Oxidative stress has been reported to induce cognitive impairment in Parkinson's disease. This paper aimed to determine the effect of quercetin, a substance possessing antioxidant activity, on the cognitive function in a rat model of Parkinson's disease. Male Wistar rats, weighing 200–250 g, were orally given quercetin at doses of 100, 200, 300 mg/kg BW once daily for a period of 14 days before and 14 days after the unilateral lesion of right substantia nigra induced by 6-hydroxydopamine (6-OHDA). Their spatial memory was assessed at 7 and 14 days of treatment and neuron density was determined, malondialdehyde (MDA) level, the activity of superoxide dismutase (SOD), catalase (CAT), and glutathione peroxidase (GPx) were evaluated at the end of the experiment. In addition, the activity of acetylcholinesterase (AChE) was also measured. It was found that all doses of quercetin enhanced spatial memory. Therefore, it is suggested that the cognitive-enhancing effect of quercetin occurs partly because of decreased oxidative damage resulting in increased neuron density.

The systemic administration of lipopolysaccharide (LPS) has been recognized to induce neuroinflammation which plays a significant role in the pathogenesis of neurodegenerative diseases such as Alzheimer’s disease and Parkinson’s disease. In this study, we aimed to determine the protective effect of Zingiber cassumunar (Z. cassumunar) or Phlai (in Thai) against LPS-induced neuronal cell loss and the upregulation of glial fibrillary acidic protein (GFAP) of astrocytes in the hippocampus. Adult male Wistar rats were orally administered with Z. cassumunar extract at various doses (50, 100, and 200 mg/kg body weight) for 14 days before a single injection of LPS (250 μg/kg/i.p.). The results indicated that LPS-treated animals exhibited neuronal cell loss and the activation of astrocytes and also increased proinflammatory cytokine interleukin- (IL-) 1β in the hippocampus. Pretreatment with Z. cassumunar markedly reduced neuronal cell loss in the hippocampus. In addition, Z. cassumunar extract at a dose of 200 mg/kg BW significantly suppressed the inflammatory response by reducing the expression of GFAP and IL-1ß in the hippocampus. Therefore, the results suggested that Z. cassumunar extract might be valuable as a neuroprotective agent in neuroinflammation-induced brain damage. However, further investigations are essential to validate the possible active ingredients and mechanisms of its neuroprotective effect.

Chronic hyperglycemia causes nerves to be more susceptible to compression, which often occurs as a result of hyperglycemia-induced oxidative stress. Oxidative stress impairs nerve function and delays nerve recovery. Azadirachta indica, a herb from Thailand, possesses antioxidant and antidiabetic properties. The aim of the present study was therefore to investigate the effect of A. indica flower extract on the functional recovery of a sciatic nerve crush injury in rat models of diabetes mellitus (DM). Male Wistar rats were randomly assigned into seven groups including the control rats, rats with DM subjected to sham surgery and treated with vehicle, and rats with DM subjected to the crush surgery and treated with vehicle or A. indica flower extract at a dose of 250, 500 or 750 mg/kg animal body weight, or with vitamin C. DM was induced using a single intraperitoneal injection of streptozotocin (55 mg/kg animal body weight). Rats subjected to a sciatic nerve crush injury or sham surgery were orally treated with either vehicle, A. indica flower extract or vitamin C for 21 days. Functional recovery was assessed every 3 days using a walking track analysis, foot withdrawal reflex test and rotarod test. At the end of the study, the rats were sacrificed and their left sciatic nerves were harvested in order to determine malondialdehyde levels, superoxide dismutase activity and axon density. The treatment with A. indica flower extract significantly improved functional recovery, especially motor and sensory functions. The extract significantly decreased malondialdehyde levels, and increased superoxide dismutase activity and axon density. The results of the current study indicate that the mechanism underlying the enhanced functional recovery of the sciatic nerve following treatment with A. indica flower extract may be associated with an antioxidative effect. However, further studies are required to confirm the current results.

Injury to the peripheral nerve may lead to deficits in nerve function. An increase in the levels of free radicals plays a role in inhibition of nerve regeneration following damage. The aim of this study was to investigate the effects of lotus essential oil (LEO) on neurite outgrowth in vitro and nerve regeneration in vivo in a rat model of sciatic nerve crush injury. Gas chromatography-mass spectrometry analysis showed that the principal constituent of LEO was palmitic acid ethyl ester (25.12%). The radical scavenging activity of LEO was evaluated using the DPPH method, and was determined to be IC 50 =29.01±2.93 µg/ml. LEO-treated sensory neurons exhibited increased neurite outgrowth and upregulated levels of phospho-ERK. Sensory and motor functions were improved in rats treated with 50 and 100 mg/kg LEO, and this was accompanied by an increase in the number of neurons in the dorsal root ganglia, as well as an increase in the nerve axon diameters following nerve injury. Taken together, these results suggests that LEO may serve as a novel pharmacological option for the management of peripheral nerve injury.

The aim of this study was to evaluate whether an aqueous extract of Azadirachta indica A. Juss. (A. indica) flower had anxiolytic and antidepressant-like effects in the stressed rats. Male Wistar rats were randomly allocated to one of two experimental groups: control or stress. The stress groups were received restraint stress for 3 h. The stressed rats were administered a vehicle, diazepam, fluoxetine, and A. indica at doses of 250, 500, and 1000 mg/kg BW for 30 days. The elevated plus-maze test (EPMT), the forced swimming test (FST), and the open field test (OFT) were used to assess anxiolytic and antidepressant-like behaviors. In the EPMT, the percentage of the number of open arm entries and the duration spent in open arms were measured. These measurements were considerably enhanced in the stressed rats treated with diazepam and A. indica flower extract at a dose of 500 mg/kg BW. Furthermore, the stressed rats given fluoxetine and A. indica flower extract at all doses employed in this study showed a significant reduction in the amount of time the rats were immobilized in the FST. However, there was no significant difference in spontaneous locomotor activity between any of the groups. Additionally, the stressed rats treated with either positive control medications or A. indica flower extract exhibited significantly higher brain dopamine (DA) and serotonin (5-HT) levels, but lower blood cortisol levels as compared to the stressed rats treated with vehicle. Moreover, A. indica flower extract had no harmful effect on the stressed rats' liver tissue.