ABSTRACT
Emergencies of epistaxis in students caused by environmental pollution have rarely been reported to date. This study aimed to explore the cause of an emergency of epistaxis in elementary students by using a field epidemiological investigation. Twenty-two epistaxis cases from a single school with differences in gender, age, and classroom, were diagnosed within a period of 7 days. The air concentration of chromic acid mist (Cr6+) in the electroplating factory area, new campus, and residential area exceeded the limit of uncontrolled emissions. The emission of HCL and H2SO4 was also observed. Formaldehyde levels in the classrooms exceeded the limits of indoor air quality. Abnormal nasal mucosa was significantly more frequent in the case group (93.3%) and control group 1 (of the same school) (66.7%) than in control group 2 (from a mountainous area with no industrial zone) (34.8%; P < 0.05 and P < 0.01, respectively). On the basis of the pre-existing local nasal mucosal lesions, excessive chromic acid mist in the school's surrounding areas and formaldehyde in the classrooms were considered to have acutely irritated the nasal mucosa, causing epistaxis. Several lessons regarding factory site selection, eradication of chemical emissions, and indoor air quality in newly decorated classrooms, should be learned from this emergency.
Subject(s)
Child , Female , Humans , Male , Air Pollutants , Toxicity , Air Pollution, Indoor , Case-Control Studies , China , Epidemiology , Emergencies , Epidemiology , Environmental Exposure , Environmental Monitoring , Epistaxis , Epidemiology , Schools , StudentsABSTRACT
OBJECTIVE: To evaluate the proliferation inhibitory effect of Lappaconitine (LAP) on non-small cell lung cancer cell line A549 cells in vitro and its possible mechanism. METHODS: A549 cell was cultured with different concentrations of LAP. Cellular proliferation was determined with MTT. Cell cycle and apoptosis were detected with FCM technology. The Cyclin E1 gene expression was checked by Real-time Quantitative PCR method. RESULTS: LAP could inhibit the proliferation of A549 cells in vitro in a dose-dependent manner. LAP could induce apoptosis of A549 cell. Cell cycle was stopped at the G1 + G0 phase by LAP with FCM technology. With the increasement of LAP concentration, the ratio of G1 + G0 phase was increased and the ratio of S phase and G2 + M phase was decreased; The apoptotic rate was gradually increased, and the Cyclin E1 gene expression was down-regulated. CONCLUSION: LAP has the inhibitory effect on the growth of A549 cells, which is related to the cell cycle arrest in G0/G1 phase, apoptosis and down-regulation of Cyclin E1 gene expression.
Subject(s)
Aconitine/analogs & derivatives , Aconitum/chemistry , Antineoplastic Agents, Phytogenic/pharmacology , Apoptosis/drug effects , Carcinoma, Non-Small-Cell Lung/pathology , Cell Proliferation/drug effects , Aconitine/pharmacology , Carcinoma, Non-Small-Cell Lung/metabolism , Cell Cycle/drug effects , Cell Line, Tumor , Cyclin E/genetics , Cyclin E/metabolism , Dose-Response Relationship, Drug , Down-Regulation , Drugs, Chinese Herbal/pharmacology , Flow Cytometry , Humans , Lung Neoplasms/metabolism , Lung Neoplasms/pathology , RNA, Messenger/genetics , RNA, Messenger/metabolism , Real-Time Polymerase Chain ReactionABSTRACT
This research is aimed on reversing multidrug resistance (MDR) of chemotherapy in lung cancer. According to our previous research, chemotherapeutic drugs resistance in lung cancer is mainly due to high expression of multidrug resistance-associated protein (MRP) gene and activation of caspases. The effect of stephania tetrandra-containing Chinese herbal formula, namely Supplement Energy and Nourish Lung (SENL), is effective in enhancing efficacy and reducing toxicity of chemotherapy in lung cancer. However, the underlying mechnism is largely unknown. To understand whether and how SENL herbs function on multidrug-resistance lung cancer cells, we treated a multidrug resistance lung cancer cell line, SW1573/2R120 with SENL herbs alone or together with a chemotherapeutic drug, Adriamycin (ADM). We observed that SENL herbs had a significant synergistic effect with ADM in inhibiting the growth of SW1573/2R120 cells. SENL alone and particularly together with ADM could significantly increase cell apoptotic death via mitochondria- and caspase-dependent pathway. Furthermore, we showed that SENL herbs could reverse drug resistance of lung cancer cells by decreasing MRP expression and increasing accumulation of intracellular ADM, which in turn increase the sensitivity of cancer cells to ADM. Taken together, the mechanism underlying reversal effect of drug resistance by SENL treatment was reported here and further systematical investigation on SENL herbs may lead to solve drug resistance in lung cancer chemotherapy.
Subject(s)
Drug Resistance, Multiple , Drug Resistance, Neoplasm , Lung Neoplasms/pathology , Plant Extracts/pharmacology , Stephania tetrandra/chemistry , Antineoplastic Agents/pharmacology , Apoptosis , Base Sequence , Cell Line, Tumor , DNA Primers , Doxorubicin/pharmacology , HumansABSTRACT
OBJECTIVE: To explore the effect of supplement energy and nourish lung (SENL) herbs on the growth of drug-resistance lung cancer cells, expression of multidrug resistance-associated protein (MRP) and mechanisms of mitochondrial and Caspase signal. METHODS: Drug-resistance lung cancer cell line SW1573/2R120 was treated with SENL herbs and Adriamycin. Cellular toxicity with MTT colorimetric assay, expression of MRP protein with flow microscopy, the fluorescence intensity of mitochondria membrane potetional and Ca2+ with laser confocal microscopy, the activities of caspase-3 and caspase-8 with colorimetric assay were detected. RESULTS: Compared with control group, cellular inhibitory rate was increased obviously, expression of MRP protein was decreased, mitochondria membrane potetional and intracellular Ca2+ were decreased, the activities of caspase-3 and caspase-8 were increased in the group of SENL herbs. CONCLUSION: SENL herbs can interfere and reverse drug resistance in lung cancer by the mechanism of decreasing mitochondria membrane potetional and increasing the activities of caspase-3 and caspase-8.
