• Korean Journal of Environmental Biology
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• v.29 no.1
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• pp.61-67
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• 2011

N-acetyl-L-cysteine (NAC) having a thiol, a precursor for glutathione (GSH), is known as one of the antioxidants. NAC used as a radioprotector against ionizing radiation (IR)-induced injury and damage. The aim of this study was to evaluate the radioprotective effects of NAC against IR-induced cell damage in Saccharomyces cerevisiae and the antioxidative effect of NAC on transcriptional level of yeast antioxidant enzyme genes such as superoxide dismutase (SOD) and catalase. In the present study, yeast cells were pretreated with various concentrations of NAC and/or irradiated with various doses of gamma rays. The cell viability was measured by counting the cell forming unit (CFU). The quantitative real-time PCR was performed for analysis of gene expression of SOD and catalase. The viability of irradiated cells was not improved by pretreatment with NAC. Ionizing radiation with 100 Gy highly induced the gene expression of antioxidant enzymes. In the irradiated group with NAC pretreatment, the gene expression of SOD and catalase was gradually reduced with the increased concentrations of NAC. These results indicate that NAC can act as a useful antioxidant to scavenge reactive oxygen species in vivo, but does not protect cells against IR-induced cell death in S. cerevisiae.

• Herbal Formula Science
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• v.29 no.2
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• pp.71-80
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• 2021

Objectives : This study investigated cellular-protective effects of Nardotidis seu Sulculii Concha water extract (NSCE) against oxidative stress induced by arachidonic acid (AA)+iron or tert-butylhydroperoxide (tBHP). Methods : In vitro, MTT assay was assessed for cell viability, and immunoblotting analysis was performed to detect expression of AMP-activated kinase (AMPK) signaling pathway and autophagy related proteins. In vivo, mice were orally administrated with the aqueous extract of NSCE of 500 mg/kg for 3 days, and then injected with CCl₄ 0.5 mg/kg body weight to induce acute damage. The level of liver damage was measured by serum aspartate aminotransferase (AST), alanine aminotransferase (ALT) and lactate dehydrogenase (LDH) analysis. Results : Treatment with NSCE inhibited cell death induced by AA+iron and tBHP. NSCE induced the phosphorylation of AMPK, and this compound also induced the phosphorylation of LKB1, an upstream kinase of AMPK, and Acetyl-CoA carboxylase (ACC), a primary downstream target of AMPK. NSCE increased the protein levels of autophagic markers (LC3II and beclin-1) and decreased the phosphorylation of mammalian target of rapamycin (mTOR) and simultaneously increased the phosphorylation of unc-51-like kinase-1 (ULK-1) in time-dependent manner. Conclusions : NSCE has the ability 1) to protect cells against oxidative stress induced by AA+iron or tBHP. NSCE 2) to activate AMP-activated protein kinase (AMPK), and 3) to regulate autophagy, an important regulator in cell survival.

• Applied Microscopy
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• v.39 no.3
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• pp.261-266
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• 2009

This study aim to disclose a possible mechanism for the neuronal cell death induced by peripheral nerve injury following a spinal nerve ligation (SNL) as a neuropathic pain model. Male Sprague-Dawley rats (270~290 g) were used for this study. Pain threshold was evaluated for their response to mechanical (von Frey hairs) stimuli 1, 3, and 7 days after a tight ligation of L5 ventral ramus. In control group, the small ganglion cells were strongly stained with routine toluidine blue (TB), whereas the large ganglion cells showed a little bit weak stainity. Each large ganglion cell is surrounded by perineuronal satellite cells. In experimental groups, small ganglion cells showing apparent degenerative changes increased on 1 day, and showed a peak in degenerative cell number at 3 days group, and decreased gradually at 7 days group. We also found a small number of large-sized ganglion cells showing mild degenerative changes. However their satellite cells ware relatively intact with no typical findings throughout this experiment. Under the electron microscope, small ganglion cells showed various stage and typical features of the dark degeneration including mitochondrial swelling.

• The Korean Journal of Physiology and Pharmacology
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• v.1 no.4
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• pp.345-353
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• 1997

The effects of crude saponin (SAP) and alkaloid (ALK) fractions of Panax ginseng C.A. Meyer on the detrimental effects of electroconvulsive shock (ECS) and scopolamine on passive avoidance response (PAR) were studied in male Sprague-Dawley rats, referring their effects on the neuronal injury and plasticity of hippocampus in response to electrolytic lesion of left entorhinal cortex (ECL). The detrimental ECS effect on PAR was attenuated by pre- and post-treatments with SAP and ALK, respectively, or by pretreatment with aminoguanidine (AG), an inhibitor of diamine oxidase and NO synthase. And the detrimental scopolamine effect on PAR was also inhibited by pre-treatment with ALK or AG, and by post- treatment with SAP or ALK, respectively. On the 7th day after ECL, the brain sections stained by cresyl violet and by acetylcholinesterase (AChE) histochemistry, respectively, showed the chromatolysis and numeral decrease of neurons and the reduction of AChE reactivity in the hippocampus CA1 area and to a lesser extent, in the dentate gyrus. The neuronal cell death of the CA1 area was significantly reduced by SAP, ALK, or AG, and the reduction of AChE reactivity was significantly attenuated by SAP or ALK and to a lesser extent by AG. These results suggests that the protective effect of ginseng SAP and ALK fractions on ECS- or scopolamine-induced impairment of PAR may be ascribed in part to preservation of hippocampal neurons, particularly cholinergic neurons.

• Journal of Haehwa Medicine
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• v.26 no.1
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• pp.1-10
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• 2017

Objectives: The aim of this study is (1) to investigate the historic changes and pharmacological efficacies of Woohwangchungsim-won and (2) to discuss the necessities for Woohwangchungsim-won's clinical applications. Methods: This study was performed through (1) investigating the ancient literature records related with Woohwangchungsim-won and analyzing Woohwangchungsim-won's composition, dosage and indications, (2) searching articles about Woohwangchungsim-won on 10 major Korean web and 3 major foreign web article search engines and analyzing Woohwangchungsim-won's pharmacological efficacies and indications. Results: Woohwangchungsim-wom has been used for cerebrovascular diseases such as stroke and palpitation. Also, there are some ancient literature records of Woohwangchungsim-won's clinical applications in neuropsychiatric disorders such as depression and bipolar disorder. In addition, there have been a number of experimental studies which demonstrate Woohwangchungsim-won's neuroprotective effect on cerebral cortex and hippocampus injury. So, it is possible to infer that Woohwangchungsim-won can be used for the treatments of neuropsychiatric disorders associated with neuronal cell death in cerebral cortex and hippocampus. But there have been no or less experimental studies which demonstrate the pharmacological efficacy of Woohwangchungsim-won on such disease. Conclusion: It is necessary that further experimental studies which demonstrate Woohwangchungsim-won's pharmacological efficacy on neuropsychiatric disorders should be done and Woohwangchungsim-won's clinical applications should be expanded on the basis of those related experimental results.

• Korean Journal of Acupuncture
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• v.21 no.1
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• pp.15-27
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• 2004

Objectives : Acupuncture has been used to prevent and treat the cerebrovascular accident, such as a stroke, and many studies of acupuncture and moxibustion concerning to the stroke have been undertaken in the human and various animals. Also, herbal acupuncture, namely aqua acupuncture has been applied and developed to various diseases including the cerebrovascular accident. FOLIUM ARTEMISIAE ARGYI is the dry leaf of Artemisia argyi Levl. et Vant. collected in summer before the plant blooms and used to moxibustion and has been recommended for use as an analgesic and hemostatic. In this study, effects of FOLIUM ARTEMISIAE ARGYI (艾葉)' herbal acupuncture on the $LR_3$, namely Taechung on neuroprotection after the transient forebrain ischemia were investigated in Sprague-Dawely rats. Methods : Expressions of neuronal nitric oxide synthase (nNOS) protein in the hippocampus and cortex were observed at 2 hrs after transient forebrain ischemia by immunohistochemistry. Results : Expression of nNOS protein was increased in the hippocampus and cortex at 2 hrs after transient forebrain ischemia. However, pretreatment with FOLIUM ARTEMISIAE ARGYI' herbal acupuncture on $LR_3$ significantly decreased expression of nNOS protein protein compared to ischemia group. These features were observed in the motor cortex and the hippocampus. Conclusions : These results suggest that pretreatment with FOLIUM ARTEMISIAE ARGYI' herbal acupuncture on $LR_3$ inhibits the expression of nNOS protein induced by transient forebrain ischemia and may modulate excitatory toxicity of neuron related to neuronal cell death.

• Archives of Plastic Surgery
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• v.34 no.6
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• pp.765-770
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• 2007

Purpose: Peritendinous adhesion is one of the most notorious complication after the flexor tendon injury. In this study, $Alloderm^{(R)}$(LifeCell Corp., Branchburg, N.J.), which is the decellularized human dermal analogue with its intact native basement membrane components, was used for the prevention of peritendinous adhesions following flexor tendon repair. Methods: Thirty New Zealand white male rabbits were divided equally into 3 groups. In all groups, the flexor digitorum profundus of the third finger of the right back foot was cut totally and repaired by modified Kessler suture technique. Following tendon repair, $Alloderm^{(R)}$ was wrapt around the repaired tendon in the first group and sodium hyaluronate gel was sprayed to the operation field in the second group. In the control group, no external material was applied. The right back foot were immobilized for 6 weeks to optimize the formation of adhesion ingrowth. After death, the third finger that repaired tendons and sheaths was removed en bloc. We checked range of motion. and studied histologically for all groups. Results: The experimental groups had better range of motion than the control group. We checked that the range of motion was 73.5 degrees in $Alloderm^{(R)}$ group, 55.9 degrees in the hyaluronic acid group, and 38.3 degrees in the control group. in the histological study, the experimental group had less adhesions compared with the control group. Conclusion: This study concludes that $Alloderm^{(R)}$ can decrease peritendinous adhesions following flexor tendon repairs in rabbits. We think the method could be used in clinical cases.

• Animal cells and systems
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• v.7 no.4
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• pp.309-315
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• 2003

Renal dipeptidase (RDPase, membrane dipeptidase, dehydropeptidase 1, EC 3.4.13.19) has been widely studied since it was first purified from porcine kidney brush border membrane. It was reported that RDPase activity in urine samples of acute and chronic renal failure patients decreases. Nitric oxide (NO) is a highly reactive free radical involved in a number of physiological and pathological processes. NO is able to act in a dual mode, leading either to induction of apoptosis or to blunted execution of programmed cell death. NO inhibited the RDPase release from porcine renal proximal tubules, which could be blocked by L-NAME. Chitosan, the linear polymer of D-glucosamine in $\beta$(1\longrightarrow4) linkage, not only reversed the decreased RDPase release by NO but also increased NO production in the proximal tubule cells. The stimulatory effect of NO on RDPase release from proximal tubules in the presence of chitosan must be different from the previously proposed mechanism of RDPase release via NO signaling pathway. Chitosan stimulated the RDPase release in the proximal tubules and increased RDPase activity to 220% and 250% at 0.1% and 1%, respectively. RDPase release was decreased to about 40% in the injured proximal tubules and was recovered in proportion to the increase of chitosan. Chitosan may be useful in recovery of renal function from $HgCl_2$injury.

• Korean Journal of Pharmacognosy
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• v.42 no.2
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• pp.175-181
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• 2011

Oxidative stress or accumulation of reactive oxygen species (ROS) leads neuronal cellular death and dysfunction, and it contributes to neuronal degenerative disease such as Alzheimer's disease, Parkinson's disease and stroke. Glutamate is one of the major excitatory neurotransmitter in the central nervous system (CNS). Glutamate contributes to fast synaptic transmission, neuronal plasticity, outgrowth and survival, behavior, learning and memory. In spite of these physiological functions, high concentration of glutamate causes neuronal cell damage, acute insults and chronic neuronal neurodegenerative diseases. Heme oxygenase-1 (HO-1) enzyme plays an important role of cellular antioxidant system against oxidant injury. NNMBS020, the water-insoluble fraction of the 70% EtOH extract of root barks of Dictamnus dasycarpus, showed dominant neuroprotective effects on glutamate-induced neurotoxicity in mouse hippocampal HT22 cells by induced the expression of HO-1 and increased HO activity. In mouse hippocampal HT22 cells, NNMBS020 makes the nuclear accumulation of Nrf2 and stimulates extracellular signal-regulated kinase (ERK) pathway. The ERK MAPK pathway inhibitor significantly reduced NNMBS020-induced HO-1 expression, whereas the JNK and p38 inhibitors did not. In conclusion, the water-insoluble fraction of the 70% EtOH extract of root barks of D. dasycarpus (NNMBS020) significantly protect glutamate-induced oxidative damage by induction of HO-1 via Nrf2 and ERK pathway in mouse hippocampal HT22 cells.

• The Korean Journal of Physiology and Pharmacology
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• v.23 no.6
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• pp.483-491
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• 2019

Cordycepin exerts neuroprotective effects against excitotoxic neuronal death. However, its direct electrophysiological evidence in Alzheimer's disease (AD) remains unclear. This study aimed to explore the electrophysiological mechanisms underlying the protective effect of cordycepin against the excitotoxic neuronal insult in AD using whole-cell patch clamp techniques. ${\beta}$-Amyloid ($A{\beta}$) and ibotenic acid (IBO)-induced injury model in cultured hippocampal neurons was used for the purpose. The results revealed that cordycepin significantly delayed $A{\beta}$ + IBO-induced excessive neuronal membrane depolarization. It increased the onset time/latency, extended the duration, and reduced the slope in both slow and rapid depolarization. Additionally, cordycepin reversed the neuronal hyperactivity in $A{\beta}$ + IBO-induced evoked action potential (AP) firing, including increase in repetitive firing frequency, shortening of evoked AP latency, decrease in the amplitude of fast afterhyperpolarization, and increase in membrane depolarization. Further, the suppressive effect of cordycepin against $A{\beta}$ + IBO-induced excessive neuronal membrane depolarization and neuronal hyperactivity was blocked by DPCPX (8-cyclopentyl-1,3-dipropylxanthine, an adenosine $A_1$ receptor-specific blocker). Collectively, these results revealed the suppressive effect of cordycepin against the $A{\beta}$ + IBO-induced excitotoxic neuronal insult by attenuating excessive neuronal activity and membrane depolarization, and the mechanism through the activation of $A_1R$ is strongly recommended, thus highlighting the therapeutic potential of cordycepin in AD.