Glibenclamide ameliorates the expression of neurotrophic factors in sevoflurane anaesthesia-induced oxidative stress and cognitive impairment in hippocampal neurons of old rats

Introduction Several antidiabetic medications have been proposed as prospective treatments for cognitive impairments in type 2 diabetes patients, glibenclamide (GBC) among them. Our research aimed to evaluate the impact of GBC on hippocampal learning memory and inflammation due to enhanced neurotrophic signals induced by inhalation of sevoflurane. Material and Methods Rats (Sprague Dawley, both sexes) were assigned to four groups: a control (vehicle, p.o.), GBC (10 mg/kg b.w.; p.o.), low-dose sevoflurane and low-dose sevoflurane + GBC (10 mg/kg b.w.; p.o.) for 23 days. Terminal deoxynucleotidyl transferase dUTP nick end labelling (TUNEL) staining was performed to analyse the count of apoptotic cells and ELISA was conducted to assess the protein signals. A Western blot, a Y-maze test, and a Morris maze test were performed, and the results analysed. Blood and tissues were collected, and isolation of RNA was performed with qRT-PCR. Results The Morris maze test results revealed an improvement in the length of the escape latency on days 1 (P < 0.05), 2 (P < 0.01), 3, and 4 in the low-dose Sevo group. Time spent in the quadrant and crossing axis and the percentage of spontaneous alterations showed a substantial decrease in the low-dose Sevo group which received GBC at 10 mg/kg b.w. Significant increases were shown in IL-6 and TNF-α levels in the low-dose Sevo group, whereas a decrease was evident in the GBC group. Conclusion Our results indicate that glibenclamide may be a novel drug to prevent sevoflurane inhalation-induced impaired learning and reduce brain-derived neurotrophic factor release, which may be a vital target for the development of potential therapies for cognitive deficits and neurodegeneration.

Roles of Glucose and Sucrose Intakes on the Brain Functions Measured by the Working Ability and Morris Maze

Sugars such as glucose or sucrose are considered hazardous foods because their intakes lead to obesity, further causing diabetes mellitus (DM), or cardiovascular diseases. However, glucose is needed for many brain functions such as memory and emotion among others. Glucose induces the secretion of insulin, which is needed for transportation of tryptophan from the blood to the brain. Serotonin, which is converted from tryptophan, is important for mood stability, control of emotion, and feeding is inhibited by serotonin in the hypothalamus. We discuss transportation of glucose from the blood to the glia cells. After glycolysis of glucose in the glia lactic acid is transported to cells such as glutaminergic neurons. After the release from neurons glutamic acid is taken up into glia cells and further to neurons again. Sucrose is degraded into glucose and fructose in the intestine thus intake of sucrose increases plasma levels of glucose. We show that intake of sucrose enhanced memory measured by Morris maze in rats and improved the working ability in humans. Roles of glucose and sucrose intakes are discussed together with the function of serotonin in feeding.

Aqueous Extract of Black Maca (Lepidium meyenii) on Memory Impairment Induced by Ovariectomy in Mice

The present study aims to test two different doses of aqueous extract of black maca on learning and memory in ovariectomized (OVX) mice and their relation with malonalehyde (MDA), acetylcholinesterase (Ache) and monoamine oxidase (MAO) brain levels. Female mice were divided into five groups: (i) naive (control), (ii) sham, (iii) OVX mice and OVX mice treated with (iv) 0.50 g kg−1and (v) 2.00 g kg−1black maca. Mice were orally treated with distilled water or black maca during 35 days starting 7 days after surgery. Memory and learning were assessed using the water Morris maze (from day 23–27) and the step-down avoidance test (days 34 and 35). At the end of each treatment, mice were sacrificed by decapitation and brains were dissected out for MDA, Ache and MAO determinations. Black maca (0.5 and 2.0 g/kg) increased step-down latency when compared to OVX control mice. Black maca decreased MDA and Ache levels in OVX mice; whereas, no differences were observed in MAO levels. Finally, black maca improved experimental memory impairment induced by ovariectomy, due in part, by its antioxidant and Ache inhibitory activities.