No abstract

The decrease of brain-derived neurotrophic factor (BDNF) has been reported in alcohol use disorder and major depression. The effective treatment of these comorbid diseases remains undiscovered. Nutraceutical products are therefore proposed as an alternative approach to overcome this challenge. Ginseng extract G115, the standardized extract of Panax ginseng, is a widely-used nutraceutical that is beneficial for various central nervous system disorders. This study aimed to determine the antidepressant effect of ginseng extract G115 in ethanol-treated mice models. Mice received either water, amitriptyline, or various doses of G115 (p.o.) followed by water or ethanol (i.p.) for 8 days. The antidepressant activity was evaluated using forced swimming test. BDNF levels were measured from hippocampal and prefrontal cortex tissues. The results demonstrated that the increase of immobility time in depressant mice induced by ethanol was reversed by both G115 and amitriptyline treatment. A significant increase of BDNF levels in the hippocampus and prefrontal cortex was observed in ethanol-treated mice receiving G115. Taken together, this study provides scientific information on the use of G115 as an antidepressant that could be further used as a dietary supplement in comorbid alcohol use and major depressive disorders.

Oxyresveratrol, a polyphenolic compound, has been reported as having antioxidant and anti-inflammatory effects. This study determined the neuroprotective effects of oxyresveratrol, extracted from the heartwood of Artocarpus lakoocha Roxburgh (Moraceae), on parkinsonism induced by rotenone. Male Wistar rats were divided into control, rotenone (PD), and rotenone plus oxyresveratrol (OXY) groups. The OXY rats received oxyresveratrol (300 mg/kg orally) on days 1-20. Rotenone (3 mg/kg subcutaneously) was given to PD and OXY rats on days 15, 16, 18, and 20. Motor function was determined by the rotarod test. Brains were collected to analyze dopaminergic neurons, malondialdehyde (MDA) levels, and superoxide dismutase (SOD) and catalase activities. OXY rats exhibited a longer latency to fall than PD rats in the rotarod test ( P < 0.01) on day 16. The number of dopaminergic neurons in PD rats was lower than that in controls ( P < 0.01), while that of OXY rats was not different from controls. OXY rats showed a reduction in MDA levels ( P < 0.01) and increased catalase activity ( P < 0.05), while SOD activity was unaltered. The results suggest that oxyresveratrol pretreatment ameliorates motor impairment induced by rotenone and preserves dopaminergic neurons. The neuroprotective mechanism of oxyresveratrol is involved with its antioxidant properties.

No abstract

TRPA1 channels have been implicated in mechanical and cold hypersensitivity in chronic pain. But how TRPA1 mediates this process is unclear. Here we show that IQ-motif containing GTPase activating protein 1 (IQGAP1) is responsible using a combination of biochemical, molecular, Ca2+ imaging and behavioural approaches. TRPA1 and IQGAP1 bind to each other and are highly colocalised in sensory DRG neurons in mice. The expression of IQGAP1 but not TRPA1 is increased in chronic inflammatory and neuropathic pain. However, TRPA1 undergoes increased trafficking to the membrane of DRG neurons catalysed by the small GTPase Cdc42 associated with IQGAP1, leading to functional sensitization of the channel. Activation of PKA is also sufficient to evoke TRPA1 trafficking and sensitization. All these responses are, however, completely prevented in the absence of IQGAP1. Concordantly, deletion of IQGAP1 markedly reduces mechanical and cold hypersensitivity in chronic inflammatory and neuropathic pain in mice. IQGAP1 thus promotes chronic pain by coupling the trafficking and signalling machineries to TRPA1 channels.