Aluminium and its compounds when taken orally can have negative impacts on a variety of enzymes leading to neurotoxicity. Apurinic endonuclease 1 (APE-1), a protein that performs multiple functions, including deoxyribonucleic acid (DNA) repair, is essential for cell survival. Thus, the determination of APE-1 with aluminium chloride (AlCl3) induced neuro-inflammation in Wistar rats was performed in this study. Wistar rats were divided into four groups, each with six animals. Group 1 received 100 mg/kg AlCl3 orally, Group 2 received 150 mg/kg eugenol, Group 3 received both 100 mg/kg AlCl3 and 150 mg/kg eugenol, and Group 4 received 0.8 ml/kg distilled water. Rats were euthanized after eight weeks, and brain tissues were homogenized and analysed. Oral administration of AlCl3 resulted in significant (p<0.01) decreased APE-1, superoxide dismutase (SOD) and amyloid beta-40 (Aβ-40), and significant (p<0.01) increased tumour necrosis factor-α (TNF-α), interleukin-1 (IL-1), inducible nitric oxide synthase (iNOS), myeloperoxidase, and nitric oxide (NO). Co-administration of AlCl3 and eugenol significantly increased (p<0.01) APE-1, Aβ-40 and SOD, while significantly decreasing (p<0.01) TNF-α, IL-1, iNOS and MPO levels. Our findings suggest that eugenol, by targeting these most potent hallmarks of neurodegeneration could be an effective alternative in its treatment.
Objective: Xylopia aethiopica is a common plant in West Africa, with wide applications in trado-medical management of several diseases. Thus, our study aimed to analyze the histology and hormonal effects of ethanol extracts of Xylopia aethiopica seeds on cadmium chloride-induced reproductive dysfunction in female Wistar rats. Methods: We used twenty-five rats weighing 120-150g for this study. The rats were divided into five groups (n=5). Group 1: received only distilled water orally; Group 2: received 2 mg/kg cadmium chloride orally; Group 3: received 2 mg/kg cadmium chloride plus 50 mg/kg Xylopia aethiopica seeds orally; Group 4: received 2 mg/kg cadmium chloride plus 100 mg/kg Xylopia aethiopica seeds orally, and Group 5: received 100 mg/kg Xylopia aethiopica seeds only, orally. We administered the extracts for 14 days, after which we slaughtered the animals following chloroform anesthesia. We took the blood samples by cardiac puncture for hormonal assay. The ovaries and uterus were harvested for histology. We analyzed the data using ANOVA, and the differences in mean values were considered significant at p <0.05. Results: The body weight of the rats showed a dose-dependent reduction ( p <0.05), compared with the controls. Xylopia aethiopica seeds significantly ( p <0.05) reversed the detrimental effects of Cadmium on LH and FSH. The histological analysis of the ovary showed significant improvement upon treatment with Xylopia aethiopica extract in a dose-dependent manner. Conclusions: The ameliorative effects of Xylopia aethiopica against cadmium chloride-induced reproductive toxicity in female Wistar rats may be attributed to its antioxidant properties.
Diabetic encephalopathy and its associated end organ damage have become a major global epidemic in many patients with diabetes mellitus. These diseased conditions are complex and poorly understood, therefore the need to seek for alternative management measures to attenuate the complications associated with it. The aim of this study was to evaluate the effects of co-administration of melatonin and magnesium on the cytoarchitecture of the hippocampus of streptozotocin (STZ) induced diabetic rats. STZ was used to induce type 1 diabetes mellitus. Fifty four rats: Forty eight diabetic and six normoglycaemic rats distributed in nine groups as follow; normal control, diabetic control (DC), melatonin low dose (MLD, 10 mg/kg), magnesium low dose (MgLD, 240 mg/kg), melatonin and magnesium combined dose (MMgLD, 10 mg/kg+240 mg/kg, respectively), melatonin high dose (MHD, 20 mg/kg), magnesium high dose (MgHD, 480 mg/kg), melatonin and magnesium high dose (MMgHD, 20 mg/kg+480 mg/kg, respectively) and insulin (IN, 500 mg/kg). Melatonin and insulin were administered through intraperitoneal injections while magnesium was orally. The control groups were given placebo and all treatments were for twenty-one days. Results showed distortion of hippocampal CA1 area in the diabetic control, MgLD, MgHD, MMgHD and IN groups. MLD, MHD and MMgLD groups showed organized structures of hippocampus CA1 area with no cellular distortions, while there were less positive GFAP in the MLD, MHD and MMgLD groups. The DC, MgLD. MgHD, MMgHD and IN groups showed strong GFAP reactivity. In conclusion, MLD, MHD and MMgLD increased neuroprotection of hippocampal neurocytes
Over the years, Formaldehyde (FA) has been linked to increased generation of reactive oxygen species (ROS), leading to oxidative stress and cognitive decline. However limited numbers of studies have shown the effect of eugenol on FA induced toxicity in Wistar rats. Therefore this study aimed at investigating the effects of eugenol on the FA induced toxicity in Wistar rats. A total of twenty male Wistar rats where divided into four groups: (Group I. 150 mg/kg eugenol; Group II, 5 mg/kg FA; Group III, 150 mg/kg eugenol + 5 mg/kg FA; Group IV/control, 2ml/kg distilled water) for thirty days. FA and eugenol were administered orally. Rats were humanely sacrificed under 0.8 mg/kg ketamine anaesthesia administered intraperitoneally. Cognitive tests using Morris water maze and Novel object recognition test were carried out, Oxidative stress parameters, acetylcholine activity and histometric analysis of hippocampal Cornu Ammonis (CA 1 and 3) pyramidal neuronal cells. Administration of FA resulted in significant (p<0.05) increased activity of malondialdehyde (MDA), intra-mitochondrial accumulation of 8-hydroxydeoxyguanosine (8-OHdG), reduced activity level of superoxide dismutase (SOD) and acetylcholine levels. However co-administration of eugenol and FA resulted in significant (p<0.05) enhancement of cognitive ability and also significantly (p<0.05) reduced MDA and 8-OHdG levels, and increased SOD and acetylcholine levels. Our results indicate that eugenol would provide therapeutic value against FA induced oxidative stress and cognitive impairments.
The aim of this study was to evaluate the effects of co-administration of melatonin and magnesium on BCL-2 and Bax expression in the Hippocampus of streptozotocin-induced Type 1 diabetic Wistar rats. To achieve this aim sixty-four Wistar rats were used in the study. Streptozotocin (STZ) was used to induce chemical type 1 diabetes mellitus (T1DM) after two weeks acclimatization period in fifty-eight Wistar rats. Fifty-three rats were diabetic and fourty-eight diabetic rats were randomly distributed in eight groups and six normal normoglycaemic rats were used as control. The animals were assigned into nine groups as follows, Normal control group (NC), Diabetic control (DC) group, Melatonin Low dose group of 10 mg/kgb (MLD), Magnesium low dose group of 240 mg/kgbw (MgLD), Melatonin and magnesium combined low dose group of 10mg/kgbw + 240mg/kgbw (MMgLD), Melatonin high dose group of 20mg/kgbw (MHD), Magnesium high dose group of 480mg/kgbw (MgHD), Melatonin and magnesium high dose combined group of 20mg/kgbw + 480mg/kgbw (MMgHD) and Insulin at 500mg/kgbw group (IN). Melatonin and insulin were administered through intraperitoneal injections (IP) while magnesium was by oral administration. The control groups were given placebo and all group treatment was for twenty-one days. At the end of the study, the animals were aestheticized and euthanized to harvest the brain organ. The harvested organs were weighed and their relative weight recorded. They were fixed in neutral buffered formaldehyde (NBF). The Brain tissues were evaluated using BCL-2 mouse polyclonal antibodies to evaluate the level of neuroprotection of hippocampal neurocytes by melatonin and magnesium co-administration. The immunohistochemical test showed that melatonin and magnesium co-administration at low doses increased neuroprotection of hippocampal neurocytes by upregulation of BCL-2 protein and down regulation of Bax proteins. Reports published by the World Health Organization (WHO) states that diabetes mellitus (DM) is a common disease with a global prevalence estimated to be 9% among adults aged 18+ years and above [1]. Populationbased studies of neuropathy in persons with diabetes indicate that
Background: Improve insulin secretion and cellular availability to reduced blood glucose levels in diabetic subjects by bioactive compound especially antioxidants are the new focus to ameliorate the complication with diabetes mellitus. Aims and objectives: The aim of this study was to evaluate the effects of administration of melatonin and magnesium on the cytoarchitecture of the pancreatic tissue and to access immunohistochemically insulin release in streptozotocin-induced diabetic Albino rats. Materials and methods: To achieve this aim six normoglycaemic rats and fourty eight Streptozotocin (STZ) induced diabetic rats was used in the study after two weeks acclimatization period. The animals were assigned into nine groups as follows, Normal control group (NC), Diabetic control (DC) group, Melatonin at 10 mg/kgb (MLD), magnesium dose group of 240 mg/kgbw (MgLD), melatonin and magnesium combined group of 10mg/kgbw+240mg/kgbw (MMgLD), melatonin group of 20mg/kgbw (MHD), melatonin and magnesium high dose combined group of 20mg/kgbw+480mg/kgbw (MMgHD) and insulin at 500mg/kgbw group (IN). Melatonin and insulin were administered through intraperitoneal injections (IP) while magnesium was by oral administration. The control groups were given placebo and all groups’ treatment was for twenty-one days. At the end of the study, the animals were aestheticized and euthanized to harvest pancreatic organ. The organs were fixed in neutral buffered formaldehyde (NBF). They were histologically prepared and stained using haematoxylin and eosin and immunohistochemically stained using insulin antibody to access insulin release. Results: Melatonin treatment at 10mg/kgbw and at 20 mg/kgbw showed histological improvement in histological tissues and insulin release while when combined with magnesium at dose of 10mg/kgbw and at 240 mg/kgbw showed better results. The administration of magnesium at 240 mg/kgbw, 480 mg/kgbw and when combined with melatonin at high doses does not show significant improvement in islet β-cell proliferation and insulin release. Conclusion: The administration of melatonin and magnesium at low doses regenerates pancreatic islet histoarchitecture and augments insulin release from treated diabetic albino rats.
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