• Archives of Pharmacal Research
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• v.17 no.2
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• pp.100-103
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• 1994

The limonoid compound (28-deacetyl sendanin0 isolated from the fruit of Melia toosendan SIEB. et ZUCC. was evaluated on anticancer activity. According to a standard in vitro cytotoxicity assy, eight human cancer cell lines and SRB assay were introduced for present evaluation. As a positive standard, adriamycin was tested in parallel. The cell lines were originated from six different organs. In view of dose-response profiles to 28-deacetyl sendanin, the most sensitive cells were SF-539 and PC-3 which were derived from CNS and prostate, respecitively. In contrast, all the cell lines responded similarly to adriamycin to give rise to nearly indentical six cell lines were more sensitive to 28-deacetyl sendanin and two were more resistant. As a result, 28-deacetyl sendanin had more senstive and selective inhibitory effects on in vitro growth of human cancer cell lines in a comparison with adriamycin.

• Journal of the East Asian Society of Dietary Life
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• v.9 no.4
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• pp.427-434
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• 1999

This study was conducted to investigate the effects of vitamin I supplementation on renal function in high fat diet and adriamycin (ADR) induced experimental nephrotic syndrome in model rats. The effects of vitamin E supplementation on renal function in high fat diet and ADR treated rats were as follows. Kidney weight was decreased by vitamin E supplementation. Serum total protein was increased by the excess supplementation. Blood urea nitrogen(BUN) was decreased by the high supplementation. However, serum albumin and creatinine showed no significant differences between groups. Urinary volume tended to increase by vitamin I supplementation. Urinary urea-N tended by vitamin I supplementation. Particularly glomerular filtration rate(GFR) was significantly decreased by vitamin E supplementation. These results suggested that vitamin E supplementation could alleviate the adverse effects caused in renal function by highfatdiet and ADR treatments.

• The Journal of Internal Korean Medicine
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• v.32 no.4
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• pp.610-615
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• 2011

Objectives : To observe the mitigating effects of a Traditional Korean Medicine treatment program, called Wheel Balanced Cancer Therapy (WBCT), with Adriamycin and 5-FU chemotherapy on a breast cancer patient. Methods : A 26 year old female patient diagnosed with stage IIb breast cancer was admitted to the East-West Cancer Center (EWCC) in February of 2010. She received Adriamycin and 5-FU from February 22nd, to July 20th, 2010 followed by WBCT consisting of herbal medicine, acupuncture, moxibustion and physiotherapy for 5 months. Her symptoms were measured by Common Terminology Criteria for Adverse Events (CTCAE) and her quality of life was measured by Eastern Cooperative Oncology Group (ECOG). Results : WBCT significantly alleviated chemotherapy-induced nausea, oral dryness, and peripheral neuropathy. Quality of life also significantly improved. Conclusions : This case study potentiates WBCT's significant efficacy in aiding breast cancer patients suffering from Adriamycin plus 5-FU chemotherapy induced adverse effects.

• The Journal of Natural Sciences
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• v.9 no.1
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• pp.31-37
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• 1997

Apoptosis is an important event in the anticancer drug therapy. p53 was demonstrated to serve a key component to lead tumor cell death by inducing apoptosis. However, recent study showed the presence of p53 independent apoptotic pathway (Gaftenhaus et al., 1996). We were curious to know it apoptosis induced by adriamycin, a genotoxic anticancer agent, involved p53 gene mutation. Thus this study investigated the p53 gene mutation status among HeLa cell population during apoptosis induced by adriamycin. Under our experimental condition, 12 hour treatment of 1 ${\mu}m$ adriamycin caused apoptosis which was monitored by DNA fragmentation assay. In order to see the p53 gene mutation status, exons of 5, 7 and 8 of p53 gene, where previously reported p53 mutation hot spots reside, were amplified by PCR and nucleotide sequence change was scanned. However, no nucleotide change was observed among apoptotic HeLa cell population. Therefore this study demonstrated that adriamycin induced apoptosis without causing p53 gene damage.

• The Journal of Internal Korean Medicine
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• v.21 no.3
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• pp.443-452
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• 2000

Objective : This study was designed to evaluate the synergistic effect on cytotoxicity of combination with adriamycin and Palginhonhapwhajucwhan, a traditional prescription for cancer treatment in oriental medicine, in Chang, HL-60, Hep-3B and Alexander cells. Methods : We observed cell viability in Chang, HL-60, Hep-3B, and Alexander cells by crystal violet staining. Those cells were treated with various concentrations of adriamycin alone, Palginhonhapwhajucwhan alone and combination of two medications for 10 hr. On condition of $0.5{\mu}l/ml$ adriamycin alone, $15.6{\mu}l/ml$ Paljintanghapwhajucwhan alone and combination of two medications, at first, we observed colony forming of Chang and HL-60 cells. Second, we observed DNA fragmentation by agarose electrophoresis in Chang, HL-60, Hep-38 and Alexander cells. Third, we measured the catalytic activation of caspase-1, 2, 3, 6, 8, and 9 protease in Chang cells and caspase-3 protease in Chang, HL-60, Hep-3B and Alexander cells by using fluorogenic substrate. Finally, we isolated mRNA of Fas in Chang, HL-60, Hep-38 and Alexander cells and observed that Fas gene was amplified by RT-PCR Results : 1. The combination of adriamycin and Palginhonhapwhajucwhan synergistically augmented the cytotoxicity of Chang and HL-60 cells whereas did not in Hep-38 and Alexander cells. 2. Cotreatment of two drugs also markedly inhibited the colony forming ability both in Chang and HL-60 cells. 3. The cytotoxicity of these medicatons was revealed as apoptosis characterized by high molecular wight DNA fragmentaton. 4. The apoptotic cytotoxicity was mediated by activation of caspase-3 protease in Chang cells. 5. Synergistic increase in apoptotic cytotoxicity by combination of two medications was dependent on the expression of Fas in cancer cells. Conclusions : Combination of adriamycin and Palginhonhapwhajucwhan significantly augmented apoptotic cytotoxicity of Fas-positive cells such as Chang and HL-60 cells via acticaton of apoptosis signaling pathway.

• Journal of Life Science
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• v.13 no.3
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• pp.241-247
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• 2003

While the DNA-protein kinase (DNA-PK) complex, comprised of DNA-PKcs and Ku80, is primary involved in the repair of DNA double-strand breaks, it is also believed to participate in additional cellular processes. Here, treatment of embryo fibroblasts (MEFs) derived from either wild-type (Wt) or DNA-PKcs-null (DNA-$PKcs^{-/-}$) mice with various stress inducing agents revealed that adriamycin was markedly more cytotoxic for $Ku80^{-/-}MEFs$ and led to their long-term accumulation in the $G_2$/M phase. This differential response was not due to differences in DNA repair, since adrimycin-triggered DNA damage was repaired with comparable efficiency in both Wt and $Ku80^{-/-}MEFs$, but was associated with differences in the expression of important cell cycle regulatory genes. Our results support the notion that Ku80-mediated cytoprotection and $G_2$/M-progression are not only dependent on the cell's DNA repair but also may reflect Ku80's influence on additional cellular processes such as gene expression.

• Archives of Pharmacal Research
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• v.27 no.1
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• pp.77-82
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• 2004

DA-125, a novel derivative of adriamycin, is known for its anti-cancer activity. In this study, the inhibitory mechanism of DA-125 on topoisomerase was investigated in the simian virus 40 (SV40) replicating CV-1 cell by studying the SV40 DNA replication intermediates and DNA-topoisomerase complexes. DNA-protein complexes that were formed in the drug-treated cells were quantitated by using a glass filter assay. SV40 DNA replication intermediates that were accumulated in the drug-treated CV-1 cell were analyzed in a high resolution gel. DA-125 did not accumulate B-dimers of SV40 DNA replication intermediates which were found in the adriamycin-treated CV-1 cells. DA-125 induced a dose-dependent formation of the DNA-protein complexes, while adriamycin did not. When adriamycin and etoposide (VP16) were added to the SV40-infected cells at the same time, adriamycin blocked the formation of the DNA-protein complexes induced by VP16 in a dose-dependent manner. However, DA-125 blocked the formation of the DNA-protein complexes induced by VP16 up to the maximum level of the DNA-protein complexes that were induced by DA-125 alone. Adriamycin and DA-125 did not inhibit the formation of the DNA-protein complexes that were caused by camptothecin, a known topoisomerase I poison. DA-125 is bifunctional in inhibiting topoisomerase II because it simultaneously has the properties of the topoisomerase II poison and the DNA intercalator. As a topoisomerase II poison, DA-125 alone induced dose-dependent formation of the DNA-protein complexes. However, as a DNA intercalator, it quantitatively inhibited the formation of the DNA-protein complexes induced by a strong topoisomerase II poison VP16. Furthermore considering that the levels of the DNA-protein complex induced by VP16 were decreased by DA-125 in terms of the topoisomerase II poison, we suggest that DA-125 has a higher affinity to the drug-binding sites of DNA than VP16 has.

• Journal of Physiology & Pathology in Korean Medicine
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• v.16 no.6
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• pp.1207-1210
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• 2002

To examine the cardiotoxic effect of adriamycin on cultured rat myocardial cells, cytotoxicity was measured by MTT assay after cultured myocardial cells were grown with various concentrations of adriamycin(ADA) for 48 hours. The protective effect of Benincasae Semen(BS) on ADR-induced cardiotoxicity was also examined in these cultures. ADR decreased cell viability of cultured rat myocardial cells remarkably in a dose- and time-dependent manners. In protective effect of BS, it was very effective in blocking ADR-induced cytotoxicity. From these results, it is suggested that ADR shows cardioxicity, and the herba extract, as is very effective in preventing ADR-induced cytotoxicity on cultured rat myocardial cells.

• Biomolecules & Therapeutics
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• v.8 no.3
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• pp.241-247
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• 2000

The present study was designed to assess the protective effect of a selective thromboxane $A_2$ receptor antagonist, KT2-962 (KT2) and possible mechanisms of adriamycin(AD)-induced nephrotoxicity in rats. The male Wistar rats were given either of AD (7.5 mg/kg, i.v.) alone in the AD-group (n=5) or in KT2+AD- group (n=5) which is a combination of AD and KT2 (30 mg/kg/day, i.p.) for 10 days from 3 days before and 7 days after AD injection. The body weight, 24-hours urine volume, urine protein and urinary N-acetyl-$\beta$-D-glu-cosaminidase (NAG) activity were measured with an interval of 2 days during 1 week. BUN, serum creatinine and creatinine clearance were measured on the 7th day. KT2 has significantly suppressed AD-induced change of body weight, 24-hours urine volume, urine protein and urinary NAG activity in the KT2+AD-group. The change of BUN, serum creatinine and creatinine clearance were significantly inhibited in the B7T2+AD-group. Based on these results, it is concluded that KT2 prevents AD-induced nephrotoxicity and suggests that endogenous thromboxane A2 may play an important role in AD-induced nephrotoxicity in rats.

• Journal of Nutrition and Health
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• v.25 no.6
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• pp.501-510
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• 1992

The present study was designed to evaluate the effect of pretreatment with coenzyme {{{{ { Q}_{10 } }}}} on adriamycin-induced myocardial ultrastructural changes in rats. Except control group 6 treat-ments included three levels of dietary conenzyme {{{{ { Q}_{10 } }}}} (0, 0.1 or 0.5g/kg diet) and two levels of ADR(1.0 or 2.0mg/kg B.W/week) Adriamycin treatment significantly decreased growth perfo-rmance of rats. But this decrement was not modified by dietary supplementation of coenzyme{{{{ { Q}_{10 } }}}} Electron microscopic examination revealed a progression of myocardial lesions were depen-dent upon the level of ADR injection. The most frequently observed fin structural alterations in rat myocardium were mitochondrial swelling dilation of the sarcoplasmic reticulum and the appearance of a perinuclear vacuolication. But these structural changes were somewhat reduced by dietary supplementation of coenzyme {{{{ { Q}_{10 } }}}}.