tannins and Memory-Disorders

Kalyanaka ghrita (KG) is an Ayurvedic formulation traditionally used in the treatment of Daurbalya (debility) and Smritidaurbalya (impairment of intellectual activities). Clinical studies have reported the effect of KG in the treatment of Manasmandata or Buddhimandyata which is associated with impaired learning, social adjustment and maturation.. The present study aims to standardization of KG and validation of its use in experimental models of neurodegeneration.. KG was Standardized for biomarkers curcumin, gallic acid, tannic acid, chebulagic acid, and berberine. In male wistar rats, neurodegeneration was induced by administration of intracerebroventricular Amyloid β (Aβ. A novel HPLC method has been developed for the standardization of KG. Treatment with KG significantly improved cognition and memory and increased brain BDNF and antioxidant status in Aβ. The findings suggest that KG has neuroprotective potential and along with its nootropic property could be a promising therapy for neurodegenerative diseases like Alzheimer's disease.

Topics: Acetylcholinesterase; Alzheimer Disease; Amyloid beta-Peptides; Animals; Antioxidants; Berberine; Brain-Derived Neurotrophic Factor; Curcumin; Cytokines; Disease Models, Animal; Male; Maze Learning; Memory Disorders; Neuroprotective Agents; Nootropic Agents; Rats; Rats, Wistar; Tannins

Tannic acid (TA) is a natural compound present abundantly in fruit such as grapes and green tea. In this study, we have evaluated the therapeutic efficacy of TA against Lipopolysaccharide (LPS)-induced oxidative stress-mediated memory impairment, neuroinflammation, insulin signaling impairment, and Amyloid Beta (Aβ) deposition in adult male mice. The LPS was administered once per week and TA twice a week to adult male mice for three months consecutively. Behavioral studies were performed using different behavioral models such as balance beam, novel object recognition (NOR), Morris water maze (MWM), and Y-maze tests. The protein expression of different mediators such as TNF-α, p-JNK, pIRS636, BACE1, APP, and Aβ was evaluated through western blot and immunofluorescence staining techniques. Biochemical assays were carried out to assess the antioxidant activities of TA. The computational study was conducted to predict the binding mode of TA with target sites of TNF-α. Behavioral studies showed that the TA-treated mice exhibited gradual memory improvement. TA significantly inhibited BACE1 activity and reduced production and accumulation of Aβ in the hippocampus of mice brains. Moreover, the TA significantly inhibited LPS-induced ROS production and enhanced the glutathione levels. Furthermore, we have shown via the computational method for the first time that TA inhibits LPS-triggered TNF-ὰ and its downstream signaling to reduce AD pathology including memory impairment, neuroinflammation, insulin signaling impairment, and Aβ deposition in adult mice. Taken together our current study demonstrates that TA is a potential candidate for the abrogation of LPS-induced neurotoxicity and AD pathology in rodent's models.

Topics: Alzheimer Disease; Amyloid beta-Peptides; Amyloid Precursor Protein Secretases; Animals; Aspartic Acid Endopeptidases; Cognitive Dysfunction; Disease Models, Animal; Insulins; Lipopolysaccharides; Male; Maze Learning; Memory Disorders; Mice; Tannins; Tumor Necrosis Factor-alpha

Tannic acid (TA) is a hydrolysable glycosidic polyphenol polymer of gallic acid, which possesses neuroprotective properties. The aim of this study was to evaluate the effect of TA treatment on cognitive performance and neurochemical changes in an experimental model of sporadic dementia of Alzheimer's type (SDAT) induced by intracerebroventricular (ICV) injection of streptozotocin (STZ) and to explore the potential cellular and molecular mechanisms underlying these effects. Adult male rats were divided into four groups: control, TA, STZ, and TA + STZ. Animals from TA and TA + STZ groups were treated with TA (30 mg/kg) daily, by gavage, for 21 days; others groups received water (1 mL/kg). Subsequently, an ICV injection of STZ (3 mg/kg) was administered into the lateral ventricles of animals from STZ and TA + STZ groups, while other groups received citrate buffer. Cognitive deficits (short-term memory), neuronal survival, neuroinflammation as well as expression of SNAP-25, Akt, and pAkt were evaluated in the cerebral cortex. TA treatment protected against the impairment of memory in STZ-induced SDAT. STZ promoted an increase in neuronal death and the levels of proinflammatory cytokines (IL-6 and TNF-α) and a decrease in Akt and pAkt expression; TA was able to restore these changes. Neither STZ nor TA altered SNAP-25 expression or the levels of IL-12 and IL-4 in the cerebral cortex. Our study highlights that treatment with TA prevents memory deficits and reestablishes Akt and pAkt expression, protecting against neuronal death and neuroinflammation in STZ-induced SDAT in rats.

Topics: Alzheimer Disease; Animals; Avoidance Learning; Cell Death; Inflammation Mediators; Male; Memory Disorders; Proto-Oncogene Proteins c-akt; Rats; Rats, Wistar; Streptozocin; Tannins

Mice were subcutaneously injected with d-galactose (D-gal, 150 mg/kg per day) for 6 weeks and were administered high molecular weight persimmon condensed tannin (HMWPT) simultaneously. After 6 weeks of treatment, the animal behavior was observed in the open field test and water maze test, and the morphology of hippocampus and skin were checked. Meanwhile, the activities of antioxidant enzymes, the levels of non-enzymatic antioxidants, as well as malondialdehyde (MDA) were evaluated. The results indicated that HMWPT markedly inhibited the d-gal induced learning and memory impairment in both open field test and Morris water maze. Biochemical examination revealed that HMWPT significantly increased the decreased activities of superoxide dismutase (SOD), catalase (CAT), elevated the lowered total anti-oxidation capability (T-AOC), glutathione (GSH) and hydroxyproline (Hyp) contents (p<0.01 or p<0.05), and decreased the raised monoamine oxidase (MAO), total cholinesterase (TChE) activities and MDA level (p<0.01) in serum, liver or brain of aging mice induced by d-gal in a dose-dependent fashion. Furthermore, HMWPT significantly and (p<0.01) attenuated the d-gal induced number decrease, neuronal degeneration and karyopycnosis in cells in the hippocampus and decrease of thickness of skin epidermis and dermis.

Topics: Aging; Animals; Antioxidants; Behavior, Animal; Catalase; Cholinesterases; Cognition Disorders; Diospyros; Galactose; Glutathione; Hippocampus; Hydroxyproline; Lipid Peroxidation; Male; Malondialdehyde; Maze Learning; Memory Disorders; Mice; Molecular Weight; Monoamine Oxidase; Oxidative Stress; Skin; Superoxide Dismutase; Tannins