• Asian Pacific Journal of Cancer Prevention
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• v.14 no.8
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• pp.4635-4639
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• 2013

Multi-drug resistance (MDR) is an essential aspect of human lung cancer chemotherapy failure. Recent studies have shown that vinorelbine is involved in underlying processes in human tumors, reversing the MDR inseveral types of cancer cells. However, the roles and potential mechanism are not fully clear. In this study, we explored effects of vinorelbine in multi-drug resistance reversal of human lung cancer A549/DDP cells. We found that vinorelbine increased drug sensitivity to cisplatin and intracellular accumulation of rhodamine-123, while decreasing expression of P-glycoprotein (P-gp), multi-drug resistance-associated protein (MRP1) and glutathione-S-transferase ${\pi}$ (GST-${\pi}$) in A549/DDP cells. At the same time, we also established downregulation of p-Akt and decreased transcriptional activation of NF-${\kappa}B$ and twist after vinorelbine treatment. The results indicated that vinorelbine might be used as a potential therapeutic strategy in human lung cancer.

• The Journal of Korean Medicine
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• v.23 no.3
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• pp.33-42
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• 2002

Objective : This study was performed to investigate the activity of Whagan-Jeon (huaganjian) in protection against acetaminophen (AAP)-induced hepatotoxicity and the possible mechanisms in vivo. Methods : The following were performed : Serum ALT, depletion of hepatic glutathione (GSH) levels, the microsomal p. nitrophenol hydroxylation activity, microsomal aniline hydroxylation activity, genomic DNA fragmentation and its reversal, hepatic glutathione-S-transferase (GST) activity, and hepatic NAD(P)H:quinone oxidoreductase (QR) activity Results : Whagan-Jeon (huaganjian) protected against AAP-inducedhepatotoxicity by the increase of GSH levels, inhibition of P450 2E1-specific metabolic activities, attenuation of hepatic DNA damage, and induction of GST and QR activities in vivo. Conclusions : In conclusion, Whagan-Jeon (huaganjian) was effective in protection against AAP-induced hepatoxicity.

• Journal of Microbiology and Biotechnology
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• v.5 no.1
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• pp.31-35
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• 1995

An antitumor antibiotic named YS-1649 was isolated from the culture filtrate of a newly isolated fungus identified as Penicillium sp.. The fermentation yield reached about 40 mg per liter of the broth. YS-1649, a $\gamma$-Iactone - structured antibiotic, has the molecular fomular of $C_7H_6O_4$, Its structure was determined to be patulin by spectral analysis. It is active against some bacteria and showed cytotoxic effect on the proliferation of human breast cancer cell line, MCF-7, at concentrations of more than 0.048 $mu g/ml$. This compound also showed strong cytotoxic effect on the proliferation of human cancer cell lines, A549 and ACHN.

• Asian Pacific Journal of Cancer Prevention
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• v.13 no.11
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• pp.5619-5625
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• 2012

Gastric carcinoma is a leading cause of cancer death in the world and multi-drug resistance (MDR) is an essential aspect of gastric carcinoma chemotherapy failure. Recent studies have shown that integrin-linked kinase (ILK) is involved in metastasis of human tumors, expression silencing of ILK inhibiting the metastasis of several types of cultured human cancer cells. However, the role and potential mechanism of ILK to reverse the multi-drug resistance in human gastric carcinoma is not fully clear. In this report, we focused on roles of expression silencing of ILK in multi-drug resistance reversal of human gastric carcinoma SGC7901/DDP cells, including increased drug sensitivity to cisplatin, cell apoptosis rates, and intracellular accumulation of Rhodamine-123, and decreased mRNA and protein expression of multi-drug resistance gene (MDR1), multi-drug resistance-associated protein (MRP1), excision repair cross-complementing gene 1 (ERCC1), glutathione S-transferase -${\pi}$ (GST-${\pi}$) and RhoE, and transcriptional activation of AP-1 and NF-${\kappa}B$ in ILK silenced SGC7901/DDP cells. We also found that there was a decreased level of p-Akt and p-ERK. The results indicated that ILK might be used as a potential therapeutic strategy to combat multi-drug resistance through blocking PI3K-Akt and MAPK-ERK pathways in human gastric carcinoma.

• The Journal of Internal Korean Medicine
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• v.26 no.4
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• pp.767-775
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• 2005

This study was carried out to investigate the preventive effect of Salviae Miltiorrhizae Radix, Rhei Rhizoma and Carthami Flos combined with Samgijiwhang-Tang(SJTSRC) on streptozotocin(STZ)-induced diabetic nephropathy. Rats were divided into a control group of rats with STZ-induced diabetic nephropathy, a sample group of those given SJTSRC, and a normal group. In the experiment diabetic nephropathy was induced by giving STZ(60mg/kg) to rats via the peritoneum, and effects were assessed with measures of serum creatinine, serum BUN, secretion content of albumin and glucose content of urine, malondialdehyde(MDA) and glutathione(GSH) content in cortex of kidney. When STZ was injected into sample rat, the value of creatinine and BUN increased validly and STZ did damage to the kidney. When applying SJTSRC to sample rats, the value of serum creatinine decreased validly but the value of serum BUN decreased invalidity. It was confirmed that SJTSRC had an effect on recovery after kidney damage and secretion content of albumin increasedafter administration of SJTSRC but there was no change in glucose content of urine compared with the control group. The decrease of secretion of albumin after injection of STZ was taken to mean progressive diabetic nephropathy, and that reversal of that trend after SJTSRC administration showed that kidney function had improved, not through decreasing blood sugar, but through other factors. Results suggest that diabetic nephropathy was induced by STZ, and SJTSRC was effective in restricting the extent of damage to the kidney and halting the progression of diabetic nephropathy with improvement in levels of serum creatinine and albumin secretion. More study is needed, particularity pertaining to anti-oxidative effects in the kidney cortex.

• Molecules and Cells
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• v.37 no.12
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• pp.899-906
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• 2014

Prostaglandin $E_2$ ($PGE_2$) promotes tumor-persistent inflammation, frequently resulting in cancer. Curcumin is a diphenolic turmeric that inhibits carcinogenesis and induces apoptosis. $PGE_2$ inhibits curcumin-induced apoptosis; however, the underlying inhibitory mechanisms in colon cancer cells remain unknown. The aim of the present study is to investigate the survival role of $PGE_2$ and whether addition of exogenous $PGE_2$ affects curcumininduced cell death. HCT-15 cells were treated with curcumin and $PGE_2$, and protein expression levels were investigated via Western blot. Reactive oxygen species (ROS) generation, lipid peroxidation, and intracellular glutathione (GSH) levels were confirmed using specific dyes. The nuclear factor-kappa B ($NF-{\kappa}B$) DNA-binding was measured by electrophoretic mobility shift assay (EMSA). $PGE_2$ inhibited curcumin-induced apoptosis by suppressing oxidative stress and degradation of PARP and lamin B. However, exposure of cells to the EP2 receptor antagonist, AH6809, and the PKA inhibitor, H89, before treatment with $PGE_2$ or curcumin abolished the protective effect of $PGE_2$ and enhanced curcumin-induced cell death. $PGE_2$ activates PKA, which is required for cAMP-mediated transcriptional activation of CREB. $PGE_2$ also activated the Ras/Raf/Erk pathway, and pretreatment with PD98059 abolished the protective effect of $PGE_2$. Furthermore, curcumin treatment greatly reduced phosphorylation of CREB, followed by a concomitant reduction of $NF-{\kappa}B$ (p50 and p65) subunit activation. $PGE_2$ markedly activated nuclear translocation of $NF-{\kappa}B$. EMSA confirmed the DNA-binding activities of $NF-{\kappa}B$ subunits. These results suggest that inhibition of curcumin-induced apoptosis by $PGE_2$ through activation of PKA, Ras, and $NF-{\kappa}B$ signaling pathways may provide a molecular basis for the reversal of curcumin-induced colon carcinoma cell death.