OBJECTIVE:To probe into the general regularity and characteristics of ADR in our hospital. METHODS:117 ADR reports were analyzed retrospectively in respect of the patient’s gender,age,dosage form,route of medication,medication combination,category of drugs,involved organs and system and clinical manifestation,ect. RESULTS:Of total 117 cases of ADR,female cases of 69 accounted for 58.97% while 48 male cases 41.03%. ADR cases were mainly found in the group aged from 41 to 50(23.93%). ADR was predominantly caused by intravenous drip infusion(86.32%). 46 kinds of drugs in 10 categories were involved,in which antimicrobial drug took dominate place including 20 kinds in 10 categories(58.97%). The most common clinical symptom represented as lesion of skin and its appendants(54.70%). 117 cases were cured and improved without death case. CONCLUSION:Great importance should be attached to rational use of drug and safety of drug use of special population.

OBJECTIVE: To study the expression of Cyclin D1 in nasopharyngeal carcinoma cells processed by epigallocatechin gallate(EGCG) and it's significance, and revealed the anti-tumor mechanism of EGCG against nasopharyngeal carcinoma. METHOD: CNE-2 cells were treated by EGCG at different concentrations, the morphological changes of CNE-2 cells were observed by inverted microscope; the inhibition ratio of cell proliferation was detected by MTT colorimetric method, flow cytometry was used to analyze the changes of cell cycle. The expression of Cyclin D1 mRNA was detected by RT-PCR. RESULT: After treated by EGCG, the CNE2 cells decreased in amount and density, some of which became roll and small; Floating and dead cells can be seen in the inverted microscopy; cell proliferation was significantly inhibited in a time and dose dependent (P < 0.05). CNE-2 cells were arrested at G1/G0 phase. The expression of Cyclin D1 mRNA was down-regulated by EGCG with concentration and action time dependent (P < 0.05). CONCLUSION EGCG resisted nasopharyngeal carcinoma by inhibiting the cell proliferation, The down regulation of Cyclin D1 mRNA expression in a time and dose dependent may be the possible mechanisms.
Carcinoma ; Catechin ; analogs & derivatives ; pharmacology ; Cell Cycle ; drug effects ; Cell Line, Tumor ; Cell Proliferation ; drug effects ; Cyclin D1 ; metabolism ; Humans ; Nasopharyngeal Carcinoma ; Nasopharyngeal Neoplasms ; metabolism ; pathology

Objective To explore the role and potential mechanisms of all-trans retinoic acid （ATRA） on activation and oxidative stress of hepatic stellate cell （HSC）. Methods Platelet-derived growth factor （PDGF-bb, 10 ng/ml） was applied to induce the activation of HSCs, which was then treated with ATRA at a dosage of 5 μmol/L for 48 h. The effects of ATRA on HSC activation were evaluated by detecting changes in cell growth viability and phenotypic marker expression. The effects of ATRA on HSC oxidative stress were evaluated by detecting changes in intracellular reactive oxygen species （ROS）, reduced glutathione （GSH） and malondialdehyde （MDA）, and the expression of antioxidant genes. The effects of ATRA on HSC autophagic activity were evaluated by detecting changes in autophagy marker expression and autophagic flow. Results Compared with the PDGF-bb group, the cell viability was significantly reduced in ATRA-treated HSCs （P<0.01）, as well as the expression of α-SMA and Collagen I. The intracellular levels of ROS and MDA were significantly reduced in ATRA-treated HSCs （P<0.01）, whereas the GSH level was significantly increased （P<0.01）. The expression levels of antioxidant genes （NRF2, HO-1, and ATF4）, were significantly higher in ATRA-treated HSCs than those in the normal ones under PDGF-bb condition （P<0.01）. Meanwhile, the expression of autophagy markers Beclin 1 and LC3 Ⅱ/I, and signal of autophagy flow in ATRA-treated HSCs were found to be significantly reduced （P<0.01）. Conclusion ATRA significantly inhibited PDGF-bb-induced HSC activation and reduced the level of oxidative stress and autophagic activity of HSCs, which had potential applications in the prevention and treatment of liver fibrosis.