Hyun Kyung Chang

Treadmill exercise decreases intrastriatal hemorrhage-induced neuronal cell death via suppression on caspase-3 expression in rats

Intracerebral hemorrhage is one of the most devastating types of stroke. This disease is known to cause severe neurological damage and also has a very high mortality rate. In this study, the effect of treadmill exercise on intrastriatal hemorrhage-induced neuronal cell death was investigated. Intrastriatal hemorrhage was caused by injection of collagenase into the striatum using a stereotaxic instrument. Animals of the exercise group were made to run on a treadmill for 30 min once a day during 10 consecutive days. In the present results, treadmill exercise was shown to suppress the increase in the size of hemorrhage-induced lesions and the increase in caspase-3 expression in the striatum. Based on these results, it is possible that treadmill exercise aids in the recovery from central nervous system sequelae following intracerebral hemorrhage.

Acupuncture suppresses intrastriatal hemorrhage-induced apoptotic neuronal cell death in rats.

Intracerebral hemorrhage is one of the most devastating types of stroke. In the present study, the effect of acupuncture on intrastriatal hemorrhage-induced neuronal cell death in rats was investigated via Nissl staining, terminal deoxynucleotidyl transferase-mediated dUTP nick end labeling assay, and immunohistochemistry for caspase-3. The present results showed that lesion size and apoptotic neuronal cell death in the striatum were significantly increased following intrastriatal hemorrhage in rats and that acupunctural treatment at the Zusanli acupoint suppressed the hemorrhage-induced increase in lesion size and apoptotic neuronal cell death in the striatum. In the present study, it can be suggested that acupunctural treatment, especially at the Zusanli acupoint, may aid in the recovery following central nervous system sequellae following intracerebral hemorrhage.

Administration of Ginseng radix Decreases Nitric Oxide Synthase Expression in the Hippocampus of Streptozotocin-Induced Diabetic Rats

Nitric oxide (NO) is synthesized from L-arginine by nitric oxide synthase (NOS). Alternation of NOS expression is implicated in the pathogenesis of numerous secondary complications of diabetes. Aqueous extract of Ginseng radix has traditionally been used for the various disorders including diabetes. In this study, the effect of Ginseng radix on the NOS expression in the hippocampus of streptozotocin (STZ)-induced diabetic rats was investigated via nicotinamide adenine dinucleotide phosphate-diaphorase (NADPH-d) histochemistry. Enhanced NOS expression was detected in the hippocampus of diabetic rats and administration of Ginseng radix suppressed NOS expression. Ginseng radix may aid the treatment of central nervous system complications in diabetes.

Modulation of cyclooxygenase-2 on glycine- and glutamate-induced ion currents in rat periaqueductal gray neurons

Cyclooxygenase (COX) is a key enzyme in the conversion of arachidonic acid to prostaglandins. Two isoforms of COX are known: COX-1 and COX-2. In the present study, the modulatory effect of COX-2 on glycine- and glutamate-induced ion currents in periaqueductal gray (PAG) neurons was investigated using the nystatin-perforated patch clamp method. Continuous application of lipopolysaccharides on PAG neurons resulted in increased glycine-induced ion current and decreased glutamate-induced ion current. In contrast, continuous application of celecoxib, selective COX-2 inhibitor, resulted in decreased glycine-induced ion current and increased glutamate-induced ion current. These results demonstrate that COX-2 modulates neuronal activity of PAG, and it can be suggested that COX-2 participates in the regulation of the descending pain control system in the level of PAG neurons.

Treadmill exercise suppresses diabetes-induced increment of neuropeptide Y expression in the hypothalamus of rats

Diabetes mellitus is a metabolic disorder with serious sequelae in humans. Hyperphagia is a characteristic symptom of diabetes and is a central nervous system-mediated disorder. Neuropeptide Y (NPY) is a 36-amino-acid peptide and is concentrated in the hypothalamus which is an appetite-regulating area. NPY is known to stimulate appetite and decrease energy expenditure. In the present study, the effect of treadmill exercise on the hypothalamic NPY expression in rats with streptozotocin (STZ)-induced diabetes was investigated via immunohistochemistry. Enhanced NPY expression in the paraventricular nucleus and arcuate nucleus was observed in the STZ-induced diabetic rats. Treadmill exercise suppressed a diabetes-induced increase of NPY expression. The present results suggest the possibility that treadmill exercise inhibits diabetes-induced increment of the desire for food.

Maternal ethanol administration inhibits 5-hydroxytryptamine synthesis and tryptophan hydroxylase expression in the dorsal raphe of rat offspring

Maternal ethanol consumption during pregnancy has a detrimental effect on the central nervous system (CNS) development of fetus. 5-Hydroxytryptamine (5-HT) is an important neurotransmitter and/or neuromodulator in the mammalian CNS. Tryptophan hydroxylase (TPH) is the rate limiting enzyme of 5-HT synthesis. Ethanol is known to induce neuropsychiatric disorders by alteration of the central serotonergic system. In the present study, the effects of maternal ethanol intake on the 5-HT synthesis and the TPH expression in the dorsal raphe of rat offspring were investigated. The present results show that the synthesis of 5-HT and the expression of TPH in the dorsal raphe of rat offspring were suppressed by maternal ethanol intake and that the suppressive effect of alcohol was more potent in the 5 weeks old rat pups compared to the 3 weeks old rat pups. Based on the present study, it can be suggested that the pathogenesis of ethanol-induced neuropsychological disorders involves ethanol-induced suppression on the 5-HT synthesis and the TPH expression in the dorsal raphe of offspring.

Bupivacaine and ropivacaine suppress glycine- and glutamate-induced ion currents in acutely dissociated rat hippocampal neurons.

Bupivacaine and ropivacaine are local surgical anesthetics with great efficacy in post-operative pain relief and labor analgesia. In the present study, the effects of bupivacaine and ropivacaine on ion currents induced by glycine and glutamate in acutely dissociated hippocampal CA1 neurons of rats were investigated via a nystatin-perforated patch clamping method at a clamped voltage. The magnitude of the glycine-induced ion currents was decreased reversibly and in a time-dependent manner by continuous application of 0.1 mg/ml of either bupivacaine or ropivacaine. The magnitude of the glutamate-induced ion currents was also suppressed time-dependently by continuous application of either bupivacaine or ropivacaine. The inhibitory action of bupivacaine and ropivacaine on currents induced by glycine and glutamate could be one of the mechanisms behind the actions of these anesthetics.

Treadmill exercise suppresses food-deprivation-induced increase of nitric oxide synthase expression in rat paraventricular nucleus

Exercise is known to potentially affect the eating patterns. In the present study, the effect of treadmill exercise on the expressions of nitric oxide synthase (NOS) and neuronal nitric oxide synthase (nNOS) in the paraventricular nucleus (PVN) of food-deprived rats was investigated using nicotinamide adenine dinucleotide phosphate-diaphorase (NADPH-d) histochemistry and nNOS immunohistochemistry. The present results showed that food deprivation increased NOS and nNOS expressions in the PVN of the hypothalamus and treadmill exercise suppressed food deprivation-induced enhancing of NOS and nNOS expressions in the PVN. The most suppressive effect of treadmill exercise on the expressions of NOS and nNOS were observed in the heavy-intensity exercise group. Based on the present study, it is possible that treadmill exercise alleviates desire for food under food-deprivation conditions via modulation of NOS expression.

Aqueous Extract of Ma huang Suppresses Neuropeptide Y Expression in Food-Deprived Rat Hypothalamus

Ma huang, the dried plant stem of ephedra intermedia Schrenk et C.A., contains an ephedrine-type alkaloid and has been used for weight loss. Neuropeptide Y (NPY), a 36-amino acid peptide, is concentrated in the hypothalamus and stimulates feeding desire. In this study, the effect of ma huang on the expressions of NPY in the hypothalamus of rats was investigated using immunohistochemistry. Food-deprivation enhanced the NPY expression in the hypothalamus. ma huang suppressed the food-deprivation-induced enhancement of NPY expression. Present results suggest that ma huang curbs the food desire by suppressing the NPY expression under food-deprivation conditions.

EGFR protein expression using a specific intracellular domain antibody and PTEN and clinical outcomes in squamous cell lung cancer patients with EGFR-tyrosine kinase inhibitor therapy.

Purpose The aim of this research was to examine the molecular and clinical features that are related with EGFR-tyrosine kinase inhibitor (EGFR-TKI) efficacy in previously treated patients with squamous cell carcinoma of the lung (SCCL). Materials and methods This retrospective study included 67 SCCL patients with obtainable lung cancer tissue and records on EGFR-TKI treatment response and survival. EGFR protein expression in lung cancer tissue was measured by immunohistochemistry with a specific antibody that recognizes the intracellular domain (ID) of EGFR. PTEN expression in lung cancer tissue was also evaluated with immunohistochemistry. PI3KCA gene amplification was detected by quantitative real-time polymerase chain reaction, and FGFR1 amplification was assessed by fluorescent in situ hybridization. Results EGFR ID expression (hazard ratio [HR] 0.53, P=0.022) and Eastern Cooperative Oncology Group (ECOG) performance status (PS) (HR 0.43, P=0.022) were significantly related with progression-free survival following EGFR-TKIs treatment. PTEN expression (HR 0.52, P=0.025) was significantly related to overall survival. The group of EGFR-positive or PTEN-positive patients with ECOG PS of 0 or 1 had better clinical outcomes than patients who were EGFR-negative and PTEN-negative or who had poor ECOG PS with longer median progression-free survival (2.1 vs 1.0 months, P=0.05) and overall survival (6.2 vs 2.1 months, P=0.05). Conclusion EGFR expression using an ID-specific antibody and PTEN protein expression may be used to identify SCCL patients who might benefit from EGFR-TKI treatment.