Effect of Combined Treatment with Levofloxacin and Metformin on Diabetes-the Diabetes Related Behavioral and Biochemical Alterations.

Objectives: The current experiment was conducted to investigate the combined effect of levofloxacin (LVX) and metformin treatment on blood glucose levels, malondialdehyde (MDA),nitrite levels, and anxiety in streptozotocin (STZ)+ nicotine adenine dinucleotide (NAD)-induced diabetic rats.

Materials And Methods: In this study, Wistar rats have been used. After receiving a single dose of STZ + NAD (45 mg/kg, + 50 mg/kg, ), the rats developed diabetes.

Brain insulin resistance mediated cognitive impairment and neurodegeneration: Type-3 diabetes or Alzheimer's Disease.

Insulin resistance is a condition characterized by the attenuated biological response in the presence of normal or elevated insulin level and therefore is characterized by the impaired sensitivity to insulin and impaired glucose disposal and utilization. Insulin resistance in brain/Brain insulin resistance (BIR) is accompanied by the various manifestations including alteration in glucose sensing by hypothalamic neurons, impaired sympathetic outflow in response to hypoglycemia, increased ROS production, impaired mitochondrial oxygen consumption in the brain, cognitive deficits and neuronal cell damage. It has been reported that the disrupted insulin signaling is accompanied by the reduced expression of insulin receptor (IR)/insulin receptor substrate 1 (IRS1)/PI3K/AKT and IGF-1 receptor (IGF-1R)/IRS2/PI3K pathways.

Caffeic acid differentially modulates behavior and neurochemicals in chronic unpredictable mild stress and dexamethasone induced models of depression.

In the present study authors studied the effect of caffeic acid (CA) in chronic unpredictable mild stress (CUMS) and dexamethasone (DEXA) model of depression. CUMS (21 days) and DEXA (1.5 mg/kg × 21 days) was used for the induction of depression and anxiety related behavior.

Therapeutic potential of vasopressin in the treatment of neurological disorders.

Vasopressin (VP) is a nonapeptide made of nine amino acids synthesized by the hypothalamus and released by the pituitary gland. VP acts as a neurohormone, neuropeptide and neuromodulator and plays an important role in the regulation of water balance, osmolarity, blood pressure, body temperature, stress response, emotional challenges, etc. Traditionally VP is known to regulate the osmolarity and tonicity.

Hypoglycemia and anxiolysis mediated by levofloxacin treatment in diabetic rats.

Purpose: The present study was designed to determine the effect of levofloxacin (LVX) treatment on the blood glucose level, insulin sensitivity, anxiety level, nitrite and MDA level of STZ induced diabetic rats.

Methods: Wistar rats were used in the present study. The rats were made diabetic by the administration of single dose of STZ (45 mg/kg, i.

Therapeutic Potential of Myricetin in the Treatment of Neurological, Neuropsychiatric, and Neurodegenerative Disorders.

Myricetin (MC), 3,5,7,3',4',5'-hexahydroxyflavone, chemically belongs to a flavonoid category known to confer antioxidant, antimicrobial, antidiabetic, and neuroprotective effects. MC is known to suppress the generation of Reactive Oxygen Species (ROS), lipid peroxidation (MDA), and inflammatory markers. It has been reported to improve insulin function in the human brain and periphery.

Possible involvement of NO-cGMP signaling in the antidepressant like Effect of Amantadine in mice.

In the present study, antidepressant like effect of amantadine was studied in mice using tail suspension test (TST) and forced swim test (FST). Further the effect of amantadine treatment on the brain nitrite, glutamate and serotonin levels was also determined. Amantadine (AMT) (50, 100 and 150 mg/kg, i.

Antidepressant Like Effect of Ascorbic Acid in Mice: Possible Involvement of NO-sGC-cGMP Signaling.

The present study was designed to determine the antidepressant like activity of ascorbic acid (AA) in mice. Further the influence of NO-sGC-cGMP signaling in the antidepressant like effect of AA in mice was determined. Male swiss albino mice were used in the present study.

Delineation of Neuroprotective Effects and Possible Benefits of AntioxidantsTherapy for the Treatment of Alzheimer's Diseases by Targeting Mitochondrial-Derived Reactive Oxygen Species: Bench to Bedside.

Alzheimer's disease (AD) is considered the sixth leading cause of death in elderly patients and is characterized by progressive neuronal degeneration and impairment in memory, language, etc. AD is characterized by the deposition of senile plaque, accumulation of fibrils, and neurofibrillary tangles (NFTs) which are responsible for neuronal degeneration. Amyloid-β (Aβ) plays a key role in the process of neuronal degeneration in the case of AD.

Possible involvement of NO-sGC-cGMP signaling in the antidepressant like effect of pyridoxine in mice.

The present study was designed to determine the antidepressant like effect of pyridoxine in mice. Pyridoxine (12.5, 25 and 50 mg/kg, i.

Therapeutic potential of mangiferin in the treatment of various neuropsychiatric and neurodegenerative disorders.

Xanthones are important chemical class of bioactive products that confers therapeutic benefits. Of several xanthones, mangiferin is known to be distributed widely across several fruits, vegetables and medicinal plants. Mangiferin has been shown to exert neuroprotective effects in both in-vitro and in-vivo models.

Anxiolytic like effect of L-Carnitine in mice: Evidences for the involvement of NO-sGC-cGMP signaling pathway.

L-Carnitine (LC) is an endogenous compound synthesized from the essential amino acids lysine and methionine. LC act as an antioxidant and modulates the levels of neurochemicals such as glutamate, GABA, NO etc. implicated in the regulation of anxiety and related behavior.

Amantadine exerts anxiolytic like effect in mice: Evidences for the involvement of nitrergic and GABAergic signaling pathways.

Amantadine is a glutamatergic antagonist that works by inhibiting the NMDA receptor. Besides the inhibition of NMDA receptors amantadine also stabilizes the glutamatergic system and protects the neurons against the NMDA toxicity. Amantadine treatment also reduces the production of NO and metabolism of GABA.

Lithium potentiated, pyridoxine abolished and fluoxetine attenuated the anxiolytic effect of diazepam in mice.

In the present study, the anxiolytic effect of diazepam (1 and 2 mg/kg, i.p.) was determined alone and in combination with lithium (50 mg/kg, i.

Nitrergic signaling modulation by ascorbic acid treatment is responsible for anxiolysis in mouse model of anxiety.

The present study was designed to investigate the effect of ascorbic acid (AA) treatment on the anxiety related behavioral and neurochemical alterations. AA (50, 100 and 200 mg/kg, i.p.

NO-sGC-cGMP signaling influence the anxiolytic like effect of lithium in mice in light and dark box and elevated plus maze.

Glutamate is an excitatory neurotransmitter implicated in the pathogenesis of psychiatric disorders. Glutamate results in the activation of an enzyme called glycogen synthase kinase-3 (GSK-3) acting through N-methyl-d-aspartate (NMDA) receptors. Impaired expression of GSK-3 affects behavior and neurochemicals level in the brain responsible for the pathogenesis of mood disorders.

Anxiolytic-like effect of pyridoxine in mice by elevated plus maze and light and dark box: Evidence for the involvement of GABAergic and NO-sGC-cGMP pathway.

Present study was carried out to investigate the 'anxiolytic-like' effect of pyridoxine in mice. Pyridoxine (90, 180 and 360 mg/kg) was administered by intraperitoneal (i.p.