• Journal of Microbiology and Biotechnology
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• v.31 no.8
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• pp.1069-1078
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• 2021

Sevoflurane postconditioning (SPostC) has been proved effective in cardioprotection against myocardial ischemia/reperfusion injury. It was also reported that heat shock protein 70 (HSP70) could be induced by sevoflurane, which played a crucial role in hypoxic/reoxygenation (HR) injury of cardiomyocytes. However, the mechanism by which sevoflurane protects cardiomyocytes via HSP70 is still not understood. Here, we aimed to investigate the related mechanisms of SPostC inducing HSP70 expression to reduce the HR injury of cardiomyocytes. After the HR cardiomyocytes model was established, the cells transfected with siRNA for HSP70 (siHSP70) or not were treated with sevoflurane during reoxygenation. The lactate dehydrogenase (LDH) level was detected by colorimetry while cell viability and apoptosis were detected by MTT and flow cytometry. Reverse transcription-quantitative polymerase chain reaction (RT-qPCR) and Western blotting were used to detect HSP70, apoptosis-, cell cycle-associated factors, iNOS, and Cox-2 expressions. Enzyme-linked immuno sorbent assay (ELISA) was used to measure malondialdehyde (MDA) and superoxide dismutase (SOD). SPostC decreased apoptosis, cell injury, oxidative stress and inflammation and increased viability of HR-induced cardiomyocytes. In addition, SPostC downregulated Bax and cleaved caspase-3 levels, while SPostC upregulated Bcl-2, CDK-4, Cyclin D1, and HSP70 levels. SiHSP70 had the opposite effect that SPostC had on HR-induced cardiomyocytes. Moreover, siHSP70 further reversed the effect of SPostC on apoptosis, cell injury, oxidative stress, inflammation, viability and the expressions of HSP70, apoptosis-, and cell cycle-associated factors in HR-induced cardiomyocytes. In conclusion, this study demonstrates that SPostC can reduce the HR injury of cardiomyocytes by inducing HSP70 expression.

• Journal of Ginseng Research
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• v.47 no.1
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• pp.89-96
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• 2023

Background and aim: Panax ginseng, a key herbal medicine of replenishing Qi and tonifying Spleen, is widely used in the treatment of gastrointestinal diseases in East Asia. In this study, we aim to investigate the potential effects and mechanisms of polysaccharides from P. ginseng (PGP) on intestinal mucosal restitution which is one of the crucial repair modalities during the recovery of mucosal injury controlled by the Ca²⁺ signaling. Methods: Rat model of intestinal mucosal injury was induced by indomethacin. The fractional cell migration was carried out by immunohistochemistry staining with BrdU. The morphological observations on intestinal mucosal injury were also performed. Intestinal epithelial cell (IEC-6) migration in vitro was conducted by scratch method. Western-blot was adopted to determine the expressions of PLC-𝛾1, Rac1, TRPC1, RhoA and Cav-1. Immunoprecipitation was used to evaluate the levels of Rac1/PLC-𝛾1, RhoA/TRPC1 and Cav-1/TRPC1. Results: The results showed that PGP effectively reduced the assessment of intestinal mucosal injury, reversed the inhibition of epithelial cell migration induced by Indomethacin, and increased the level of Ca²⁺ in intestinal mucosa in vivo. Moreover, PGP dramatically promoted IEC-6 cell migration, the expression of Ca²⁺ regulators (PLC-𝛾1, Rac1, TRPC1, Cav-1 and RhoA) as well as protein complexes (Rac1/PLC-𝛾1, Cav-1/TRPC1 and RhoA/TRPC1) in vitro. Conclusion: PGP increases the Ca²⁺ content in intestinal mucosa partly through controlling the regulators of Ca²⁺ mobilization, subsequently promotes intestinal epithelial cell migration, and then prevents intestinal mucosal injury induced by indomethacin.

• Journal of Trauma and Injury
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• v.26 no.3
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• pp.63-73
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• 2013

Spinal cord injury (SCI) is a serious condition associated with social and familial burden, as well as significant neurologic deficit. Despite the many advances in the treatment of spinal cord injury, a fundamental treatment for neurologic functional recovery has not yet been developed. In this article, we review two directions of development for spinal cord injury treatment: neuroprotective pharmacological agents and axon-regenerating cell therapy. We expect developments in these two to lead to improve functional recovery in patients with spinal cord injuries and to reduce burdens on society, as well as the patients' families.

• The Korea Journal of Herbology
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• v.20 no.4
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• pp.53-60
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• 2005

Objectives : This study was carried out to determine if Dendrobii Herba have protective effect against cell injury induced by various toxic agents in rat kidney slices. Water(DWe) and methanol(DMe) extracts were prepared for this experiment. Methods : Cell injury was estimated by measuring lactate dehydrogenase(LDH). Lipid peroxidation was examined by measuring malondialdehyde, a product of lipid peroxidation. Results : DMe prevented the LDH release by $CCl_4$, menadione, tert-butyl hydroperoxide and mercury treatment in vitro in kidney slices, but DWe prevented the LDH release by $CCl_4$ and mercury. DMe also prevented reduction in GSH and lipid peroxidation induced by $CCl_4$ and mercury. Conclusion : Thus, DMe may have more powerful efficacy on anti-oxidative effects when compared with DWe. And further studies have to be followed concerned with extraction of Dendrobii Herba and its change of effects.

• Journal of the Korean Chemical Society
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• v.38 no.1
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• pp.74-79
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• 1994

The participation of superoxide in initiating tissue damage derived from xenobiotics is best illustrated by paraquat intoxication. In the present study, the roles of superoxide dismutase and catalase on paraquat-induced cell injury were investigated using primary cultured rat skin fibroblast. The degree of cell injury was assassed by the conversion of reduced MTT to a blue formazan. Paraquat produced concentration-and time-related cell injury in cultured rat skin fibroblast. Paraquat induced-cell injury was aggravated by pretreatment of aminotriazol (AT: 10 mM), an catalase inhibitor, and attenuated by addition of catalase (100∼500 unit/ml). However, the effects of diethyldithiocarbamate (DDC : 10 mM), copper- and zinc-containing superoxide dismutase (Cu, Zn-SOD) inhibitor, and Cu, Zn-SOD on paraquat-induced injury were not significant. These results suggest that hydrogen peroxide might be more responsible factor than superoxide in the pathogenesis of paraquat-induced cell injury.

• Journal of Microbiology and Biotechnology
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• v.31 no.6
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• pp.794-802
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• 2021

In this study we investigated the role and mechanism of cardamonin on IL-1β induced injury in OA. CHON-001 cells were treated with cardamonin and IL-1β and transfected with silencing nuclear factor erythroid 2-related factor 2 (siNrf2). Cell viability was detected by Cell Counting Kit-8 assay and flow cytometer assay was utilized for cell apoptosis assessment. IL-6, IL-8, TNF-α and Nrf2 mRNA expression was tested by qRT-PCR. Western blot was employed to evaluate MMP-3, MMP-13, Collagen II, Nrf2, NQO-1, NLRP3, Caspase 1 and apoptosis-associated speck-like protein containing a caspase-1 recruitment domain (ASC) protein levels. In CHON-001 cells, IL-1β suppressed cell viability and Collagen II level while promoting cell apoptosis and expression of pro-inflammatory cytokines (IL-6, IL-8, TNF-α), MMPs (MMP-3, MMP-13), NQO-1, and NLRP3 inflammasome (NLRP3, Caspase 1 and ASC), with no significant influence on Nrf2. Cardamonin reversed the effect of IL-1β on cell viability, cell apoptosis, pro-inflammatory cytokines, MMPs, Collagen II, and NLRP3 inflammasome levels. In addition, cardamonin advanced Nrf2 and NQO-1 expression of CHON-001 cells. SiNrf2 reversed the function of cardamonin on IL-1β-induced cell apoptosis and expression of pro-inflammatory cytokines, Nrf2, NQO-1, and NLRP3 inflammasome in chondrocytes. Taken together Cardamonin inhibited IL-1β induced injury by inhibition of NLRP3 inflammasome via activating Nrf2/NQO1 signaling pathway in chondrocyte.

• The Journal of Korean Medicine
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• v.23 no.3
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• pp.188-199
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• 2002

Objectives : Banhasasim-tang has been clinically used to treat upper gastric intestinal discomfort. The object of this study is to examine the defense effect of Banhasasim-tang for acute duodenal injury of the mouse. Methods and Materials : Twenty-one rats were divided into 3 groups and treated as follows: the control group was untreated mice. The ADE group was acute duodenal-damage-elicited mice. The BST group was Banhasasim-tang treated mice before acute duodenal damage elicitation. The groups were examined with common morphology, paneth cells in intestinal crypt, absorptive cells and goblet cells in epithelium, cell division in mucose, COX-l as mucosal protector, COX-2 (which appears to play an important role in inflammation), IL-2R-inducing cellular immuno-chainreaction, and the distribution of apoptotic cells. Results : 1. Common morphology: the ADE group was observed with duodenal injury - loss of villi, infiltration of cells concerned to inflammation (lymphocytes, granular leukocytes) to submucosal layer - by hemorrhagic erosions, while the BST group was seen the same as normal in proportion to increasing treatment time before injury. 2. Histochemical change: the ADE group was observed with noticeable decreased distribution of absorptive cells with microvilli, acid mucin secreted goblet cell, neutral mucin secreted goblet cell, paneth cells compared to the normal group. The BST group was seen to have distribution of epithelium cells resembling normal in proportion to increasing treatment time before injury. 3. Imnunohistochemical change: the ADE group showed a change of factors leading to duodenal injury as reduce of cytokinesis, COX-1, increase of COX-2, IL-2R-. In contrast, the BST group tended to reduction of cytokinesis, COX-1, increase of COX-2, IL-2R- in proportion to increasing taking time before injury. 4. Apoptosis change: the ADE group showed increasing apoptosis cells, in contrast to the BST group which was the same as normal in proportion to increasing treatment time before injury. Conclusions : According to the above results, by increasing the defense system of mucosal epithelium, Banhasasim-tang is thought to effectively protect tissue against ulcers resulting from acute duodenal injury.

• Journal of Haehwa Medicine
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• v.14 no.1
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• pp.201-211
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• 2005

Cdc2 kinase is a prototypical cyclin-dependent kinase critical for G2 to M phase cell cycle transition. Yet, its function in the nervous system is largely unknown. Here, we investigated possible role of Cdc2 in axonal regeneration using sciatic nerve system in rat. Cdc2 protein levels and activity were increased in the injured sciatic nerves 3 and 7 days after crush injury and then decreased to basal level 14 days later. Administration of Cdc2 kinase inhibitor roscovitine in vivo at the time of crush injury significantly inhibited axonal regeneration when regrowing axons were analyzed using retrograde tracers. Cdc2 protein levels in cultured Schwann cells which were prepared from sciatic nerves 7 days after crush injury were much higher compared with those from uninjured sciatic nerves, suggesting that Cdc2 protein expression was primarily induced in the Schwann cells. To further investigate Cdc2 function in Schwann cell, we examined changes in cultured Schwann cell proliferation and migration in culture system. Both the number of proliferating Schwann cells and the extent of neurite outgrowth from co-cultured DRG neurons were significantly decreased by Cdc2 inhibitor roscovitine treatment in DRG culture which was prepared from animals with sciatic nerve injury for 7 days. Also, Schwann cell migration in the injured sciatic nerve explant was significantly inhibited by roscovitine treatment. Taken together, the present data suggest that Cdc2 may be involved in peripheral nerve regeneration via Schwann cell proliferation and migration.

• Archives of Pharmacal Research
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• v.20 no.2
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• pp.103-109
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• 1997

The effects of ginseng total saponins (GTS) on hypoxic damage of primary cultures of astrocytes were studied. Hypoxia was created by placing cultures in an air tight chamber that was flushed with 95% $N_2/5%CO_2$ for 15 min before being sealed. Cultures showed evidence of significant cell injury after 24 h of hypoxia (increased lactate dehydrogenase (LDH) content in the culture medium, cell swelling and decreased glutamate uptake and protein content). Addition of GTS (0.1, 0.3 mg/ml) to the cultures during the exposure to hypoxic conditions produced dose-dependent inhibition of the LDH efflux. GTS (0.1, 0.3 mg/ml) also produced significant inhibition of the increased cell volume of astrocytes measured by $[^3H]$ O-methyl-D-glucose uptake under the hypoxic conditions. Decreased glutamate uptake and protein content was inhibited by GTS. These data suggest that GTS prevents astrocytic cell injury induced by severe hypoxia in vitro.

• Herbal Formula Science
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• v.8 no.1
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• pp.147-167
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• 2000

Reactive oxygen species (ROS) play an important role in the pathogenesis of a variety of life threatening conditions such as atherosclerosis, myocardial infarction and cerebral stroke. In this study, the effect of Sunghyangchungisan (SHCS) as a cytoproctant against ROS-induced cell injury was studied by investigating its effect on $H_{2}O_2-induced$ cell injury in cultured endothelial cells derived from the human umbilical vein. SHCS effectively proteced the cells against $H_{2}O_2-induced$ injury determined by trypan blue exclusion ability and lactate dehydrogenase (LDH) release. The effect of SHCS was concentration-dependent and the concentrations to inhibit by 50% the cell death and LDH release were $0.9{\pm}0.1$ and $1.2{\pm}0.1\;mg/ml$, respectively. In addition, SHCS effectively protected the cells against t-butylhydroperoside- and menadione-Induced injury as well. SHCS inhibited lipid peroxidation determined by malondialdehyde production. SHCS exerted as an effective scavenger of ROS produced by exposing the cells to $H_{2}O_2$ The activities of the intracellular ROS scavenging enzymes such as superoxide dismutase, catalase and glutathione peroxidase were not Influenced by SHCS.These results indicate that SHCS might exert as an effective cytoprotectant against ROS-induced cell injury. Further intensive studies would provide us insights into mechanisms of the pharmacological actions of SHCS.