Abstract:The purpose of the present study was to examine the effect of Lycii Radicis Cortex (LRC) and betaine (BT) on immobility and neurochemical change in the forced swimming test (FST) in the rat. LRC, BT or fluoxentine was administered intraperitoneally to Sprague-Dawley rats three times (1, 5 and 23.5 h) before the FST. To investigate antidepressant-like effect, serotonin (5-HT) and norepinephrine (NE) were examined in the hippocampus and hypothalamus of rats. LRC (100 mg/kg) and BT (30, 100 mg/kg) significantly d… Show more
“…On the other hand, D-serine (Malkesman et al 2012) and glycine transporter-I inhibitor sarcosine (Chen et al 2015;Huang et al 2013), which are assumed to potentiate NMDAR function through glycine site, can also improve depression-like behaviors in rodent models and in human depression (Huang et al 2013). Modulation of NMDAR glycine site might be majorly contributed to the rapid and sustained antidepressant-like effect of betaine, although betaine elevated 5-HT levels and has been suggested to be like a traditional antidepressant (Kim et al 2013).…”
Section: Discussionmentioning
confidence: 96%
“…Based on the structural similarity to glycine, we have examined if betaine can affect the NMDAR function and demonstrated that betaine acts like a NMDAR glycine binding site partial agonist (Lee and Chen 2014). Furthermore, betaine exhibits antidepressant-like effects in rats (Kim et al 2013). Accordingly, it is hypothesized that betaine can promote the antidepressant-like but antagonize the psychotomimetic effect of ketamine.…”
Ketamine is emerging as a new hope against depression, but ketamine-associated psychotomimetic effects limit its clinical use. An adjunct therapy along with ketamine to alleviate its adverse effects and even potentiate the antidepressant effects might be an alternative strategy. Betaine, a methyl derivative of glycine and a dietary supplement, has been shown to have antidepressant-like effects and to act like a partial agonist at the glycine site of N-methyl-D-aspartate receptors (NMDARs). Accordingly, betaine might have potential to be an adjunct to ketamine treatment for depression. The antidepressant-like effects of ketamine and betaine were evaluated by forced swimming test and novelty suppressed feeding test in mice. Both betaine and ketamine produced antidepressant-like effects. Furthermore, we determined the effects of betaine on ketamine-induced antidepressant-like and psychotomimetic behaviors, motor incoordination, hyperlocomotor activity, and anesthesia. The antidepressant-like responses to betaine combined with ketamine were stronger than their individual effects. In contrast, ketamine-induced impairments in prepulse inhibition, novel object recognition test, social interaction, and rotarod test were remarkably attenuated, whereas ketamine-induced hyperlocomotion and loss of righting reflex were not affected by betaine. These findings revealed that betaine could enhance the antidepressant-like effects, yet block the psychotomimetic effects of ketamine, suggesting that betaine can be considered as an add-on therapy to ketamine for treatment-resistant depression and suitable for the treatment of depressive symptoms in patients with schizophrenia.
“…On the other hand, D-serine (Malkesman et al 2012) and glycine transporter-I inhibitor sarcosine (Chen et al 2015;Huang et al 2013), which are assumed to potentiate NMDAR function through glycine site, can also improve depression-like behaviors in rodent models and in human depression (Huang et al 2013). Modulation of NMDAR glycine site might be majorly contributed to the rapid and sustained antidepressant-like effect of betaine, although betaine elevated 5-HT levels and has been suggested to be like a traditional antidepressant (Kim et al 2013).…”
Section: Discussionmentioning
confidence: 96%
“…Based on the structural similarity to glycine, we have examined if betaine can affect the NMDAR function and demonstrated that betaine acts like a NMDAR glycine binding site partial agonist (Lee and Chen 2014). Furthermore, betaine exhibits antidepressant-like effects in rats (Kim et al 2013). Accordingly, it is hypothesized that betaine can promote the antidepressant-like but antagonize the psychotomimetic effect of ketamine.…”
Ketamine is emerging as a new hope against depression, but ketamine-associated psychotomimetic effects limit its clinical use. An adjunct therapy along with ketamine to alleviate its adverse effects and even potentiate the antidepressant effects might be an alternative strategy. Betaine, a methyl derivative of glycine and a dietary supplement, has been shown to have antidepressant-like effects and to act like a partial agonist at the glycine site of N-methyl-D-aspartate receptors (NMDARs). Accordingly, betaine might have potential to be an adjunct to ketamine treatment for depression. The antidepressant-like effects of ketamine and betaine were evaluated by forced swimming test and novelty suppressed feeding test in mice. Both betaine and ketamine produced antidepressant-like effects. Furthermore, we determined the effects of betaine on ketamine-induced antidepressant-like and psychotomimetic behaviors, motor incoordination, hyperlocomotor activity, and anesthesia. The antidepressant-like responses to betaine combined with ketamine were stronger than their individual effects. In contrast, ketamine-induced impairments in prepulse inhibition, novel object recognition test, social interaction, and rotarod test were remarkably attenuated, whereas ketamine-induced hyperlocomotion and loss of righting reflex were not affected by betaine. These findings revealed that betaine could enhance the antidepressant-like effects, yet block the psychotomimetic effects of ketamine, suggesting that betaine can be considered as an add-on therapy to ketamine for treatment-resistant depression and suitable for the treatment of depressive symptoms in patients with schizophrenia.
Objectives : This study aimed to compare the anti-diabetic efficacy of Lycii Radicis Cortex (Lycium chinense Mill.) and Corni Fructus (Cornus officinalis) on streptozotocin (STZ)-induced diabetes in rats.Methods : Male Sprague-Dawley rats were divided into four groups; normal, STZ-control, Lycii Radicis Cortex extract-administrated group (LRC) and Corni Fructus extract-administrated group(CF). Diabetes in rats was induced by intraperitonal injection with streptozotocin (STZ) at doses of, 30 ㎎/㎏ (body weight) for 5 days (once per a day). STZ-induced diabetic rats were orally administrated LRC and CF extract daily for 4 weeks at doses of 300 ㎎/㎏. Fasting blood glucose, total cholesterol (TC), triglyceride (TG), blood urea nitrogen (BUN) and creatinine were measured in sera of rats. Histopathological changes of kidney, liver and lung tissues were observed by microscope after H&E staining. Results : There were no differences in body and kidney weights, food intake and water intake in LRC-and CF-administrated groups compared with STZ control group. However, glucose, TC and TG levels in serum were significantly decreased in LRC-administrated groups compared with STZ-control group. In histopathological analysis of kidney, liver and lung, both LRC-and CF-administrated groups showed the inhibition of morphological damage. Conclusions : These results suggest that LRC and CF have a biological action on STZ-induced diabetes in rats via decreasing the serum TG and TG levels and may protect the morphological changes of kidney, liver and lung.
“…In addition, LRC inhibits hepatic damage induced by CC14 (Cho and Kim ) and depressed state (Kim et al . ) in mice. Furthermore, tyramine derivatives or phenolic amides from LRC exhibit hypocholesterolemic, antioxidative or anti‐inflammatory effects (Cho et al .…”
An oxidative defense system imbalance leads to overproduction of reactive oxygen species (ROS) and is implicated in the progression of neurodegenerative ailments such as Parkinson's disease (PD). In the present study, we examined the protective effects of the ethanolic extract of Lycii Radicis Cortex (LRCE) in an in vitro PD model induced by 6‐hydroxydopamine (6‐OHDA), which induces selective dopaminergic cell death through oxidative stress. LRCE resulted in significant protective effects in SH‐SY5Y cells and showed strong radical scavenging effects. In addition, LRCE inhibited intracellular ROS and extracellular nitrite production and glutathione depletion induced by 6‐OHDA. Furthermore, LRCE blocked the destabilization of the mitochondrial membrane potential and the activation of caspase‐3. Moreover, dopaminergic neuronal protection of LRCE from 6‐OHDA exposure was confirmed in the rat primary mesencephalic culture system. LRCE is therefore considered to exert beneficial effects on dopaminergic neurons, resulting to antiparkinsonian effects via antioxidant activities.
Practical Applications
The current findings suggest that owing to its effects on antioxidant activity, Lycii Radicis Cortex may be useful as an alternative therapy to prevent and treat neurodegeneration including dopaminergic neuron dysfunction.
scite is a Brooklyn-based organization that helps researchers better discover and understand research articles through Smart Citations–citations that display the context of the citation and describe whether the article provides supporting or contrasting evidence. scite is used by students and researchers from around the world and is funded in part by the National Science Foundation and the National Institute on Drug Abuse of the National Institutes of Health.