Aluminum is a potent neurotoxin used in animal models of neurodegenerative diseases like Alzheimer’s disease (AD), in which oxidative stress mediates tissue pathogenesis in vivo. N-acetyl cysteine (NAC) is a glutathione precursor with reported antioxidant and neuroprotective potentials. Recent therapy for combating AD is known to provide only symptomatic relief thus necessitating the discovery of new drugs and their mechanism of action. This study was aimed to demonstrate the in vivo neuroprotective effect of NAC against aluminum (Al³⁺)-induced neuro-degeneration in rats (a model for AD). Twenty- five (25) adult male Wistar rats used for this study were divided into 5 groups: Group A = Control, B = Aluminum chloride (200 mg/kg), C = 1000 mg/kg of NAC + Aluminum chloride (200 mg/kg), D = 1000 mg/kg of NAC, E = Aluminum chloride (200 mg/kg) was orally administered daily for 3 weeks and discontinued for one week. Frontal Cortex harvested for histological analysis using Haematoxylin and Eosin stain, Cresyl Fast Violet stain for Nissl granules and Glial fibrillary acidic protein immunohistochemistry specific for astrocytes. Aluminum significantly induced oxidative stress, coupled with marked neurons necrosis, chromatolysis and gliosis in the frontal cortex, upon NAC administration, there was neuro anti-inflammatory response as seen in the significant reduction in astrocytes expression, neuronal cell death and Nissl body aggregation which attenuates neuropathological deficits induced by Al³⁺. It was shown that aluminum is a neurotoxin mediating AD-like oxidative stress, NAC has a therapeutic potential associated with its potent in vivo interaction with astrocytes in response to Al³⁺ neuro-inflammation seen in positive expression of Nissl granules and glial cells in addition to possibility of endogenous glutathione neuroprotection after withdrawal of stress mediator in neurodegeneration.

Neurodegenerative disorders are linked to oxidative tissue damage characterized by gradual loss of cognitive functions and neuronal cells. Alpha-lipoic acid (AHA) has a strong antioxidant property. Scopolamine is an anti-muscarinic agent used to study the mechanism of memory loss in an animal model. This study is aimed at evaluating the antioxidant role of alpha lipoic acid in reversing scopolamine induced memory loss and neurodegenerative process in the prefrontal cortex of Wistar rats. Twenty adult male Wistar rats used were divided into four groups (n = 5): Group 1 received vehicle (Control), Group 2 had scopolamine (1 mg/kg, i.p) for 4 days, Group 3 received AHA (200 mg/kg, p.o) for 10 days while Group 4 were pretreated with scopolamine (1 mg/kg, i.p) for 4 days followed by oral administration of 200 mg/kg of AHA for 10 days. The rats were subjected to Y-maze test to assess their spatial memory. The rats were euthanized, the prefrontal area was excised and fixed in 10% formol-calcium and processed for Haematoxylin and Eosin, Cresyl fast violet for Nissl Bodies (Ribosome), and Glial Fibrillary Acidic Protein (GFAP) stains. Scopolamine caused a significant decline in spatial working memory, prefrontal neuron cell loss, and increased proliferation of reactive astrocytes (astrogliosis) when compared with the control and AHA treated group. AHA process of reversing scopolamine-induced memory deficit, prefrontal neuron cell loss, and generation of reactive astrocytes (astrogliosis) is mediated by its antioxidant mediated positive modulation of astrocyte-neuronal interaction during neuroinflammation in response to oxidative tissue damage.

The study’s goal was to ascertain the contraceptive effects of Aqueous extract of Carica papaya on female rats by assessing changes in the body weight, estrous cycle, serum progesterone level and the cyto-architecture of the Utero-ovarian tissue. We used twenty (20) healthy young Adult Female Albino rats. The study ran for 7 and 21 days, respectively. Each study group has their Experimental (treated 200mg/kg aqueous extract of Carica papaya seed extract) and Control group (n=5). We determined daily the phases and frequencies of the estrous cycles of the rats during the administration of the extract. We processed the utero-ovarian tissue for histological analysis, and we assessed serum progesterone level and the oestrus cycle pattern. There was a significant increase in body and Ovarian weights after 21 days of treatment when compared to controls and those treated for 7 days. However, uterine weight reduced significantly (p<0.05), serum progesterone level decreased (p<0.05) in the treated rats, mostly in those submitted to 21 day-treatments; the ovary showed marked degeneration of the theca cells, granulosa and corpus luteum, and loss of mucin granules in the uterine tissues. Carica papaya administered for 7 and 21 days caused the animals to have more proestrus and diestrus phases as compared to the control animals. The estrous cycle became irregular, with prolonged diestrous and proestrus phase. The aqueous extract of Carica papaya seeds caused antifertility, anti-implantation, by a reduction in progesterone level, disruption of oestrus pattern and histological alteration of utero-ovarian tissue.