Maternal diet supplemented with African walnuts enhances cortico-hippocampal gene expression and histomorphology in rat offspring.

BACKGROUND: The brain is built up during pregnancy. How it functions afterwards depends on how the expectant mother's diet nourishes it. Walnuts contain significant quantities of polyunsaturated fatty acids (PUFAs) and bioactive phytochemicals, which enhance brain health and function even with advancing age. This study examined the effects of a walnut-enriched diet (WED) on corticohippocampal histoarchitecture and gene expression in rat offspring. MATERIALS AND METHODS: Twenty-eight female adult Wistar rats (n= 7) averaging about 185 g in weight were used for this study. After mating, pregnant dams were split randomly into four groups: A (standard rat chow/control), B (WED from GD 0 - PND 21), C (WED from GD 0 - PND 1), D (WED from PND 1 - PND 21). Offspring of dams were sacrificed at adolescence (PND 35), with brain tissues of interest harvested for subsequent analyses. RESULTS: We observed no significant correlates in litter size, body, and brain weights across the experimental groups. Histomorphology revealed no distortion in cellular layering and delineation of cells in the PFC and dentate gyrus of both control and WED groups. Nissl staining intensity was enhanced in the offspring of dams exposed to WED versus the control, indicating improved proteostasis. Upregulated mRNA expression of DNMT3a, H2Ax, OPA1, and BDNF was observed in cortical and hippocampal tissues of WEDexposed offspring compared with the control group. CONCLUSION: A diet enriched with African walnuts during early development induced changes predictive of cognitive improvements and enhanced stress-response signalling, plasticity, and neural resilience in rat offspring.

African walnut (Tetracarpidium conophorum) extract upregulates glucocerebrosidase activity and circumvents Parkinsonian changes in the Hippocampus via the activation of heatshock proteins.

BACKGROUND: Neurodegenerative illnesses like Parkinson's and Alzheimer's are largely caused by the accumulation of aggregated proteins. Heat shock proteins (HSPs), which are molecular chaperons, have been linked with the modulation of ß-glucocerebrosidase (GCase) function encoded by GBA1 and Synucleinopathies. Herein, the chaperonic properties of African walnut ethanolic extract (WNE) in manganese-induced Parkinsonian neuropathology in the hippocampus was examined. METHODOLOGY: 48 adult male rats weighing 185 g ± 10 g were randomly assigned into 6 (A - F) groups (n = 8) and treated orally as follows: A-PBS (1 ml daily for 28 days), B-WNE (200 mg/kg daily for 28 days), C- WNE (400 mg/kg daily for 28 days), D-Mn (100 mg/kg daily for 28 days), E-Mn plus WNE (100 mg/kg Mn + 200 mg/kg WNE daily concomitantly for 28 days), F-Mn plus WNE (100 mg/kg Mn + 400 mg/kg WNE daily concomitantly for 28 days). RESULTS: Rats treated with WNE showed increased levels of HSP70 and HSP90 in comparison with the Mn-intoxicated group. GCase activity also increased significantly in animals treated with WNE. Our results further revealed the therapeutic tendencies of WNE against Mn toxicity by modulating oligomeric α-synuclein levels, redox activity, and glucose bioenergetics. Furthermore, immunohistochemical evaluation revealed reduced expression of neurofibrillary tangles, and reactive astrogliosis following WNE treatment. CONCLUSION: The ethanolic extract of African Walnut induced the activation of HSPs and increased the expression of GBA1 gene in the hippocampus. Activated heat shock proteins suppressed neurodegenerative changes due to Manganese toxicity. WNE was also shown to modulate neuroinflammatory, bioenergetics and neural redox balance in Parkinson-like neuropathology. This study was limited to the use of crude walnut extract and the evaluation of non-motor cascades of Parkinson's disease.

Histological and Biochemical Alterations in the Superior Colliculus and Lateral Geniculate Nucleus of Juvenile Rats Following Prenatal Exposure to Marijuana Smoke.

Introduction: Prenatal exposure to Marijuana (MJN) has been associated with various brain deficits. The main activity in marijuana, Δ9-Tetrahydrocannabinol (THC), crosses the placenta and affects fetal brain development. Despite this, marijuana remains a commonly abused substance among pregnant women. The current study examined the histological and biochemical changes in the Superior Colliculus (SC) and Lateral Geniculate Nucleus (LGN) in rat brains prenatally exposed to marijuana. Methods: Four groups of pregnant rats (n=5 rats/group) were exposed to the smoke of 10 g/kg marijuana at various days during their gestational period, with a group (control), i.e., not exposed. After parturition, the litters from each group were sacrificed by cervical dislocation on postnatal days 7, 14, and 21; the superior colliculi and lateral geniculate nuclei were excised. Tissue sections were prepared for histological studies using Haematoxylin and Eosin stains. Biochemical studies were performed on alkaline phosphatase, acid phosphatase, lactate dehydrogenase, and glucose-6-phosphate dehydrogenase activity levels. The histological and biochemical analyses of tissues were performed. Results: Prenatal exposure to marijuana resulted in spontaneous abortion and affected neuronal morphology in the SC and LGN of the progeny. Furthermore, the levels of enzyme activities were altered following maternal exposure to MJN. Conclusion: These data suggested that histological changes in the SC and LGN were associated with oxidative damage. Highlights: Prenatal exposure to marijuana smoke in early gestation induced spontaneous abortion.Prenatal exposure to marijuana smoke-induced damage to the visual pathway in the progeny.Prenatal exposure to marijuana-induced histological changes in juvenile rats' superior colliculus and lateral geniculate nucleus.Prenatal exposure to marijuana smoke resulted in biochemical alterations in juvenile rats' superior colliculus and lateral geniculate nucleus. Plain Language Summary: Marijuana is the most widely used psychoactive substance in the western world, consumed for recreational, medicinal, and spiritual purposes. Although marijuana consumption by pregnant women has been linked with neurodevelopmental consequences, little is known of its effect on the visual pathway of the progeny. We examined juvenile rats using the rat model, the effect of prenatal exposure to marijuana smoke on the superior colliculus and lateral geniculate body (regions of the brain involved in visual information processing). Our result reveals that marijuana use in early gestation induces spontaneous abortion. Also, prenatal exposure to marijuana smoke produced histological changes in the brain mentioned above regions involved in visual information of the progeny. Our findings also include biochemical alterations in these regions. Hence, we highlight the damaging effects of marijuana smoke on the developing brain, specifically the superior colliculus and lateral geniculate nucleus, i.e., involved in visual information processing, of juvenile rats following prenatal exposure.

Cerebellar Molecular and Cellular Characterization in Rat Models of Alzheimer's Disease: Neuroprotective Mechanisms of Garcinia Biflavonoid Complex.

BACKGROUND: Recent evidences suggest that cerebellar degeneration may be associated with the development of Alzheimer's disease (AD). However, previous reports were mainly observational, lacking substantial characterization of cellular and molecular cerebellar features during AD progression. PURPOSE: This study is aimed at characterizing the cerebellum in rat models of AD and assessing the corresponding neuroprotective mechanisms of Garcinia biflavonoid complex (GBc). METHODS: Male Wistar rats were grouped and treated alone or in combination with PBS (ad libitum)/day, corn oil (CO; 2 mL/kgBw/day), GBc (200 mg/kgBw/day), sodium azide (NaN3) (15 mg/kgBw/day) and aluminium chloride (AlCl3) (100 mg/kgBw/day). Groups A and B received PBS and CO, respectively; C received GBc; D received NaN3; E received AlCl3; F received NaN3 then GBc subsequently; G received AlCl3 then GBc subsequently; H received NaN3 and GBc simultaneously while I received AlCl3 and GBc simultaneously. Following treatments, cerebellar cortices were processed for histology, immunohistochemistry and colorimetric assays. RESULTS: Our data revealed that cryptic granule neurons and pyknotic Purkinje cell bodies (characterized by short dendritic/axonal processes) correspond to indistinctly demarcated cerebellar layers in rats treated with AlCl3 and NaN3. These correlates, with observed hypertrophic astrogliosis, increased the neurofilament deposition, depleted the antioxidant system-shown by expressed superoxide dismutase and glutathione peroxidase, and cerebellar glucose bioenergetics dysfunction-exhibited in assayed lactate dehydrogenase and glucose-6-phosphate dehydrogenase. We further showed that GBc reverses cerebellar degeneration through modulation of neurochemical signaling pathways and stressor molecules that underlie AD pathogenesis. CONCLUSION: Cellular, molecular and metabolic neurodegeneration within the cerebellum is associated with AlCl3 and NaN3-induced AD while GBc significantly inhibits corresponding neurotoxicity and is more efficacious when pre-administered.

Sodium azide-induced degenerative changes in the dorsolateral prefrontal cortex of rats: attenuatingmechanisms of kolaviron

Identification of therapeutic targets following neurodegeneration is of major biomedical importance. Kolaviron (Kv) is a biflavonoid complex isolated from seeds of Garcina kola - a common oral masticatory agent in Nigeria known to hold medicinal value. Therefore this study evaluated the therapeutic potential of Kv on cells of the dorsolateral prefrontal cortex (DLPFC), before or after sodium azide (NaN3)-induced neurodegeneration. Rats were randomly assigned into 5 groups (6 each) and treated daily (orally) as follows: 1 ml of corn-oil (vehicle of Kv, 21 days); Kv only (200 mg/kg) for 21 days; NaN3 only (20 mg/kg for 5 days); NaN3 (20 mg/kg for 5 days) followed by Kv (200 mg/kg for 21 days); Kv (200 mg/kg for 21 days) followed by NaN3 (20 mg/kg for 5 days). After treatments, rats were sacrificed and perfused transcardially (with 4% PFA) with brains fixed in accordance with the technique to be used. The DLPFC was examined using histology (H&E), immunoperoxidase (GFAP), immunofluorescence (iNOS & nNOS) and Western blotting (MAPT, MAP2, Bax, BCL-2 and CAD). Quantitative analysis was done using ImageJ software and statistical analysis with Graphpad prism (ANOVA) at p<0.05. NaN3 treatment induced neuronal damage, characterized by reduced relative brain weight, pyknosis, karyorrhesis, astrogliosis, axonal/dendritic damage and cytoskeletal dysregualtion that subsequently resulted in increased expressions of apoptotic regulatory proteins. These degenerative changes were relatable to the observed iNOS and nNOS upregulations. However, Kv administration attenuated the NaN3- initiated destructive molecular cascades in the DLPFC of rats through mechanisms that involved inhibition of stressor molecules and toxic proteins, prevention of stress related biochemical redox, preservation of neuronal integrity, cytoskeletal framework and subsequently, reduced the level of apoptotic regulatory proteins. We conclude that Kv conferred therapeutic benefits on NaN3- induced neurodegeneration, particularly when administered before more than after the insult

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Kolaviron was protective against sodium azide (NaN3) induced oxidative stress in the prefrontal cortex.

Kolaviron is a phytochemical isolated from Garcina kola (G. kola); a common oral masticatory agent in Nigeria (West Africa). It is a bioflavonoid used--as an antiviral, anti-inflammatory and antioxidant--in relieving the symptoms of several diseases and infections. In this study we have evaluated the neuroprotective and regenerative effect of kolaviron in neurons of the prefrontal cortex (Pfc) before or after exposure to sodium azide (NaN3) induced oxidative stress. Separate groups of animals were treated as follows; kolaviron (200 mg/Kg) for 21 days; kolaviron (200 mg/Kg for 21 days) followed by NaN3 treatment (20 mg/Kg for 5 days); NaN3 treatment (20 mg/Kg for 5 days) followed by kolaviron (200 mg/Kg for 21 days); 1 ml of corn-oil (21 days-vehicle); NaN3 treatment (20 mg/Kg for 5 days). Exploratory activity associated with Pfc function was assessed in the open field test (OFT) following which the microscopic anatomy of the prefrontal cortex was examined in histology (Haematoxylin and Eosin) and antigen retrieval Immunohistochemistry to show astroglia activation (GFAP), neuronal metabolism (NSE), cytoskeleton (NF) and cell cycle dysregulation (p53). Subsequently, we quantified the level of Glucose-6-phosphate dehydrogenase (G6PDH) and lactate dehydrogenase (LDH) in the brain tissue homogenate as a measure of stress-related glucose metabolism. Kolaviron (Kv) and Kolaviron/NaN3 treatment caused no prominent change in astroglia density and size while NaN3 and NaN3/Kv induced astroglia activation and scar formation (astrogliosis) in the Pfc when compared with the control. Similarly, Kolaviron and Kv/NaN3 did not alter NSE expression (glucose metabolism) while NaN3 and NaN3/Kv treatment increased cortical NSE expression; thus indicating stress related metabolism. Further studies on enzymes of glucose metabolism (G6PDH and LDH) showed that NaN3 increased LDH while kolaviron reduced LDH in the brain tissue homogenate (P < 0.001). In addition kolaviron treatment before (P < 0.001) or after (P < 0.05) NaN3 treatment also reduced LDH expression; thus supporting its role in suppression of oxidative stress. Interestingly, NF deposition increased in the Pfc after kolaviron treatment while Kv/NaN3 showed no significant change in NF when compared with the control. In furtherance, NaN3 and NaN3/Kv caused a decrease in NF deposition (degeneration). Ultimately, the protective effect of KV administered prior to NaN3 treatment was confirmed through p53 expression; which was similar to the control. However, NaN3 and NaN3/Kv caused an increase in p53 expression in the Pfc neurons (cell cycle dysregulation). We conclude that kolaviron is not neurotoxic when used at 200 mg/Kg BW. Furthermore, 200 mg/Kg of kolaviron administered prior to NaN3 treatment (Kv/NaN3) was neuroprotective when compared with Kolaviron administered after NaN3 treatment (NaN3/Kv). Some of the observed effects of kolaviron administered before NaN3 treatment includes reduction of astroglia activation, absence of astroglia scars, antioxidation (reduced NSE and LDH), prevention of neurofilament loss and cell cycle regulation.

Moringa oleifera impairs the morphology and functions of the kidney in adult Wistar rats / Moringa oleifera altera la morfología y funciones del riñón en ratas Wistar adultas

We tested the hypothesis that Moringa oleifera impairs the morphology and functions of the kidney in rats. Twenty-four adult male Wistar rats were employed in the study. Rats of Control Group I received physiological saline while rats of Groups II ­ IV received 250, 500 and 750 mg/kg bodyweight of methanolic extract of Moringa oleifera respectively for twenty one days. No behavioral anomalies were observed in rats of Groups I ­ IV. Rats of Control Group I gained statistically significant increased bodyweight while rats of Groups II ­ IV experienced non-significant decreased bodyweight during experimental procedure. (P0.05). No statistical significant differences (P0.05) were observed in the analyses of the relative weights of kidneys of rats of Groups I ­ IV. Histological examinations showed normal cyto-architecture of the kidneys of rats of Group I while the Capsular spaces of the kidneys of rats of Groups II ­ IV appeared wider than those of Group I. Statistical analyses showed significant higher levels (P0.05) of Alanine and Aspartate Transaminases, and serum urea in rats of Groups II ­ IV in a non- dose-dependent manner when compared to rats of Group I. Our findings are consistent with the stated hypothesis.

Se puso a prueba la hipótesis que Moringa oleifera altera la morfología y función del riñón en ratas. Fueron utilizadas 24 ratas Wistar macho adultas. El grupo control recibió suero fisiológico mientras que los Grupos II a IV recibieron 250, 500 y 750 mg/kg peso corporal del extracto metanólico de Moringa oleifera respectivamente, durante 21 días. No se observaron anomalías en el comportamiento en ratas de los Grupos I - IV. En las ratas del grupo de control se registró un aumento de peso corporal estadísticamente significativo, mientras que las ratas de los grupos II - IV experimentaron una disminución no significativa de peso corporal durante el procedimiento experimental (P0,05). No se observaron diferencias estadísticamente significativas (P0,05) en el análisis de los pesos relativos en riñones de las ratas de los grupos I - IV. Los exámenes histológicos mostraron citoarquitectura normal de los riñones de las ratas del grupo I, mientras que en ratas de los grupos II ­ IV los espacios capsulares de los riñones aparecían más amplios que los del Grupo I. Los análisis estadísticos mostraron niveles superiores significativos ( P 0,05 ) de la alanina y aspartato aminotransferasa, y de urea en suero en ratas de los Grupos II - IV no dependiente de la dosis, en comparación con las ratas del Grupo I. Estos resultados coinciden con la hipótesis planteada.

Cytoprotective activities of Anacardium occidentale (Linn) on the testis of streptozotocin-induced diabetic rats

This study presents the protective effects of methanolic Anacardium occidentale leaf extract (AOLE) on the testes of streptozotocin (STZ)-induced diabetic rats. Forty male wistar rats (Rattus norvegicus) were randomly divided into four experimental groups A,B,C and D. Hyperglycaemia was induced by a single intraperitoneal injection of 0.1 M STZ (70 mg/kg b.w). Five days after the confirmation of hyperglycaemia by using a glucometer (Roche(R)) and compatible glucose test strips, groups A and B were treated with 300 mg/kg b.w of the extract and 1 I.U/kg b.w insulin respectively. Groups C and D served as hyperglycaemic and normal controls and received 1 ml/kg b.w citrate buffer respectively.After 16 days of treatment, blood was collected through retro-orbital puncture for insulin and reproductive hormone (FSH, LH and testosterone) analysis; the animals were then sacrificed and the testes were processed for histological staining. Data obtained were expressed as means of ten (10) replicates ± SEM and subjected to one-way analysis of variance (ANOVA) and the Scheffe’s post hoc test for multiple comparisons.Results showed that the levels of testosterone, FSH and LH in the AOLE- and insulin-treated rats increased significantly compared to the hyperglycaemic controls (P<0.05).Histological sections revealed improved cellularity, germinal epithelium, tubular diameter, cross-sectional area and luminal spermatids in the AOLE- and insulin-treated rats when compared with the hyperglycaemic control.AOLE improved the structural integrity of the testes, promoted spermatogenesis, and improved the profile of reproductive hormones (AU)

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Liver enzymes derangement and the influence of diet in animals given oral albendazole.

BACKGROUND: Albendazole is used as an anthelmintic in the treatment of some parasitic infections. This study determined how the effects of albendazole on liver enzymes are influenced by diet. MATERIALS AND METHOD: Thirty adult male Wistar rats of mean weight 304.12 ± 11.34 g were randomly grouped into five: Group A: Control, was given rat pellets and water only; Group B received 15 mg/kg/d of albendazole while fasting; Group C received 15 mg/kg/d of albendazole with fatty meal; Group D received 15 mg/kg/d of albendazole with normal diet (rat pellets); and, Group E received 30 mg/kg/d of albendazole with normal diet (rat pellets); they were given orally for 3 consecutive days. The animals were sacrificed thereafter and blood samples obtained for quantitative study of the serum activities of alanine aminotransferase (ALT), aspartate aminotransferase (AST), and alkaline phosphatase (ALP). RESULTS: Significant elevation in the serum levels of the transaminases especially in animals which were on their normal diet (rat pellets), while ALP was either reduced or increased based on dietary factors. CONCLUSIONS: Oral administration of albendazole before meal or with a fatty diet could help limit severe elevation of liver enzymes associated with its use, while still ensuring optimal efficacy.

Effect of ethanolic extract of Khaya senegalensis on some biochemical parameters of rat kidney.

The effect of administration of ethanolic extract of Khaya senegalensis (2mg/kg body weight) on some biochemical parameters of rat kidney were investigated. Experimental animals were randomly divided into the control, those administered with the extract for 6 days and those administered with extract for 18 days, respectively. The prolonged administration of the extract resulted in significant reduction in the alkaline phosphatase activities of the kidney and its body weight ratio (P<0.05). In contrast, the same prolonged administration of the extract resulted in significant increase in the serum sodium ion concentration (P<0.05) while there was no significant difference in serum potassium ion concentration when compared to control (P>0.05). Administration of the extract for 6 days produced no significant difference from the control values in all the parameters investigated except in serum urea concentration which produced a significant increase (P<0.05). The available evidence in this study suggest that the ethanolic extract of Khaya senegalensis exerted more deleterious effect on the kidney when administered continuously over a prolonged period than a short one and this will adversely affect the functioning of the kidney.