Fumiko Suzuki

Antidepressant-like effects of a water-soluble extract from the culture medium of Ganoderma lucidum mycelia in rats

BackgroundGanoderma lucidum is a popular medicinal mushroom used for promoting health and longevity in Asian countries. Previously, we reported that a water-soluble extract from a culture medium of Ganoderma lucidum mycelia (MAK) exerts antioxidative and cerebroprotective effects against ischemia–reperfusion injury in vivo. Here, we evaluated the antidepressant and anxiolytic activities of MAK in rats.MethodsMAK (0.3 or 1 g/kg, p.o.) was administered in the experimental animals 60 min before the forced swimming, open-field, elevated plus-maze, contextual fear-conditioning, and head twitch tests. Additionally, the mechanisms involved in the antidepressant-like action of MAK were investigated by the serotonin precursor 5-hydroxy-L-tryptophan (5-HTP)- or 5-HT2A agonist (±)-1-(2,5-dimethoxy-4-iodophenyl)-2-aminopropane hydrochloride (DOI)-induced head twitch responses.ResultsTreatment with MAK (1 g/kg) exhibited antidepressant-like effects in the forced swimming test, attenuated freezing behavior in the contextual fear-conditioning test, and decreased the number of head twitches induced by DOI, but not with 5-HTP. No significant response was observed in locomotion or anxiety-like behavior, when the animals were evaluated in the open-field or elevated plus-maze test, respectively.ConclusionsThese data suggest that MAK has antidepressant-like potential, which is most likely due to the antagonism of 5-HT2A receptors, and possesses anxiolytic-like effects toward memory-dependent and/or stress-induced anxiety in rats.

Diabetes-Mediated Exacerbation of Neuronal Damage and Inflammation After Cerebral Ischemia in Rat: Protective Effects of Water-Soluble Extract from Culture Medium of Ganoderma lucidum Mycelia

Diabetes mellitus is a metabolic disorder, suffered by hundreds of millions of people throughout the world, which is characterized by hyperglycemia resulting from insufficiency of insulin secretion and/or action (Wild et al., 2004). Complications associated with diabetes affecting vessels, eyes, kidney, and peripheral nerves reduce the QOL of diabetic patients. Also, diabetes is widely recognized as a major risk factor for atherosclerotic disease such as acute brain ischemia. Indeed, diabetic patients have a higher risk of stroke compared with non-diabetic patients (Baynes 1991; Stephens et al., 2009). Additionally, they are more likely to have a poor prognosis and increased mortality after stroke (Biller et al., 1993; Vinik et al., 2002). Previous studies have demonstrated that the diabetic state increases oxidative stress in the brain and aggravates cerebral ischemic injury in both type I (Li et al., 2004; Saito et al., 2005; Rizk et al., 2005) and type II diabetic animal models (Anabela et al., 2006; Tureyen et al., 2011). In addition to neuronal damage attributed to hypoxia and ATP depletion caused by vascular obstruction in ischemic core region, cerebral injury caused by subsequent reperfusion is also involved in the pathophysiology of transient ischemia (Doyle et al., 2008; Nakka et al., 2008; Wang et al., 2010). During reperfusion, the production of reactive oxygen species (ROS) and reactive nitrogen species (RNS) is enhanced by abrupt re-oxygenation (Cuzzocrea et al., 2001; Saito et al., 2005). Besides direct injurious effects to the cell membrane, proteins and DNA by