are associated with incidence of oxidative stress-related diseases such as certain carcinomas. Bioactive compounds represent an alternative for preventing this oxidative stress. The aim of this study was to elucidate the impact of blood groups on the erythroprotective potential of fucoxanthin, ß-Carotene, gallic acid, quercetin and ascorbic acid as therapeutic agents against oxidative stress. The impact of ABO blood groups on the erythroprotective potential was evaluated via the antioxidant capacity, blood biocompatibility, blood susceptibility and erythroprotective potential (membrane stabilization, in vitro photostability and antihemolytic activity). All tested antioxidants exhibited a high antioxidant capacity and presented the ability to inhibit ROO•-induced oxidative stress without compromising the cell membrane, providing erythroprotective effects dependent on the blood group, effects that increased in the presence of antigen A. These results are very important, since it has been documented that antigen A is associated with breast and skin cancer. These results revealed a probable relationship between different erythrocyte antigens with erythroprotective potential, highlighting the importance of bio-targeted drugs for groups most susceptible to certain chronic-degenerative pathologies. These compounds could be applied as additive, nutraceutical or encapsulated to improve their bioaccessibility.

Impact of ambulatory EEG in the management of patients with epilepsy in resource-limited Latin American populations.

Objective: Ambulatory electroencephalography (AEEG) monitoring allows for prolonged recordings in normal environments, such as patients' homes, and is recognized as a cost-effective alternative to inpatient long-term video-EEG primarily in resource-limited countries. We aim to describe the impact of AEEG on the assessment of patients with suspected or confirmed epilepsy in two independent Latin-American populations with limited resources. Methods: We included 63 patients who had undergone an AEEG due to confirmed/suspected epilepsy. Clinical (demographic, current antiseizure medication and indication) and electroencephalographic (duration of the study, result, and impact on clinical decision-making) were reviewed and compared. Results: The main indication for an AEEG was the differentiation of seizures from non-epileptic events with 57% of patients. It was categorized as positive in 36 patients and did have an impact on the clinical decision-making process in 57% of patients. AEEG captured clinical events in 35 patients (20 epileptic and 15 non-epileptic). Conclusions: AEEG proves to be a valuable tool in resource-limited settings for assessing suspected or confirmed epilepsy cases, with a significant impact on clinical decisions. Significance: Our study provides valuable insights into the use of AEEG in under-resourced regions, shedding light on the challenges and potential benefits of this tool in clinical practice.

Association between IL-17A, IL-17F and IL-17RA gene polymorphisms and susceptibility to psoriasis and psoriatic arthritis: a meta-analysis.

BACKGROUND: Psoriasis (Ps) is a chronic dermatosis characterized by erythematous-squamous plaques derived from an inflammatory response. The effect of polymorphisms in the genes that encode the members of the IL-17 family and their receptors has been studied to find an association with the susceptibility to Ps. However, the findings have not been conclusive. OBJECTIVES: To describe the association between IL-17A, IL-17F and IL-17RA gene polymorphisms and susceptibility to Ps. METHOD: A systematic review was conducted using the PubMed and Scopus databases to identify studies that evaluated the association between IL-17A, IL-17F, and IL-17RA gene polymorphisms and Ps susceptibility. This meta-analysis included reports published until June 2021. Heterogeneity was assessed using Cochran's Q-statistic test and I2 statistics. The associations between polymorphisms and Ps susceptibility were determined by pooled OR with a 95% CI. RESULTS: Fifteen studies were included. The frequency of the T allele of the IL-17F rs763780 polymorphism was significantly lower in patients with vulgar Ps (OR = 0.732, p = 0.026). The TT genotype of the IL-17F rs763780 polymorphism was significantly associated with a decreased frequency in individuals with Ps and psoriatic arthritis (PsA) (TT:TC + CC OR = 0.664, p = 0.046). Regarding IL-17RA polymorphisms, the AG genotype of the rs4819554 polymorphism showed a near-significant decrease in psoriasis risk compared to the GG genotype (AG:GG OR = 0.604, p = 0.050). Other polymorphisms in IL-17A, IL-17F and IL-17RA showed no association with Ps. CONCLUSIONS: The T allele and TT genotype of the IL-17F rs763780 polymorphism may be associated with a decreased risk of psoriasis. Therefore, the implications of this variant on psoriasis pathogenesis and treatment require further investigation.

The anticonvulsant effect of sparteine on pentylenetetrazole-induced seizures in rats: a behavioral, electroencephalographic, morphological and molecular study.

Abnormal synchronous activity in neurons generates epileptic seizures. Antiepileptic drugs (AEDs) are effective in 70% of patients, but this percentage is drastically lower in developing countries. Sparteine is a quinolizidine alkaloid synthesized from most Lupine species and has a probable anticonvulsive effect. For this reason, the objective of the present work was to study the anticonvulsant effect of sparteine using a dose-effect curve and to determine its effectiveness against seizures using behavioral, electroencephalographic, morphological and molecular data. Wistar rats were grouped into control [saline solution (0.9%), pentylenetetrazole (90 mg/kg), and sparteine (13, 20 and 30 mg/kg), intraperitoneal (i.p.)] and experimental (sparteine + pentylenetetrazole) groups. The rats were implanted with surface electrodes to register electrical activity, and convulsive behavior was evaluated according to Velisek's scale. The rats were perfused to obtain brain slices for cresyl violet staining and cellular density quantification as well as for immunohistochemistry for NeuN and GFAP. Other animals were used to determine the hippocampal mRNA expression of the M2 and M4 acetylcholine receptors by qPCR. Sparteine exhibited a better anticonvulsant effect at a dose of 30 mg/kg (i.p.) than at the other doses used. This anticonvulsant effect was characterized by a decrease in the severity of convulsive behavior, 100% survival, an inhibitory effect on epileptiform activity 75 min after pentylenetetrazole administration, and the conservation of the cellular layers of CA1, CA3 and the dentate gyrus (DG); however, astrogliosis was observed after 30 mg/kg sparteine treatment. In addition, sparteine treatment increased the mRNA expression of the M4 receptor three hours after administration. According to our findings, the effective dose of sparteine as an anticonvulsant agent by i.p. injection is 30 mg/kg. The astrogliosis that was observed after sparteine administration may be a compensatory mechanism to diminish excitability and maintain neuronal homeostasis, possibly through redistributing potassium and glutamate. The increase in the mRNA expression of the M4 receptor may suggest the participation of the M4 receptor in the anticonvulsive effect of sparteine, as the activation of this receptor may inhibit acetylcholine release and facilitate the subsequent release of GABA. However, the precise mechanisms by which sparteine produces these effects are not known, and therefore, further experiments are necessary.

Effect of Chronic Krill Oil Supplement on Seizures Induced by Pentylenetetrazole in the Hippocampus of Adult Rats with Previous Febrile Seizures.

We evaluated the effect of krill oil (KO) supplement on seizures induced by pentylenetetrazole (PTZ) in animals with previous febrile seizures (FSs) induced by hyperthermia to determine its effectiveness in seizure susceptibility and as an anticonvulsant. Male Wistar rats with FS separated into water (W, 1 mL), palm oil (PO, 300 mg/kg, total volume 1 mL), or KO (300 mg/kg, total volume 1 mL) groups. All drugs were administered chronically via the intragastric route. Electrical activity was recorded by intracranial EEG simultaneously with convulsive behavior. All animals' brains were processed by immunofluorescence against GFAP, NeuN, and connexins (Cx); cellular quantification was performed in hippocampus and pyramidal or granular layer thickness was evaluated with cresyl violet (CV) staining. The results showed a significant delay in convulsive behavior and a slight increased survival time after PTZ administration in the group treated with KO compared with PO and W groups. The epileptiform activity showed high amplitude and frequency, with no significant differences between groups, nor were there differences in the number and duration of discharge trains. KO and PO increased the number of astrocytes and the number of neurons compared with the W group. KO and PO decreased the expression of Cx36 without affecting Cx43 expression or the thickness of layers. Based on these data, we consider it important to perform more experiments to determine the anticonvulsant role of KO, taking into account the partial effect found in this study. KO could be used as a coadjuvant of traditional anticonvulsive treatments. PRACTICAL APPLICATION: In this study was evaluated the anticonvulsive effect of a chronic krill oil (KO) supplement in animals with seizures. Results showed that KO had partial anticonvulsive effects measured by EEG activity and convulsive behavior analysis. These data justify further research that looks at KO supplementation as a prospective coadjuvant of pharmacologic management of seizure disorder.

γ-Aminobutyric acid quantification in small volume biological samples through enzymatically induced electrochemiluminescence.

γ-Aminobutyric acid (GABA) is a well-known neurotransmitter that regulates inhibitory neurotransmission in the mammalian central nervous system and participates in several processes outside the brain. A reliable quantification method is needed to determine its role in different physiological and pathological conditions. However, GABA measurements have several challenges because GABA is neither fluorescent nor electroactive, and it is difficult to detect using enzymatic reactions because no oxidases or dehydrogenases have been identified. Several methods have been developed to quantify GABA concentrations based on the instrumentation available, the sensitivity required, and the volume of samples analyzed. Most of these methods use high-performance liquid chromatography (HPLC). Here, we describe a method for quantifying GABA concentrations in small volume samples using enzymatically-induced electrochemiluminescence with the well-known GABAse complex, which produces glutamate for use in a luminescent reaction with glutamate oxidase and luminol in an electrochemiluminescence cell. The luminescence obtained was proportional to the GABA concentrations in the micromolar range (1-1000), with linear r2 values > 0.95. GABA standards were treated with the enzymatic reactors to generate glutamate (Glu), which was measured simultaneously with an HPLC technique, to validate this new procedure. The assay was further used to determine GABA concentrations in hippocampal extracts. This alternative may be used to quantify GABA levels in fluid samples, such as microdialysates, other perfusates and tissue extracts. Thus, the method presented here is a good alternative for monitoring GABA levels with good sensitivity compared with the traditional methods that are still in use.

Sparteine as an anticonvulsant drug: Evidence and possible mechanism of action.

Sparteine is a quinolizidine alkaloid extracted from Lupinus that has numerous pharmacological properties both in humans and animal models. In the central nervous system, sparteine reduces locomotor activity, has light analgesic effects, also has no effects on short-term memory or spatial learning and does not induce changes in behavior or electroencephalographic (EEG) activity. However, the anticonvulsant profile of sparteine is not fully characterized in experimental animals and there are no data in humans. Therefore, the present review focuses on the experimental evidence supporting the anticonvulsant action of sparteine in models of acute seizures and status epilepticus (SE), as well as its possible mechanisms of action. The evidence that supports the anticonvulsant effect of (-)-Sparteine sulfate includes the inhibition of seizures induced by maximal electro-stimulation, a delay in the onset of convulsive behavior and the prolongation of survival time in mice treated with pentylenetetrazole (PTZ). Additionally, sparteine delays the onset of convulsive behavior and decreases the severity and mortality of rats treated with PTZ and pilocarpine. Sparteine decreases amplitude and frequency or blocks the epileptiform activity induced by PTZ, pilocarpine and kainic acid. Sparteine may decrease hyperexcitability through the activation of the M2 and M4 subtypes of mAChRs, which is a probable mechanism of action that together with its systemic effects may favor its anticonvulsant effects against seizures and SE.

Effect of sparteine on status epilepticus induced in rats by pentylenetetrazole, pilocarpine and kainic acid.

The long-term effects of status epilepticus (SE) include severe clinical conditions that result in disorders of various organs and systems as well as neurological damage that could lead to death. Sparteine is a quinolizidine alkaloid synthesized from most Lupine species, and its anticonvulsive effect was evaluated in the pentylenetetrazole model of SE. However, efforts to clearly determine the anticonvulsive effect of sparteine have not been made previously. For this reason, we consider it important to study the anticonvulsant effects of sparteine at the level of behavior and EEG activity in three different SE models. The animals of the control groups, which received intraperitoneal pentylenetetrazole (90 mg/kg), kainic acid (9 mg/kg) or pilocarpine (370 mg/kg), exhibited convulsive behavior and epileptiform activity. After sparteine pretreatment (13 mg/kg, administered 30 min before the convulsive drug), the animals administered pentylenetetrazole and pilocarpine exhibited reduced mortality rates compared with the corresponding control groups, while the animals administered kainic acid exhibited a delayed onset of convulsive behavior and decreased seizure duration compared with the corresponding control group. In the three models of SE, a significant reduction in the amplitude and frequency of discharge trains was observed. These results support the anticonvulsant effect of low doses of sparteine and allow us to direct our efforts to other new anticonvulsant strategies for seizure treatment. However, it is necessary to perform more experiments to determine the precise mechanism through which sparteine produces an anticonvulsant effect at this concentration.