• Korean Journal of Food Science and Technology
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• v.43 no.1
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• pp.65-71
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• 2011

Eupatorium japonicum belongs to a family of Asteraceae plants and flowers of E. japonicum have been consumed as a tea. In this study, we investigated whether E. japonicum extract inhibits lipopolysaccharide (LPS)-induced inflammatory responses in Raw264.7 macrophages. The cells were treated with various concentrations (0, 1, 2.5, 5, or 10 mg/L) of 70% ethanol extract from E. japonicum flowers (EJE) in Raw264.7 cells. LPS-induced nitric oxide (NO) and prostaglandin $E_2$ ($PGE_2$) production were inhibited by EJE up to 67% and 49% of these productions, respectively without any reduction of viable cell numbers. EJE reduced LPS-induced expression of inducible NO synthase (iNOS) and cyclooxygenase (COX)-2 proteins and their corresponding mRNA levels. Additionally, EJE decreased the levels of interleukin (IL)-6, IL-1${\beta}$, and tumor necrosis factor (TNF)-${\alpha}$ mRNA. EJE was further fractionated with water, butanol, ethylacetate (EA), hexane, or methylene chloride (MC). Among the resulting five fractions, EA and MC, respectively from EJE significantly inhibited LPS-induced NO production (each inhibition rate was 85.3% of 10 mg/L EA fraction and 97.2% of 10 mg/L MC fraction) without significant cytotoxicity in Raw264.7 cells. These results indicate that EJE exhibits powerful effects of anti-inflammation and can be developed as a potential anti-inflammatory agent.

• Journal of the Korean Society of Food Science and Nutrition
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• v.46 no.11
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• pp.1271-1277
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• 2017

As Kamisipjeondaebotang (KSD) extract is an herbal ingredient, safety is very important due to possible cell poisoning or heavy metal toxicity to organs when administered to humans or animals. Accordingly, this study examined the antioxidant and anti-inflammatory effects of KSD extract to confirm its medicinal safety by using RAW 264.7 cells after heavy metal screening, functional index test of the liver and kidney, and cell survival rate test. Heavy metals were not found in KSD extracts or were less than standard amounts. Liver function indices such as aspartate aminotransferase and alanine aminotransferase revealed low values and kidney function indices such as creatinine and blood urea nitrogen were not significantly different from the normal group. This proved the safety to the human. RAW 264.7 cells showed no poisoning compared to the control group in terms of survival rate. Regarding the antioxidant effect of KSD extract, 2,2-diphenyl-1-picrylhydrazyl radical scavenging activity and 2,2'-azino-bis(3-ethylbenzothiazo-line-6-sulphonic acid) radical scavenging activity increased at concentrations over $10{\mu}g/mL$. The anti-inflammatory effect of KSD extract significantly decreased based on the amount of nitric oxide at concentrations of 10 and $100{\mu}g/mL$ compared to the control group. Expression of interleukin (IL)-$1{\beta}$ and IL-6 decreased in a concentration-dependent manner. There was no significant difference in tumor necrosis factor-${\alpha}$ level. Based on the results, KSD can be regarded as a safe antioxidant with anti-inflammatory effects for fracture treatment.

• Journal of Life Science
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• v.20 no.7
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• pp.1027-1033
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• 2010

Liriope platyphylla has traditionally been used in Korea and China as a therapeutic drug for the treatment of coughing, sputum, neurodegenerative disorders, obesity, and diabetes. In an effort to assess the functions of a novel extract from Liriope platyphylla in diabetes therapy, the insulin secretion abilities of 10 extracts were screened via measurements of insulin concentration in the culture supernatant using an Insulin ELISA kit. The results of this assay showed the highest levels of insulin in the LP9M80-H treated group, followed by the LP-H, LP-M, LP-E and LP9M80-C treated groups, whereas other extracts did not induce insulin secretion in the HIT-T15 cells. However, the extracts capable of stimulating insulin secretion simultaneously evidenced high apoptotic activity as compared with other extracts. Therefore, one of these extracts, LP9M80-H, was initially selected as the optimal candidate for a therapeutic drug and its optimal concentration was determined. The results of the ELISA and MTT assay demonstrated that a concentration of approximately 100-125 ug/ml of LP9M80-H was optimal with regards to cell viability and insulin secretion in the HIT-T15 cells. These results suggest that LP9M80-H could be considered as an excellent candidate for a diabetes-therapeutic drug that could induce insulin secretion in pancreatic $\beta$-cells.

• Radiation Oncology Journal
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• v.28 no.2
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• pp.106-110
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• 2010

Reactivation of the hepatitis B virus (HBV) is a well-recognized complication in patients with chronic HBV infection who receive cytotoxic or other immunosuppressive therapy. In cases of patients treated by radiotherapy however, only a few of such reports exist and most of these include the patients previously treated by chemotherapy or transarterial chemoembolization. The results of this study point to a case of a patient with reactivation of HBV after radiotherapy alone. This study shows the possibility of HBV reactivation by partial hepatic irradiation alone hence, special attention should be paid to patients with HBV disease.

• Tuberculosis and Respiratory Diseases
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• v.62 no.1
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• pp.33-42
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• 2007

Background: Heme oxygenase-1 (HO-1) is known to modulates the cellular functions, including cell proliferation and apoptosis. It is known that a high level of HO-1 expression is found in many tumors, and HO-1 plays an important role in rapid tumor growth on account of its antioxidant and antiapoptotic effects. Cisplatin is a widely used anti-cancer agent for the treatment of lung cancer. However, the development of resistance to cisplatin is a major obstacle to its use in clinical treatment. We previously demonstrated that inhibiting HO-1 expression through the transcriptional activation of Nrf2 induces apoptosis in A549 cells. The aim of this study was to determine of the inhibiting HO-1 enhance the chemosensitivity of A549 cells to cisplatin. Materials and Methods: The human lung cancer cell line, A549, was treated cisplatin, and the cell viability was measured by a MTT assay. The change in HO-1, Nrf2, and MAPK expression after the cisplatin treatment was examined by Western blotting. HO-1 inhibition was suppressed by ZnPP, which is a specific pharmacologic inhibitor of HO activity, and small interfering RNA (siRNA). Flow cytometry analysis and Western blot were performed in to determine the level of apoptosis. The level of hydrogen peroxide ($H_2O_2$) generation was monitored fluoimetrically using 2',7'-dichlorofluorescein diacetate. Results: The A549 cells showed more resistance to the cisplatin treatment than the other cell lines examined, whereas cisplatin increased the expression of HO-1 and Nrf2, as well as the phosphorylation of MAPK in a time-dependent fashion. Inhibitors of the MAPK pathway blocked the induction of HO-1 and Nrf2 by the cisplatin treatment in A549 cells. In addition, the cisplatin-treated A549 cells transfected with dither the HO-1 small interfering RNA (siRNA) or ZnPP, specific HO-1 inhibitor, showed in a more significantly decrease in viability than the cisplatin-only-treated group. The combination treatment of ZnPP and cisplatin caused in a marked increase in the ROS generation and a decrease in the HO-1 expression. Conclusion: Cisplatin increases the expression of HO-1, probably through the MAPK-Nrf2 pathway, and the inhibition of HO-1 enhances the chemosensitivity of A549 cells to cisplatin.

• Journal of Life Science
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• v.26 no.4
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• pp.398-405
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• 2016

Statins, the inhibitors of 3-hydroxy 3-methylglutaryl coenzyme A (HMG-CoA) reductase, are widely used in treatments of hypercholesterolemia and newly known as anti-cancer effect of various cancer cells. Recently, several studies suggested that reactive oxygen species (ROS) play a critical role on cell death signaling. However, mechanism of ROS by rosuvastatin is currently unclear. This study aimed to explore the molecular mechanism of apoptosis by rosuvastatin in human prostate cancer PC-3 cells. Cell viability and apoptosis-related protein expression were measured by MTT assay and western blotting, respectively. In addition, the levels of apoptosis and ROS were analyzed. The results showed that rosuvastatin dramatically reduced cell viability in a dose- and time-dependent manner. We confirmed that rosuvastatin induced apoptosis through reduction of procaspase-3 and cleavage of poly (ADP-ribose) polymerase (PARP) in PC-3 cells. In addition, rosuvastatin stimulated ROS production in a dose-dependent manner and pre-treatment with N-acetylcysteine (NAC), a ROS scavenger, significantly recovered rosuvastatin-induced ROS and apoptosis. Thus, we concluded that rosuvastain induces apoptosis through generation of ROS in human prostate cancer PC-3 cells and provides a promising approach to improve the efficacy of cancer therapy.

• Journal of Life Science
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• v.26 no.9
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• pp.1088-1096
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• 2016

Despite that moderate hyperthermia can exert various antitumor activities such as direct cytotoxic effects on tumor cells, effects on tumor vasculatures and immunological effects, hyperthermia has been usually combined with radiotherapy or chemotherapy due to its limited efficacy in cancer treatment, showing some positive clinical benefits with generally well-tolerated side effects. Since heat shock responses itself can interfere with the anti-tumor effects of hyperthermia, not all of these studies might have demonstrated positive clinical outcomes in cancer patients. Therefore, the negative anti-tumor effect of hyperthermia should be reduced to enhance the effectiveness of hyperthermia. Although the responses to heat stress of tumor tissues containing vessels, immune cells, connective tissues as well as cancer cells, are very complicated, it is needed to study in the near future if some clinically available drugs, which can modulate heat stress responses, can improve the efficacy of hyperthermia in patients with cancer. In this review, the effect of clinical hyperthermia centered on non-invasive external hyperthermia using radiofrequency at moderate temperature will be discussed, since it is the state-of-the-art technology in the current clinical practice of hyperthermia, and a moderate operational temperature is used to increase the therapeutic effectiveness of conventional therapy without additional toxicity to normal tissues.

• Korean journal of food and cookery science
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• v.15 no.3
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• pp.231-237
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• 1999

The anticancer effect of the bark of Broussonetia kazinoki root extracts (hexane. chloroform, ethylacetate, butanol, aqueous) were studied. The cytotoxicity by MTT assay and inhibitory effect on the growth of sarcoma 180 cells were tested in vitro. The reduction rate of the tumor formation and spleen/body weight rate on BALB/c mouse were tested in vivo. From the tests, each fraction showed the cytotoxic effect against the sarcoma 180 cells. In addition, as the concentration of the fractions increased, cytotoxic effect tendency increased as well. The cytotoxic rate of the hexane, chloroform, ethylacetate, butanol and aqueous fractions showed by 58.7%, 40.1%, 75.7%, 52.6% and 62.7% respectively after testing by MTT assay system. And sarcoma 180 cells were incubated for 6 days at 37$^{\circ}C$ with various concentrations of each fraction. As the incubation days go on, the number of cells increased, while the inhibition rate on the growth of sarcoma 180 cells were decreased. Especially the ethylacetate fraction at the concentration of 1.0 mg/ml strongly inhibited the growth of sarcoma 180 cells by 74% compared with the control for a day 37$^{\circ}C$ The hexane, chloroform, ethylacetate, butanol and aqueous fractions inhibited on the growth of sarcoma 180 cells by 31%, 19%, 60%, 30% and 42% respectively, when sarcoma 180 cells has been incubated for 6 days at 37$^{\circ}C$. The each fraction exhibited the antitumor effect in vivo. The ethylacetate fraction reduced the tumor formation by 41% compared with the control, when sarcoma 180 cells were injected subcutaneously into the left groin of BALB/c mice. Also spleen/body weight rate of ethylacetate fraction was increased by 2.10% compared with the control (1.08%). And it is considered that there would be no toxic effect caused by each fraction of body weight and organ as there was on more changes in mouse' weight compared with the control.

• Journal of Applied Biological Chemistry
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• v.62 no.4
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• pp.327-332
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• 2019

Alzheimer's disease (AD) is a common neurodegenerative disease. Oxidative stress by amyloid beta peptide (Aβ) of neuronal cell is the most cause of AD. In the present study, protective effects of several flavonoids such as kaempferol (K), kaempferol-3-O-glucoside (KG), quercetin (Q) and quercetin-3-β-ᴅ-glucoside (QG) from Aβ_25-35 were investigated using C6 glial cell. Treatment of Aβ_25-35 to C6 glial cell showed decrease of cell viability, while treatment of flavonoids such as Q and QG increased cell viability. In addition, treatment of flavonoids declined reactive oxygen species (ROS) production compared with Aβ_25-35-induced control. The ROS production was increased by treatment of Aβ_25-35 to 133.39%, while KG and QG at concentration of 1 μM decreased ROS production to 107.44 and 113.10%, respectively. To study mechanisms of protective effect of these flavonoids against Aβ_25-35, the protein expression related to inflammation under Aβ_25-35-induced C6 glial cell was investigated. The results showed that C6 glial cell under Aβ_25-35-induced oxidative stress up-regulated inflammation-related protein expressions. However, treatment of flavonoids led to reduction of protein expression such as inducible nitric oxide synthase, cyclooxygenase-2 and interleukin-1β. Especially, treatment of KG and QG decreased more effectively inflammation-related protein expression than its aglycones, K and Q. Therefore, the present results indicated that K, Q and its glycosides attenuated Aβ_25-35-induced neuronal oxidative stress and inflammation.

• Journal of Life Science
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• v.23 no.5
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• pp.689-697
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• 2013

In the United States, about 40,000 new cases of oral cancer are diagnosed each year and nearly 7,800 patients died from it in 2012. Omega-3 polyunsaturated fatty acids have been found to have anticancer effects in a variety of cancer cell lines and animal models, but their effect in oral cancer remains unclear. This study was designed to examine the effect of docosahexaenoic acid (DHA, a kind of omega-3 fatty acid) on oral cancer cells and the molecular mechanism of its action. We found that exposure of squamous cell carcinoma-4 (SCC-4) and squamous cell carcinoma-9 (SCC-9) human oral cancer cells to DHA induced growth inhibition in a dose- and time-dependent manner. Meanwhile, in addition to the elevated levels of apoptotic markers, such as cleaved PARP, subG1 portion and TUNEL-positive nuclei, DHA led to autophagic vesicle formation and an increase in autophagic flux, indicating the involvement of both apoptosis and autophagy in the inhibitory effects of DHA on oral cancer cells. Further experiments revealed that the apoptosis and autophagy induced by DHA were linked to inhibition of mammalian target of rapamycin (mTOR) signaling by AKT inhibition and AMP-activated protein kinase (AMPK) activation in SCC-9 cells. Together, our results suggest that DHA induces apoptosis- and autophagy-associated cell death through the AMPK/AKT/mTOR signaling pathway in oral cancer cells. Thus, utilization of omega-3 fatty acids may represent a promising therapeutic approach for chemoprevention and treatment of human oral cancer.