Introducción: La isquemia cerebral constituye una de las primeras causas de muerte y la principal causa de discapacidad adquirida a nivel mundial. Actualmente se estudian nuevas variantes terapéuticas mediante la comprobación de su efecto neuroprotector o neurorreparador; para ello se utilizan los modelos in vitro que permiten entender la fisiopatología, y los mecanismos moleculares y celulares involucrados.

Objetivo: Describir la actualidad de los modelos in vitro de isquemia cerebral.

Método: Se realizó una revisión sistemática de los modelos in vitro de isquemia cerebral utilizados en los últimos cinco años. Se tuvieron en cuenta los procesos de la cascada isquémica simulada, el tipo celular y los indicadores isquémicos.

Conclusión: Se pueden definir varios tipos de modelos in vitro: los de privación de oxígeno y glucosa, que simulan el proceso isquémico desde su punto inicial, y los que reflejan procesos más específicos como los de excitotoxicidad, estrés oxidativo e inflamación. En todos los modelos se utilizan células primarias gliales, epiteliales o neuronales y se obtienen indicadores isquémicos que varían desde el aumento de citocinas proinflamatorias a la pérdida de la viabilidad celular.

Introduction: A marked or prolonged post-infarction inflammatory response leads to a pathologic remodeling, impairing the left ventricle function that is the most important predictor of heart failure development. Recent studies have investigated the modulation of inflammation by the autonomic system, mainly by electrical or drug vagal stimulation, making possible a new therapeutic approach for the modulation of the inflammation in the AMI. 

Objective: To evaluate the effect of the electrical stimulation of the aortic depressor nerve (ADN) on autonomic modulation and the possible effect on inflammatory response post AMI. Material and Methods: The animals were divided into 3 groups: Sham Group (SHAM) - 5 animals not infarcted without treatment; Infarcted group (AMI) - 10 infarcted animals without treatment; Infarcted and stimulated group (AMI+EST) - 10 infarcted animals treated with electrical stimulation of the ADN. Five sessions of 30 min of ADN stimulation were performed between days 1 and 3 post AMI.

Results: The electric current was able to reduce the median arterial pressure during the stimulation period by more than 30 mmHg in all sessions. The LF/HF ratio, which reflects the global sympathetic-vagal balance, was elevated in the AMI group (0.36±0.066) when compared to SHAM (0.18±0.015) and AMI+EST (0.16±0.022). Thus, it was possible to observe that the HF and LF parameters, important indicators of autonomic function, were similar between the SHAM and AMI+EST groups, demonstrating the beneficial effect of ADN electrical stimulation on the maintenance of autonomic modulation. The baroreflex sensitivity (BPM/mmHg) was reduced in the IAM group (ITR=1.44±0.20; IBR=-0.82±0.15) when compared to the SHAM group (TRI=2.79±0.58; BRI=1.10±0.43). The IAM+EST group presented higher induced baroreflex sensitivity (TRI=3.40±0.18; BRI=-3.32±0.43) and spontaneous compared to the AMI group, being similar or higher when compared to the SHAM group. Cardiac function assessed by echocardiography revealed a better systolic function in the AMI+EST group (Ejection Fraction %=53±3.8) when compared to the AMI group (Ejection Fraction %=43±2.0). Regarding collagen deposition in the lesion (% of collagen), the AMI group presented significantly higher values (14.24±1.75) when compared to SHAM (0.85±0.04) and AMI+EST (5.35±0, 46). Immunohistochemical analysis showed a higher concentration (cells per field) of M1 macrophages in the AMI group (131.13±11.75) in comparison to the AMI+EST group (95.46±16.27) and a higher number of M2 macrophages in the AMI+EST group (143.69±15.23) when compared to the AMI group (96.38±22.35). Oxidative stress markers indicated a higher carbonyl content of proteins (nmol/mg) in the AMI group (2.24±0.09) in comparison to the AMI+EST group (1.96±0.07). The IAM+EST group had a higher activity of the superoxide dismutase enzyme (USOD/mg) (5.55±0.04) when compared to the AMI group (5.16±0.06).

Conclusions: These findings suggest that the electrical stimulation of the ADN was able to modulate the inflammatory response post AMI, leading to a less pathological remodeling and improving the indexes of the cardiac function evaluated by echocardiography, presenting as a new therapeutic approach in the prevention of heart failure development after AMI.

Background: Several parts of Zea mays (maize) have been used for the treatment of several ailments including inflammatory conditions.

Objective: to evaluate the modulatory effect on carrageenan-induced inflammation of the methanol extract of Zea mays cob husk in Albino rats.

Methods: 9.45% maize cob husks methanol extract was obtained by soxhlet extraction and the phytochemical screening was done. The carrageenan-induced paw edema model of acute inflammation was carried out to 30 Albino rats which were divided into five groups, two controls (negative and positive) and three experimental. A single oral methanol extract (100, 200 or 400mg/Kg) were administered to the experimental groups. Indomethacin 10mg/Kg was used as positive control. The paw volume up to the tribiotural articulation was measured at 0, 1, 3 and 6^th hours. Inflammation was expressed as an increase in paw volume due to carrageenan injection and the percentage inhibition produced by the extracts was calculated to assess the anti-inflammatory activity. Acute toxicity study was conducted. ANOVA test was applied and P value less than 0.05 were considered significant.

Results: saponins, tannins and polyphenols were present in the plant extract. Doses below 5000mg/Kg were considered safe. Significant anti-inflammatory activity was shown at 400mg/Kg after sixth hours.

Conclusions: The anti-inflammatory effect of Zea mays cob husk extract may be attributed to the presence of saponins, tannins and polyphenols. Percentage inhibition of inflammation by the extracts showed dose and time dependence. The anti-inflammatory effect was found significant for safe concentrations of the plant extract.

Objective: To describe the neuroimmunological actions produced by melatonin.

Matherials and methods: A review on the subject was carried out using articles of free access in the Pubmed database from 2015 to January 2019.

Discussion: The effects of melatonin on the wake-sleep cycle are known. Recently it has been shown that this neurohormone can modulate the immune response and reduce seizures in autoimmune and rheumatologic diseases. It induces the pattern of regulatory T lymphocytes and immunomodulatory cytokines maintaining the homeostasis of the internal environment. In the Central Nervous System inhibits the formation of free radicals, has antioxidant functions and can slow neurodegenerative processes. In the peripheral nerves decreases oxidative stress and cellular apoptosis. There are drugs that use melatonin as an active ingredient for its beneficial effects. In Cuba, only the history of a publication on this hormone is collected.

Conclusions: Melatonin can be a very useful element in the management of inflammatory and neurological diseases.

Introduction: The etiology of autoimmune diseases is still unknown but different causes arise. Objective: To describe the role of factors such as hormones, feeding, stress and low grade inflammation in the etiology of autoimmune diseases. Materials and Methods: A bibliographic review was made using the Google Scholar and articles of free access in the Pubmed and Scielo database from 2015 to February 2019. The search terms were used according to the DeCS and MeSH descriptors. Development: It is well known that female hormones increase the risk of autoimmune diseases. Recently it has been observed that an imbalance in the neurohormone melatonin can generate autoreactive lymphocytes. Stress can maintain low-grade chronic inflammatory responses that cause tissue damage, initiating or aggravating the clinical manifestations of autoimmunity. An adequate diet allows the guests of the intestinal microbiota to maintain the homeostasis of the immune system. Today, glutamate is used as a flavor enhancer, especially in developed countries. Perhaps it is one of the causes of the higher incidence of autoimmune diseases in these regions. Conclusions: Autoimmune diseases are more frequent in women. Adequate nutrition allows the gut microbiota not to be altered and to maintain immunological homeostasis. Situations of stress and low-grade inflammatory processes can trigger or exacerbate the clinical manifestations of autoimmunity.

Introduction: Melatonin is a neurohormone, synthesized mainly in the pineal gland, which regulates the circadian rhythm. Objective: To describe the neuroimmunological actions produced by melatonin. Materials and methods: A review on the subject was carried out using articles of free access in the Pubmed database from 2015 to January 2019. Results: The effects of melatonin on the wake-sleep cycle are known. Recently it has been shown that this neurohormone can modulate the immune response and reduce seizures in autoimmune and rheumatologic diseases. It induces the pattern of regulatory T lymphocytes and immunomodulatory cytokines maintaining the homeostasis of the internal environment. In the Central Nervous System inhibits the formation of free radicals, has antioxidant functions and can slow neurodegenerative processes. In the peripheral nerves decreases oxidative stress and cellular apoptosis. There are drugs that use melatonin as an active ingredient for its beneficial effects. In Cuba, only the history of a publication on this hormone is collected. Conclusions: Melatonin can be a very useful element in the management of inflammatory and neurological diseases.

Introduction: The anti-inflammatory effect of Zea mays cob husk extract may be attributed to the presence of saponins, tannins and polyphenols. Objective: to evaluate the modulatory effect on carrageenan induced inflammation of the methanolic extract of Zea mays cob husk in Albino rats. Methods: The carrageenan-induced paw edema model of acute inflammation was carried out to 30 Albino rats which were divided into five groups, two controls (negative and positive) and three experimental. 9.45% maize cob husks methanol extract was previously obtained by soxhlet extraction and the phytochemical screening was done. Acute toxicity studies were conducted in 12 rats. A single oral methanol plant extract (100mg/Kg, 200mg/Kg or 400mg/Kg) were administered to the experimental groups. Indomethacin 10mg/Kg was used as positive control. The paw volume up to the tribiotural articulation was measured at 0, 1, 3, and 6^th hours. Inflammation was expressed as an increase in paw volume due to carrageenan injection and the percentage inhibition produced by the extracts was calculated to assess the anti-inflammatory activity. ANOVA was used to determine the statistical differences between the treatment groups considering a P value less than 0.05 significant. The research was conducted in conformance with the Ethical Principles for the use of animals in research with approval by the Ethical Research Committee of the Institution. Results: saponins, reducing sugars, steroids, tannins and polyphenols were present in the methanol Zea mays cob husk extract. Doses below 5000mg/Kg were considered safe. Significant anti-inflammatory activity was shown at 400mg/Kg after the sixth hour. Conclusions: The anti-inflammatory effect of Zea mays cob husk extract may be attributed to the presence of saponins, tannins and polyphenols. Percentage inhibition of inflammation by the extracts showed dose and time dependence. The antinflammatory activity was found significant for safe concentrations of the plant extract.

Introduction: Severe inflammation may induce body temperature (Tb) reduction instead of fever. In this situation, morbidity and mortality is generally higher. In mammals, based on experimental models of rats injected with endotoxin (LPS), a biphasic thermal response is suggested to be a regulated process. The initial Tb reduction, which avoids tissue hypoxia and damage because of reduction in O₂ demands, is followed by fever, which is considered to be a beneficial response when the LPS concentrations become lower throughout the time. In fact, different humoral pathways are involved in each thermal response, as for example, cyclooxygenase (COX)-1 in the Tb reduction and COX-2 during fever. The demonstration of such phenomenon in other species is important for supporting the adaptive nature of thermal responses to systemic inflammation. In this context, birds are the other endothermic vertebrate group besides mammals, which deserve investigation.

Objective: To use a precocious bird as animal model for investigating: 1) the effect of COX-2 and COX-1 inhibition on Tb changes induced by LPS; 2) the metabolic response to LPS under other two challenging conditions for O₂ demand such as food deprivation and cold.

Material and Methods: Five-day old chicks (Gallus gallus; ~100 g) injected with LPS (100 μg/kg, IM) decreased (-1.0±0.0^oC) and increased Tb (+0.9±0.2^oC) 1h and 4h after injection, respectively.

Results: The selective COX-2 inhibitor (SC-236, 1.25 mg/kg) caused no change in the initial Tb fall but attenuated the subsequent fever. In contrast, SC560 (selective COX-1 inhibitor; 1, 2.5, 5 mg/kg) did not affect the Tb reduction, but the lower doses induced a faster increase of Tb after 2h of LPS injection. Regardless the feed (food deprived or not) and thermal (cold-25^oC or neutral-30^oC) conditions, O₂ consumption was reduced 40-60 min after LPS injection, coinciding with Tb falling. The febrile response, however, was affected by cold and fasting as Tb increase was inhibited despite of no change in O₂ consumption. Conclusions: Thus, our preliminary results suggest that, similarly to rats, the febrile response to LPS is affected by other O₂ demands and may be modulated by COX-2 dependent pathways. In contrast, the initial thermal and metabolic decreases of Tb seem not to be affected by competing O₂ demands and is independent of COX-2 activity.

Keywords:   Thermal, Metabolic Biphasic Response, inflammation, chikens,  rats, Temperature, febrile response