The cagaitera (Eugenia dysenterica D.C.) is a native fruit species from the Cerrado region of Brazil. Its main use is for food, but it has medical, pharmaceutical. The aims of this work were to elaborate a fruit wine from cagaita (Eugenia dysenterica DC) pulp and to compare the fermentations conducted with free and with. The mature fruits of cagaita (Eugenia dysenterica) are harvested by hand. After cleaning (immersion in sodium hypochlorite ppm) and selection, the fruits.
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Aiming to evaluate the potential use of cagaita in pathologies involving oxidative stress, such as neurodegenerative disorders, this study investigated its antioxidant potential and neuroprotective effect. Electrochemical approaches and aluminium-induced neurotoxicity were used to determine respectively in vitro and in dysejterica antioxidant properties of cagaita.
Voltammetric experiments were carried out in a three-electrode system, whose working electrode consisted of glassy carbon. The redox behavior of CHE presented similar features to that of quercetin, a widely known antioxidant standard.
CHE prevented mouse memory impairment which resulted from aluminium intake. In addition, biochemical markers of oxidative stress catalase, superoxide dismutase activity, and lipid peroxidation were normalized by CHE treatment. The potential of CHE to prevent aluminium-induced neurotoxicity was reflected at the microscopic level, through the decrease of the number of eosinophilic necrosis phenotypes seen in treated groups.
Moreover, the protective effect of CHE eugenja similar to that of quercetin, which was taken as the standard. These findings showed that the CHE of cagaita leaves has a potential to protect the brain against oxidative-induced brain damage.
Oxidative stress is known to promote a myriad of pathological conditions due to prooxidant compound accumulation. Regarding lipid-rich organs such as the brain, reactive oxygen species ROS may ydsenterica to lipid peroxidation, thus impairing neurotransmitter signaling, which further worsens the neuronal functions [ 12 ].
Brain cells are particularly sensitive to oxidative damage due to their high oxygen uptake; therefore, the regular consumption of antioxidants is important concerning neuroprotection [ 34 ].
Physiological development of cagaita (Eugenia dysenterica).
Although brain tissue contains endogenous antioxidants capable of ROS reduction, some enzymes also contribute to promote redox homeostasis. Nevertheless, the hindrance of this antioxidant system culminates in oxidative-related neurotoxicity [ 34 ]. Moreover, exogenous factors such as heavy metals and aluminium poisoning may exert prooxidative behavior as well as promote steric hindrance of antioxidant enzyme active sites [ 56 ]. Herbal mater is regarded as the major antioxidant source in medicine due to the high reducing power of many plant secondary metabolites.
Amongst these compounds, shikimate pathway byproducts such as polyphenols are heavily sought after due to their reversible redox behavior.
Literature reports that polyphenolic-rich cagaita extracts improve glucose homeostasis of obese mice by attenuating hepatic gluconeogenesis and inflammation, as well as exhibit cytotoxic effect against SH-SY5Y human neuroblastoma cell line [ 8 ]. Amongst assessment tools capable of antioxidant evaluation, methods such as voltammetry may provide increased sensibility and selectivity when compared to colorimetric tests [ 10 ] and can be furthermore used to electrochemically characterize a complex sample such as vegetal mater.
Through such methods is possible to understand the redox features of a pool of compounds and provide important information about the thermodynamical feasibility of ROS reduction [ 1112 ]. Bovine serum albumin, quercetin, aluminium chloride, 5: Trichloroacetic acid TCA and glycine were purchased from Vetec.
All electrolyte salts, solvents, and reagents were of analytical grade. The prepared material was macerated for 48 hours and then filtered. The filtered fluid was reused to maximize extraction.
Physiological development of cagaita (Eugenia dysenterica).
The extract was thereafter concentrated in rotary evaporator and lyophilized. The measurements were performed in a 1. Experimental conditions for square wave voltammetry SWV were as follows: All voltammetric assays were performed in 0. Animals were segregated in 6 groups I to VI each group and undergone chronic treatment for 90 days. Treatment solutions were administered through gavage 0.
Treatment I was designed as a control group vehicle-distilled water ; therefore, only water was administered, while treatments II to VI were test groups. After the 45 th day, a second treatment was orally administered in the afternoon. The CHE concentrations herein used were selected according to an experimental optimization conducted by our research group data not shown.
In order to assess the neuroprotective properties of CHE against aluminium-induced neurotoxicity, three behavioral tests were conducted, namely, step-down test to evaluate short- and long-term memories [ 13 ], open-field, and chimney tests to evaluate locomotor activity [ rugenia15 ]. Mice were gently placed on the platform upon stepping four paws onto the grid eugeniaa when they received a 0.
The latency of the step-down motion was recorded, and the training consisted of one trial.
During the retention test session, mice were placed on the platform, but no shock was given when they stepped down. The latency of the step-down motion onto the grid was also recorded in the test session.
Retention test scores were expressed as test minus training step-down latency. Passive avoidance behavior based on negative reinforcement was used to examine the short- and long-term memory [ 13 dysnterica. The results were presented as time s to climb backwards out of the tube [ 15 ].
Twenty-four hours after the last behavioral test, the animals were anesthetized with isoflurane. Subsequently, mice were euthanized by blood extraction through cardiac puncture and the dysentegica tissue was removed. Thereafter, the supernatant was also used to assess thiobarbituric acid-reactive species TBARStotal superoxide dismutase activity, and catalase activity. This estimation was done by following the dysebterica mentioned by Ohkawa et al.
It is based on the reactivity of an end product of lipid peroxidation, malondialdehyde MDA with thiobarbituric acid TBA to produce a red adduct.
The principle of this method is the ability of superoxide dismutase enzyme to inhibit dysentfrica autoxidation of epinephrine. The activity of catalase enzyme can be measured by following either the decomposition of H 2 O 2 or the liberation of O 2.
The dehydrated material was clarified with xylol and embedded in Paraplast Histosec, Merck. Thirty microscopic fields were chosen at random from each experimental group six fields per animal.
The relative values were determined by counting the coincident points in the test grid and dividing them by the total number of points. All analyses were conducted using Image Pro-Plus program version 6. Statistical significance was considered to.
Figure 1 shows the evidence an anodic peak, 1a, at ca. This peak potential value is akin to the observed for catechol moiety in natural antioxidants, such as catechin and quercetin. This fact is corroborated by literature reports concerning ED leaf extract, which is described as high polyphenolic content [ 11 ]. The antioxidant activity can only eugehia deemed to assist neuroprotection when ROS reduction is thermodynamically feasible. Henceforth, CHE presents outstanding antioxidant quality, as the anodic peak occurred at 0.
Furthermore, SWV allowed the visualization of a cathodic peak 1c, which is intimately correlated to anodic peak 1a. These peaks configure reversibility, as their anodic and cathodic current ratio was quite close to 1. This pattern implies that sample compounds may repeatedly undergo oxidation to restore endogenous antioxidants in physiological environment.
Henceforth, the dyenterica reducing feasibility and their reversible profile imply that CHE possesses noteworthy antioxidant properties [ 89 ]. Behavioral tests gather important data concerning the extent of neurological damage. Aspects such as short- and long-term memories are assayed in order to study memory retention capabilities, whereas locomotor, exploratory activity, and motor impairment are assayed to study the influence of the tested compounds in motor system.
These aspects were herein assessed respectively through step-down, open-field, and chimney tests. Results are displayed in Figure 2. Figure 2 exhibits step-down test results and shows that during training, all groups presented similar profiles, whereas for short-term memory STM and long-term memory LTMgroup II presented the lowest memory retention.
Since this group was solely treated with AlCl 3it can be attested that this metal promotes memory impairment. As all polyphenols, quercetin promotes ROS scavenging, which minimizes oxidative stress and oxygen-related injuries in brain mater [ 12 — 21 ].
Animals treated with Dysentdrica exhibited crescent memory retention according to the rise in concentration. The findings herein obtained are justified by cagaita antioxidant activity, which promotes neuroprotection [ 11 ]. As seen in voltammetrical assessment, endogenous antioxidant renewal by CHE is thermodynamically feasible, which implies that ROS are efficiently scavenged.
Open-field and chimney test results evidenced that the sugenia did not impair locomotion.
Eugenia dysenterica – Useful Tropical Plants
Results imply therefore that CHE promotes memory retention without impairing motor skills. In order to complement electrochemical assessment on antioxidant quality, CHE had its antioxidant activity analyzed by assessing cortex and hippocampus response towards TBARS, superoxide dismutase, and catalase activity.
Results are displayed in Figure 3. Malondialdehyde is a lipid peroxidation dysenrerica whose increased concentrations imply elevated oxidative stress, and this compound is moreover highly reactive towards thiobarbituric acid. The aluminium-treated group II presented a rise of malondialdehyde concentration in both cortices and hippocampi of treated animals, whereas all other treatment groups did not display statistically significant variation compared to control Euhenia response.
Results evidence that AlCl 3 does promote lipid peroxidation, which is in accordance to literature. Although not a direct prooxidant, aluminium potentiates iron-mediated ROS synthesis in Fenton reaction and promotes steric hindrance of antioxidant enzyme active sites [ 56 ].
CHE as well as quercetin exhibited similar results to that of the dsyenterica group, which implies that ROS were unable to promote lipid peroxidation in these samples. Concerning total superoxide dismutase activity in cortices and hippocampi, this enzyme is known to be hindered by aluminium salts, and results display the same trend, as group II presented statistically significant activity reduction.
Although all other treated groups presented similar features to control concerning animal cortices, hippocampus response to quercetin implied that this compound hindered enzyme activity, whereas CHE increased its activity. Literature reports that polyphenols may interact with proteins depending on their chemical structure and either promote or hinder their dysrnterica [ 22 ]. Results imply therefore that CHE constituents dysentericca promote superoxide dismutase activity.
Literature reports that chronic aluminium poisoning leads to the decrease of manganese-dependent SOD activity mitochondrial SOD in mouse brain. Moreover, exposure to this metal ultimately decreases Lon protease mRNA expression. Since this enzyme is involved in the removal of oxidized proteins from mitochondria, the decline of its expression may enhance the damage promoted by ROS. Since all these biomolecules are involved in memory retention, CHE may possibly exert its neuroprotective properties through mechanisms other than plain antioxidant action; however, more studies are necessary to investigate it further [ 2425 ].
Results displayed that dysenteica activity was slightly enhanced by CHE in the cortices, whereas enzymatic activity rose significantly in the hippocampi of the treated animals. Morphoquantitative and stereological data evidenced that treatments deeply alter CA1 hippocampus pyramidal cell layer architecture and thickness, as dyseenterica in Figure 4. Results showed that in the control group, pyramidal cell dysentegica thickness was of Cells contained a single nucleus, up to three nucleoli, and basophilic cytoplasm Figure 4.
AlCl 3 exposure expressively reduced CA1 layer Both tissue architecture dysebterica cells were altered by aluminium exposure, as cell cytoplasm increased in volume and presented more vacuoles than the untreated group.