The toxicity of Chinese materia medica is the popular topic at home and abroad, and is the main barrier of Chinese materia medica in its internationalization. The safety of Chinese materia medica is the common focus in society. So, emphasis should be payed to the application and study of toxicant Chinese materia medica, correct recognition of its effct and bias is the basis of exerting its therapeutic effect thoroughly. On basis of expounding the concept and classifi cation of toxicant Chinese materia medica, this article classifyed and analyzed the heavy toxicant Chinese materia medica in government standard according to its application, and proposed thinking on study of heavy toxicant Chinese materia medica.

Objective:To explore the pharmacological basis of clinical application of Dachaihu Decoction. Methods: The relevant relation between cilnical features of Dachaihu Decoction and its pharmacological actions are analysed. Results: The various clinical curative effects rest on its relevant pharmacological actions.Conclusion: The good clinical curative effects will be achieved according to Dachaihu Decoction.

China pharmacopoeia is a civil code which is to ensure pharmaceutical quality and protect people's drug safety and effectiveness. Drug standards are consist of two parts, the pharmaceutical standards and medical standards. Medical standards include four contents, such as prescription, function and indications, usage and dosage and attentions. This paper summarized the revised contents of medical standards and suggested some propositions.
Contraindications ; Documentation ; Drug Administration Schedule ; Drug Compounding ; standards ; Drug Dosage Calculations ; Drug Prescriptions ; standards ; Drugs, Chinese Herbal ; adverse effects ; pharmacology ; standards ; Female ; Food-Drug Interactions ; Humans ; Pregnancy ; Terminology as Topic

The influence of L-arginine on endothelial nitric oxide synthase (eNOS) and cyclooxygenase 2 (COX2) was observed in experimental pulmonary thromboembolism and the action mechanism on pulmonary thromboembolism was explored. Wistar rats were randomly divided into control group, model group and treatment group. Pulmonary thromboembolism models were established by auto-blood back transfusion, and L-Arg 100 mg/kg was intraperitoneally injected after successful model preparation. The animals were sacrificed at 3 h, 1 day, 3 days and 7 days after embolism. Plasma NO, TXB2 and 6-Keto-PGFla were detected. The expression of eNOS and COX2 protein and mRNA in pulmonary tissues was detected by immunohistochemistry and RT-PCR respectively. The results showed that pulmonary thrombosis could be seen post pulmonary embolism and inflammatory reaction was significant. Plasma NO was decreased (P<0.01), and the levels of TXB2, 6-Keto-PGF1alpha and T/P ratio were all elevated. The expression of eNOS protein and mRNA in the pulmonary tissue was down-regulated (P<0.05), while that of COX2 protein and mRNA was upregulated (P<0.01). In treatment group, the level of NO was increased, the levels of TXB2 and T/P ratio were decreased, but the level of 6-Keto-PGF1alpha was increased. The expression of eNOS protein and mRNA in pulmonary tissue was upregulated (P<0.05), while that of COX2 protein and mRNA was down-regulated (P<0.05). In conclusion, L-arginine can educe the role of pulmonary tissue protection through up-regulating the expression of intra-pulmonary NOS and down -regulating COX2 in pulmonary thromboembolism.

The effects of exogenous p16(ink4a) gene on biological behaviors of human lung cancer cell line with homozygous deletion of p16(ink4a) gene were investigated. Exogenous p16(ink4a) gene was transfected by lipofectin into human lung cell line A549, in which p16(ink4a) gene was homozygously deleted. The expression of p16(ink4a) mRNA and protein was detected by RT-PCR and immunocyto-chemistry, respectively. The changes in the behaviors of the transfected cell lines in vitro and in vivo were observed. In the transfected cell line A549, the exogenous p16(ink4a) gene could be stably expressed. The growth of A549 cells transfected with p16(ink4a) gene was obviously slowed down. Flow cytometry revealed that transfection of the exogenous p16(ink4a) gene resulted in A549 cell lines arrest in G1 phase of cell cycle. The tumorigenicity of these transfected cells in nude mice could be inhibited, and the tumor growth of nude mice was significantly suppressed. It was concluded that exogenous p16(ink4a) gene may be stably expressed in human lung cancer cell line A549. The expression of the introduced p16(ink4a) could block lung cancer cells to entry into S phase of cell cycle and inhibit tumor malignant growth both in vitro and in vivo.

AIM:To investigate the effect of Polo-like kinase-1(Plk1) depletion on cell cycle progression and cell growth in lung cancer cells.METHODS:A recombinant plasmid containing antisense RNA targeting Plk1(pcDNA3-Plk1) was transfected into A549 cells by lipofectine.RT-PCR and Western blotting were used to examine Plk1 gene expression.Cell proliferation was evaluated by cell counting and BrdU labeling.Cell cycle distribution and apoptosis were examined by flow cytometry.Inhibition rate(IR) of vinorebline(NVB) was determined by MTT assay.RESULTS:After transfected with pcDNA3-Plk1 into A549 cells,the expression levels of Plk1 mRNA and protein were greatly decreased.Abnormal morphological changes of cells and growth inhibition were observed in pcDNA3-Plk1 transfected cells.The BrdU labeling index was significantly lower than that in control group(P

AIM: To localize the expression of forkhead/winged helix transcription factor(FOXP3) gene in different types of pathological lung tissues and explore its biological role in pathogenesis of human lung cancer.METHODS: By using RT-PCR and Western blotting,the expressions of FOXP3 mRNA and related protein in 153 samples including lung cancer(n=63),lung benign lesion(n=45) and normal lung tissues(n=45) were analyzed.RESULTS: The positive expressions of FOXP3 mRNA and its protein were observed in lung cancer and in benign lesion lung tissue samples with significant difference(P0.05).CONCLUSION: FOXP3 is a biomarker of CD4+CD25+ regulatory T cell.They are expressed both in lung cancer and benign lesion lung tissues,but not in normal lung tissue.The expression of FOXP3 is more intensive in cancer tissues than that in benign lesions.

AIM: To detect the changes of serum vascular endothelial growth factor(VEGF) level and the expression of peripheral blood cytokeratin 19(CK19) mRNA in patients with non-small cell lung cancer(NSCLC).METHODS: 96 patients with NSCLC,40 patients with benign lung diseases and 25 healthy controls were investigated.The VEGF level in serum was detected by ELISA and CK19 mRNA in peripheral blood was determined by using reverse transcriptase-polymerase chain reaction(RT-PCR).RESULTS: In NSCLC group,the serum VEGF level and the positive rate of CK19 mRNA in peripheral blood were(346.3?95.6) ng/L and 63.5%,which were significantly higher than those in other two groups respectively(P0.05).VEGF serum level in the patients who showed positive CK19 mRNA in peripheral blood was(407.4?121.2) ng/L.It is significantly higher than that in the negative patients(P

The influence of L-arginine on endothelial nitric oxide synthase (eNOS) and cyclooxygenase 2 (COX2) was observed in experimental pulmonary thromboembolism and the action mechanism on pulmonary thromboembolism was explored. Wistar rats were randomly divided into control group, model group and treatment group. Pulmonary thromboembolism models were established by auto-blood back transfusion, and L-Arg 100 mg/kg was intraperitoneally injected after successful model preparation. The animals were sacrificed at 3 h, 1 day, 3 days and 7 days after embolism.Plasma NO, TXB2 and 6-Keto-PGF1α were detected. The expression of eNOS and COX2 protein and mRNA in pulmonary tissues was detected by immunohistochemistry and RT-PCR respectively.The results showed that pulmonary thrombosis could be seen post pulmonary embolism and inflammatory reaction was significant. Plasma NO was decreased (P＜0.01), and the levels of TXB2,6-Keto-PGF1α and T/P ratio were all elevated. The expression of eNOS protein and mRNA in the pulmonary tissue was down-regulated (P＜0.05), while that of COX2 protein and mRNA was upregulated (P＜0.01). In treatment group, the level of NO was increased, the levels of TXB2 and T/P ratio were decreased, but the level of 6-Keto-PGF1 α was increased. The expression of eNOS protein and mRNA in pulmonary tissue was upregulated (P＜0.05), while that of COX2 protein and mRNA was down-regulated (P＜0.05). In conclusion, L-arginine can educe the role of pulmonary tissue protection through up-regulating the expression of intra-pulmonary NOS and down -regulating COX2 in pulmonary thromboembolism.

The effects of exogenous p16ink4a gene on biological behaviors of human lung cancer cell line with homozygous deletion of p16ink4a gene were investigated. Exogenous p16ink4a gene was transfected by lipofectin into human lung cell line A549, in which p16ink4a gene was homozygously deleted. The expression of pl6ink4a mRNA and protein was detected by RT-PCR and immunocytochemistry, respectively. The changes in the behaviors of the transfected cell lines in vitro and in vivo were observed. In the transfected cell line A549, the exogenous p16ink4a gene could be stably expressed. The growth of A549 cells transfected with p16ink4a gene was obviously slowed down. Flow cytometry revealed that transfection of the exogenous p16ink4a gene resulted in A549 cell lines arrest in G1 phase of cell cycle. The tumorigenicity of these transfected cells in nude mice could be inhibited, and the tumor growth of nude mice was significantly suppressed. It was concluded that exogenous p16ink4a gene may be stably expressed in human lung cancer cell line A549. The expression of the introduced p16ink4a could block lung cancer cells to entry into S phase of cell cycle and inhibit tumor malignant growth both in vitro and in vivo.