<p>OBJECTIVETo investigate the protective effect and mechanism of Ecliptae Herba extract on cigarette smoke extract-induced cytotoxicity.p><p>METHODThe effect of Ecliptae Herba extract on CSE-induced NHBE cell proliferation was detected by MTT assay. GSH content was determined by DTNB colorimetry. GST activity was measured by CDNB colorimetric assay. NQO1 activity was detected by NADPH and DCIP. The protein expression was determined by Western blot assay.p><p>RESULTEcliptae Herba extract reduced CSE's inhibitory effect on NHBE cells, recover the decrease in intracellular GSH caused by CSE and reduce the CSE-induced activity of GST and NQO1 and NQO1 protein expression.p><p>CONCLUSIONEcliptae Herba extract can reduce CSE-induced injury on NHBE cells, which may be related to phase II detoxification enzymes.p>
Cell Line ; Cell Proliferation ; drug effects ; Drugs, Chinese Herbal ; pharmacology ; Eclipta ; chemistry ; Gene Expression ; drug effects ; Humans ; NAD(P)H Dehydrogenase (Quinone) ; genetics ; metabolism ; Protective Agents ; pharmacology ; Smoke ; analysis ; Smoking ; adverse effects ; Tobacco ; chemistry

PURPOSE: NAD(P)H:Quinone Oxidoreductase 1 (NQO1) C609T missense variant (NQO1*2) and 29 basepair (bp)-insertion/deletion (I29/D) polymorphism of the NRH:Quinone Oxidoreductase 2 (NQO2) gene promoter have been proposed as predictive and prognostic factors for cancer development and progression. The purpose of this study is to investigate the relationship between NQO1/NQO2 genotype and clinico-pathological features of papillary thyroid microcarcinoma (PTMC). MATERIALS AND METHODS: Genomic DNA was isolated from 243 patients; and clinical data were retrospectively analyzed. NQO1*2 and tri-allelic polymorphism of NQO2 were investigated by polymerase chain reaction (PCR) and restriction fragment length polymorphism (RFLP) analysis. RESULTS: PTMC with NQO1*2 frequently exhibited extra-thyroidal extension as compared to PTMC with wild-type NQO1 (p=0.039). There was a significant relationship between I29/I29 homozygosity of NQO2 and lymph node metastasis (p=0.042). Multivariate analysis showed that the I29/I29 genotype was associated with an increased risk of lymph node metastasis (OR, 2.24; 95% CI, 1.10-4.56; p=0.026). CONCLUSION: NQO1*2 and I29 allele of the NQO2 are associated with aggressive clinical phenotypes of PTMC, and the I29 allele represents a putative prognostic marker for PTMC.
Adult ; Carcinoma, Papillary/*genetics/pathology ; DNA Mutational Analysis ; Female ; Genetic Predisposition to Disease ; Humans ; Immunohistochemistry ; Male ; Middle Aged ; Multivariate Analysis ; Mutagenesis, Insertional ; Mutation, Missense ; NAD(P)H Dehydrogenase (Quinone)/chemistry/*genetics ; Phenotype ; Polymorphism, Genetic ; Prognosis ; Promoter Regions, Genetic ; Retrospective Studies ; Sequence Analysis, Protein ; Sequence Deletion ; Thyroid Neoplasms/*genetics/pathology

To study the effects of triterpenoid components from Prunella asiatica on phase II detoxifying enzymes and protein expression in vitro and in vivo. Normal human bronchial epithelial (NHBE) cell model was used in vitro, and the mouse model of Kunming (KM) mice was used in vivo. CDNB assay was used to measure the activity of GST. NADPH and DCIP was used to detect the activity of NQO1. DTNB colorimetric assay was used to detect GSH. Western blot was use to detect the protein expression of NQO1. We found that triterpenoid components from P. asiatica could increase the activity of GST, NQO1 and GSH in NHBE cells and KM mice. NQO1 protein expression can also be increased in vitro. The study suggests that triterpenoid components from P. asiatica can prevent the lung cancer by regulating the body phase II detoxification enzyme activity and protein expression.
Animals ; Cell Line, Tumor ; Drugs, Chinese Herbal ; administration & dosage ; Female ; Glutathione ; metabolism ; Glutathione Transferase ; genetics ; metabolism ; Humans ; Male ; Metabolic Detoxication, Phase II ; Mice ; NAD(P)H Dehydrogenase (Quinone) ; genetics ; metabolism ; NF-E2-Related Factor 2 ; genetics ; metabolism ; Prunella ; chemistry ; Triterpenes ; administration & dosage

This study is to investigate the protection effect of schisandrin B (Sch B) against oxidation stress of HK-2 cells induced by cisplatin and the mechanisms involved. HK-2 cells were cultured and divided into different groups: solvent control group, cisplatin exposure group, positive group, Sch B treatment group. Cell viability and toxicity were evaluated by MTT and LDH assay. GSH level and SOD enzymes activities were also measured. DCFH-DA as fluorescence probe was used to detect ROS level by fluorescence microplate reader. Nrf2 translocation was detected by Western blotting. Real time Q-PCR was used to detect expressions of NQO1, HO-1 and GCLC mRNA level. The results showed that Sch B could significantly inhibit the decline of cell viability induced by cisplatin treatment (P < 0.05) and the protective effect was in a dose dependent manner. Furthermore, Sch B treatment significantly inhibited the increase of ROS level induced by cisplatin and reversed the decrease of GSH level (P < 0.05). When Sch B concentration was up to 5 micromol x L(-1), SOD enzyme activities were also enhanced significantly compared with that of the cisplatin group (P < 0.05). It was shown that Sch B could cause nuclear accumulation of Nrf2 in association with downstream activation of Nrf2 mediated oxidative response genes such as GCLC, NQO1 and HO-1. These results suggested Sch B could protect against the oxidative damage of HK-2 cells induced by cisplatin via the activation of Nrf2/ARE signal pathway.
Antineoplastic Agents ; toxicity ; Antioxidants ; isolation & purification ; pharmacology ; Cell Line ; Cell Survival ; drug effects ; Cisplatin ; toxicity ; Cyclooctanes ; isolation & purification ; pharmacology ; Glutamate-Cysteine Ligase ; genetics ; metabolism ; Glutathione ; metabolism ; Heme Oxygenase-1 ; genetics ; metabolism ; Humans ; Kidney Tubules, Proximal ; cytology ; metabolism ; L-Lactate Dehydrogenase ; metabolism ; Lignans ; isolation & purification ; pharmacology ; NAD(P)H Dehydrogenase (Quinone) ; genetics ; metabolism ; NF-E2-Related Factor 2 ; genetics ; metabolism ; Polycyclic Compounds ; isolation & purification ; pharmacology ; RNA, Messenger ; metabolism ; Reactive Oxygen Species ; metabolism ; Schisandra ; chemistry ; Signal Transduction ; Superoxide Dismutase ; metabolism