• Korean Journal of Plant Resources
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• v.30 no.2
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• pp.125-132
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• 2017

Bisphenol A (BPA), a known endocrine disruptor, induces toxicity in cells and in experimental animals. Ginseng extracts were evaluated to determine whether they can inhibit BPA-induced toxicity. The antioxidant activity of fresh ginseng extract (WGE), dried white ginseng extract (DGE), and dried red ginseng extract (RGE) was measured using the DPPH assay. WGE and RGE increased DPPH free radical scavenging activity. Cell viability was measured in HepG2 cells following treatment with BPA and ginseng extracts using the MTT assay. DGE and RGE increased HepG2 cell viability following treatment with $200{\mu}M$ BPA. RGE reduced levels of biochemical markers of liver damage, aspartate aminotransferase (AST) and alanine aminotransferase (ALT) that increased in mice following treatment with BPA. In addition, the regeneration and proliferation of damaged liver cells were significantly increased in RGE-treated mice. Moreover, RGE inhibited hepatic fibrosis in the surrounding area and in the central vein of the liver microstructure. RGE also significantly inhibited BPA-induced cytotoxicity. In addition, RGE protected liver damage and regenerated liver tissues in BPA-treated animals. These results show that RGE may represent a potential candidate drug for the treatment and prevention of liver damage caused by environmental toxins.

• The Journal of the Korean bone and joint tumor society
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• v.7 no.1
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• pp.1-12
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• 2001

Purpose : To elucidate possibility of local chemotherapy from adraimycin-impregnated bone cement. Materials and Methods : Authors used 4 kinds of bone cements, Palcos R, LVC, CMW 3, Simplex P for this experimental model, included 2.5mg, 5mg, 25mg of adriamycin, respectively. We compared the differences of eluted-adriamycin concentrations between the cylindrical shape and the flat shape of bone cements, between ddH2O, 0.45% saline, 0.9% saline, and 3% saline as one of environmental conditions. Osteosarcoma cell line, Saos-2 were cultured under $37^{\circ}C$, 5% $CO_2$ in the humidified incubator with three different concentrations of adriamycinimpregnated bone cements and cellular toxicity of adriamycin eluted from bone cement was analysed according to MTT assay. Results : Authors noticed the flat shape of bone cement eluted more concentrations of adriamycin than the cyclindrical shape, bone cement immersed in 3% saline, more than 0.9% or 0.45% saline. Concentrations of adriamycin eluted from CMW 3 or Simplex R were more than Palacos R or LVC. Saos-2 were cultured with 2.5mg, 5mg, 25mg of adriamycin-impregnated bone cement, respectively, and their cellular toxicity were 95%, 98%, 99%, each. Conclusion : Adriamycin-impregnated bone cement can be one of anticancer-drug delivery sytems as possible local chemotherapy.

• Korean Journal of Clinical Laboratory Science
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• v.52 no.4
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• pp.408-416
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• 2020

This study examined the neuronal cytotoxicity of aluminum chloride (AlCl3), a dementia inducer, and the protective effects of Aster yomena (Kitam.)(AY) extract on AlCl3-induced cytotoxicity in cultured C6 glioma cells. The antioxidative effects, such as the inhibitory ability of xanthine oxidase (XO) and superoxide anion-radical (SAR) scavenging ability, on cell viability were examined. AlCl3 decreased the cell viability significantly in a dose-dependent manner, and the XTT50 value was 130.0 μM in these cultures. The cytotoxicity of AlCl3 was determined to be mid-toxic according to the Borenfreund and Puerner' toxic criteria. Quercetin (QU), an antioxidant, increased the cell viability reduced by AlCl3-induced cytotoxicity. The protective effect of the AY extract on AlCl3-induced cytotoxicity was analyzed. The AY extract increased the cell viability remarkably compared to the AlCl3-treated group and showed the inhibitory ability of XO and SAR-scavenging ability. The cytotoxicity of AlCl3 was correlated with oxidative stress, and the AY extract effectively prevented AlCl3-induced cytotoxicity through its antioxidative effects. In conclusion, natural resources, such as the AY extract, may be a putative agent for improving the cytotoxicity of heavy metallic compounds correlated with oxidative stress, such as AlCl3, a morbid agent.

• The Journal of Korean Obstetrics and Gynecology
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• v.18 no.3
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• pp.67-76
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• 2005

Purpose : 귀전우(Euonymus alatus, EA)는 현재까지 항종양활성을 나타낸다고 보고되었지만 그 작용 메커니즘에 대해서는 아직 밝혀지지 않은 채 남아 있다. 본 연구에서는, 자궁근종세포(ULSMC)에서 EA의 분자적 수준에서의 작용메커니즘을 연구${\cdot}$검토하고자 하였다. Methods : EA의 열수추출액이 자궁근종세포(ULSMC)와 caspase-3 pretense의 활성도에 미치는 영향을 측정하였다. Results : 우리는 자궁근종에서 EA 유도 세포독성의 메커니즘을 검토하였는바, 근종 세포들은 20-200g/ml 농도의 EA추출물에 6시간 배양될 때, caspase-3가 활성화되고, 그때 세포들은 apoptosis를 유발하게 되었다. EA에 의한 apoptosis의 유도가 진행되었으며, cytochrome- c의 세포질분획에서 양적증가가 caspase-3의 활성보다도 우세하였다. GSH합성의 저해제인 5mM buthionine용액에 전처리는 EA유도 apoptosis를 용이하게 하지만 pan-caspase inhibitor인 Z-VAD-fmk용액 전 처리는 부분적으로 apoptosis유도를 억제하였다. 한편, EA는 건강한 지원자들로 부터 채취한 말초혈액 단핵세포들에 있어서는 독성의 효과는 없었다. Conclusion : 이들 결과들은 EA가 prooxidant로 작용을 하고 그리고 caspase-3 activation과 mitochondrial pathway를 경유하는 apoptosis를 유발한다는 것을 나타낸다. EA의 탕제약제로서 열수추출액이 항산화활성뿐만 아니라, 종양세포에 대한 세포독성효과를 나타낸다고 보고된 바, 이에 향후 근종치료에 대한 임상연구가 필요할 것으로 보인다.

• Journal of Life Science
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• v.30 no.8
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• pp.661-671
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• 2020

The resistance of cancer cells to anti-cancer drugs is the leading cause of chemotherapy failure. The clinical use of nonsteroidal anti-inflammatory drugs (NSAIDs) has been gradually extended to cancer treatment through combination with anti-cancer drugs. In the current study, we investigated whether NSAIDs including celecoxib (CCB), 2,5-dimethyl celecoxib (DMC), and ibuprofen (IBU) could enhance the cytotoxic effects of imatinib and TNF-related apoptosis inducing ligand (TRAIL) on human cancer cells. We found that the NSAIDs potentiated TRAIL and imatinib cytotoxicity against human hepatocellular carcinoma (HCC) cell lines SNU-354, SNU-423, SNU-449, and SNU-475/TR and against leukemic K562 cells with high level of CD44 (CD44^highK562), respectively. More specifically, CCB induced endoplasmic reticulum stress via up-regulation of ATF4/CHOP which is associated with the induction of autophagy against HCC and CD44^high K562 cells. NSAID-induced autophagic activity accelerated TRAIL cytotoxicity of HCC cells through up- and down-regulation of DR5 and c-FLIP, respectively. The NSAIDs also potentiated imatinib-induced cytotoxicity and apoptosis through down-regulation of markers in CD44^highK562 cells that express a stemness phenotype. Our results suggest that the ability of NSAIDs to induce autophagy could enhance the cytotoxicity of TRAIL and imatinib, leading to a reverse resistance to these drugs in the cancer cells. In conclusion, NSAIDs in combination with low-dose TRAIL or imatinib may constitute a novel clinical strategy that maximizes therapeutic efficacy of each drug and effectively reduces the toxic side effects.

• Journal of Chest Surgery
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• v.41 no.6
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• pp.791-794
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• 2008

Pneumomediastinum is a rare, but well recognized complication of bleomycin-induced lung toxicity. Spontaneous pneumomediastinum has to be considered as one of the causes when the dyspnea becomes aggravated in patients with bleomycin induced lung toxicity. We describe here two patients who suffered with germ cell tumor and they developed spontaneous pneumomediastinum without pneumothorax, and this was caused by bleomycin-induced lung toxicity.

• Biomedical Science Letters
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• v.2 no.2
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• pp.153-158
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• 1996

Verapamil, a potent calcium channel blocker, has been proved to be one of the modulators to overcome drug resistance in cancer chemotherapy. In the present experiment, the possibility of verapamil as a MDR modulator was investigated by using MTT assay. Sole treatment of verapamil on the HeLa and Caski cervical cancer cell line revealed dose dependent cytotoxicity within a range of tested dose. Combined treatment of verapamil with 5-FU, DDP on two human cervical cancer cell line led to a significant synergistic cytotoxicity. Therefore , these studies showed that verapamil had a possibility to be applicable to cancer chemotherapy in gynecological oncology.

• Korean Journal of Clinical Laboratory Science
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• v.50 no.4
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• pp.501-510
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• 2018

This study examined the neurotoxicity induced by lead acetate (LA) on cultured C6 glioma cells and the protective effects of Euphorbiae humifusae L. (EH) extract against LA-induced cytotoxicity. In this study, LA exhibited neurotoxicity in a dose-dependent manner compared to the control, and was determined to be highly-toxic according to the toxic criteria. The $XTT_{50}$ value of LA was calculated at a concentration of $38.6{\mu}M$ after C6 glioma cells were incubated for 72 hours in the media containing $30{\sim}50{\mu}M$ of LA, respectively. In addition, LA-induced neurotoxicity was suggested to correlate with the level of oxidative stress because vitamin E, an antioxidant, increased the cell viability damaged by LA-induced cytotoxicity. The EH extract effectively prevented cell injury from LA-induced cytotoxicity via its antioxidative effects, such as inhibitory ability of lipid peroxidation, superoxide dismutase-like activity and 1,1-diphenyl-2-picrylhydrazyl-radical scavenging activity. These antioxidative effects may result in components, such as polyphenol or flavonoids including gallic acid or quercetin. In conclusion, natural resources, such as EH extracts, may be a useful putative agent for the treatment of diseases associated with oxidative stress, such as lead neurotoxicity.

• Journal of Life Science
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• v.34 no.5
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• pp.287-295
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• 2024

Hepatocellular carcinoma (HCC) is the second leading cause of cancer-related mortality worldwide, necessitating novel therapeutic strategies. The chemotherapeutic agents used to treat HCC patients are toxic and have serious side effects. Therefore, we investigated the efficacy of anticancer drugs that reduce side effects by targeting tumor cells without causing cytotoxicity in healthy hepatocytes. Berberine, an isoquinoline alkaloid derived from plant compounds, has emerged as a potential candidate for cancer treatment due to its diverse pharmacological properties. The effect of berberine on HepG2 cell viability was determined using the 3-[4,5-dimethylthiazol-2-yl]-2,5-diphenyl tetrazolium bromide assay. HepG2 cell proliferation was determined through a colony-forming assay. The effects of berberine on HepG2 cell migration were evaluated using a wound-healing assay. Berberine inhibited the proliferation of HepG2 cells, as well as colony formation and migration. Berberine treatment increased the expression of autophagy-related genes and proteins, including Beclin-1 and LC3-II, and elevated the activities and mRNA expression of Caspase-9 and Caspase-3. Additionally, in experiments utilizing the Cell-Derived Xenograft animal model, berberine treatment reduced tumor size and weight in a concentration-dependent manner. These results demonstrate the potential of berberine as a versatile anticancer agent with efficacy in both cellular and animal models of hepatocellular carcinoma. The findings herein shed light on berberine's efficacy against HCC, presenting opportunities for targeted and personalized therapeutic interventions.

• Korean Journal of Clinical Laboratory Science
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• v.54 no.4
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• pp.298-306
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• 2022

This study sought to evaluate the mechanism of cellular injury caused by ferrous sulfate (FeSO₄) and the protective effects of Parnassia palustris L. (PP) extract against FeSO₄-induced cytotoxicity of cultured C6 glioma cells. FeSO₄ is known to cause neurotoxicity and induce Parkinson's disease. The antioxidative effects of PP, such as superoxide dismutase (SOD)-like and superoxide anion-radical (SAR)-scavenging activities, as well as effects on cell viability, were studied. FeSO₄ significantly decreased cell viability in a dose-dependent manner and the XTT₅₀ value, the concentration of FeSO₄ which reduced the cell viability by half, was measured at 63.3 μM in these cultures. FeSO₄ was estimated to be highly cytotoxic by the Borenfreund and Puerner toxicity criteria. Quercetin, an antioxidant, significantly improved cell viability, damaged by FeSO₄-induced cytotoxicity. While evaluating the protective effects of the PP extract on FeSO₄-induced cytotoxicity, it was observed that the extract significantly increased cell viability compared to the FeSO₄-treated group. Also, the PP extract showed superoxide dismutase (SOD)-like and superoxide anion radical (SAR)-scavenging activities. Based on these findings, it can be concluded that FeSO₄ induced oxidative stress-related cytotoxicity, and the PP extract effectively protected against this cytotoxicity via its antioxidative effects. In conclusion, natural antioxidant sources such as PP may be agents useful for preventing oxidative stress-related cytotoxicity induced by heavy metal compounds such as the FeSO₄, a known Parkinsonism inducer.