Histophysiological study of aluminum chloride effect on male rats

Estimation the protective role of Ginkgo biloba aqueous extract on some hormones and cerebellum tissue in male albino rats treated with aluminum chloride

“…Studies also indicate the therapeutic effects of GBE on aging-related diseases may be similar to the anti-aging effects of growth hormone secretion caused by activation of the ghrelin receptor, meaning that some of the active ingredients in this herb may mimic ghrelin to stimulate growth hormone release via the same molecular mechanism by activating the Growth Hormone Secretagogue Receptor (GHSR), stimulating growth hormone (GH) secretion, and regulating energy balance (Castaneda et al, 2010;Hsieh et al, 2016) Histological examination with H&E dye showed that oral administration of AlCl3 for 30 days caused cerebellum damage with clear degenerative changes in the nervous tissue with loss of nuclei , in addition to the loss of association between the granular and Molecular layers, while there was a clear appearance of Aβ plaques spread in the cerebellum after treatment with silver stain . The occurrence of these tissue changes may be due to the ability of aluminum to cross the blood-brain barrier (Abdul-Rassoul et al, 2009). The reason for the appearance of Aβ plaques is that AlCl3 causes an imbalance in the intracellular calcium (Ca+) balance, so it causes the depolarization of mitochondria, leading to an increase in the generation of ROS (O2.-, H2O2 -,OH), which in turn reduces the activity of Cytochrome oxidase and reduces the production of ATP energy, as well as causes an increase Activation of the amyloidogenic and nonamyloidogenic APP pathway by activation of α-secretases, γ-secretases and β-secretases that affect the APP protein and cause the generation of increased amounts of Aβ plaques (Kumar & Singh, 2015;Itkin et al, 2011), It was also found that an increase in aluminum in the synaptic cleft causes an imbalance in the ionic and affects the cholinergic system, causing a decrease in the concentration of Ach and an increase in the concentration of AchE, leading to increased formation of Aβ plaques and an increase in protein phosphorylation in nervous tissue (Silveyra et al 2011;Dey & Singh, 2022) In addition, it was found that Aβ causes a defect in the synthesis of neurons due to its ability to increase the production of ROS in the nerve cell, and the occurrence of cellular calcium imbalance, in addition to that it affects the activity of a large number of enzymes, including the flavoprotein-linked enzyme And NADPH oxidase leads to an increase in the generation of free radicals, a decrease in GSH, and a defect in the mitochondrial respiratory chain, and thus the occurrence of cell death (Sadigh-Eteghad et al, 2015;Abramova et al, 2004).…”