Table 1.
Primers used in the gene expression study.
Fig 1.
HPLC results of isolated Q and BCA.
Fig 2.
In vitro release of Q and Q-LNP at both pH 7.4 and 2.0 using 100 mL of phosphate-buffered solution and diluted HCl respectively as a release medium at 37ºC, 100 rpm.
Table 2.
Physicochemical characterization of Q-LNP.
Fig 3.
Changes in the cognitive performance in different experimental groups.
Values are expressed as means ± SE (n = 5). Mean values having different superscript letters a, b, c, and d are significantly different from each other (p < 0.05).
Table 3.
Changes in the serum levels of glucose, insulin, total cholesterol (TC) and triglyceride (TG) in different experimental groups.
Table 4.
Changes in the oxidant and antioxidant profile in the cerebral cortex of different experimental groups.
Table 5.
Changes in the neurochemical parameters in the cerebral cortex of different experimental groups.
Table 6.
Changes in the inflammatory markers in the cerebral cortex of different experimental groups.
Table 7.
Changes in the gene expression levels of inducible nitric oxide synthase (iNOS), Interleukin-1β (IL-1β), Amyloid precursor protein (APP), Presenilin 2 (PSEN2), β-secretase (BACE), insulin receptor (IR), phosphoinositide 3-kinase (PI3K), Peroxisome proliferator-activated receptor gamma (PPAR-γ), Forkhead Box 1 (FOXO-1), thymoma viral oncogene (AKT) and AMP-activated protein kinase (AMPK) in the cerebral cortex of different experimental groups.
Fig 4.
Changes in the glycogen synthase kinase-3β (GSK-3β) in the cerebral cortex of different experimental groups.
Values are expressed as means ± SE (n = 5). Mean values having different superscript letters a, b, c, and d are significantly different from each other (p < 0.05).
Fig 5.
Photomicrographs of sections in the cerebral cortex of male rats.
(A) Control rats showing normal structure of the cerebral cortex; normal pyramidal cell (green dotted arrow) and granule cell with pale open face nucleus (yellow arrow) normal blood vessel (green arrow). (B) Diabetic rats showing pericellular vacuoles (black arrow), dilatation of blood capillary with congestion (green arrow), neuronal degeneration with pyknotic nuclei (black square), encephalomelacia (red square), dark degenerated neuron (red arrow), pyknotic nuclei (blue head arrow), vacuolated neuropil (blue dotted arrow) and glial cell (green circle). (C, D, E): sections of the cerebral cortex of Diabetic+Q-LNP, Diabetic+BCA, and Diabetic+TA extract treated groups, respectively, showing slight improvement of the neuronal cells (H&E, 400X).
Fig 6.
Photomicrographs of sections in rat’s cerebral cortex, showing immunoreactivity for GFAP.
Sections in control group (A) showed negative reaction for GFAP, while cerebral cortex sections from the untreated-diabetic group (B) showed strong reaction for GFAP. Sections from Diabetic+Q-LNP, Diabetic+BCA, and Diabetic+TA extract treated groups (C, D, & E), respectively, showed reduced number and intensity of GFAP positive cells (GFAP, 400X).
Fig 7.
Changes in the mean number of GFAP labeled cells in the cerebral cortex of male rats in the different experimental groups.
Values are expressed as means ± SE (n = 5). Mean values having different superscript letters a, b, c, and d are significantly different from each other (p < 0.05).