The aim of this study is to develop the Tripterygium glycosides nanoemulsion gels and investigate its pharmacodynamics. Oleic acid was used as oil phase, polyoxyethylene castor oil as surfaetant, and 1,2-propanediol as cosurfactant to screen the formula of Tripterygium glycoside nanoemulsion using the pseudo-temary phase diagrams. Then the nanoemulsion gels was prepared. The ICR mouse ears were sensitazated by 7% DNCB, and then were excited by 0.3% DNCB to stimulate the model of mouse chronic dermatitis and eczema. The concentrations of IFN-γ, IL-4 and IL-8 in mouse blood were determined by ELISA. The results showed that Tripterygium glycosides nanoemulsion gels could significantly inhibit the swelling of mouse ears(P < 0.01) and ameliorate the edama and erythema of model mouse ears skin. Also it could significantly decrease the expression of IFN-γ and IL-4 in model mouse blood. Tripterygium glycosides nanoemulsion gels had a good therapeutic effect on mouse model of dermatitis and eczema. It was expected to provide a new and long-acting exterernal preparation for the treatment of dermatitis and eczema.
Animals ; Chemistry, Pharmaceutical ; instrumentation ; methods ; Dermatitis ; drug therapy ; immunology ; Drug Carriers ; chemistry ; Drugs, Chinese Herbal ; chemistry ; pharmacokinetics ; Emulsions ; chemistry ; Female ; Glycosides ; chemistry ; pharmacokinetics ; Humans ; Interleukin-4 ; immunology ; Interleukin-8 ; immunology ; Mice ; Mice, Inbred ICR ; Nanoparticles ; chemistry ; Tripterygium ; chemistry

OBJECTIVETo observe the cytotoxic effect of cisplatin with proteasome inhibitor on osteosarcoma cells.

METHODSCell survival was tested by MTT, apoptotic morphology was observed by electron microscopy, apoptotic rate was analyzed by flow cytometry, the transcription level of excision repair cross complementation-1 (ERCC-1) was tested by reverse transcription polymerase reaction.

RESULTSCompared with cells treated with cisplatin alone, cells treated with cisplatin and proteasome inhibitor showed a decreased survival rate, more typical apoptotic morphology, higher apoptotic rate [(14.37 +/-2.37)% vs. (50.93 +/-4.84)%, P<0.01)], and lower transcription level of excision repair cross complementation-1.

CONCLUSIONProteasome inhibitor could increase the cytotoxic effect of cisplatin on osteosarcoma cells and promote cisplatin-induced osteosarcoma apoptosis. These effects may be associated with the decreased transcription of excision repair cross complementation-1.

Animals ; Antineoplastic Agents ; pharmacology ; Apoptosis ; drug effects ; Bone Neoplasms ; pathology ; Cisplatin ; pharmacology ; Drug Synergism ; Oligopeptides ; pharmacology ; Osteosarcoma ; pathology ; Rats ; Tumor Cells, Cultured

OBJECTIVETo observe the cytotoxic effect of thermo-chemotherapy with cisplatin on osteosarcoma OS-732 cell line and to explore its mechanism.

METHODSThe osteosarcoma OS-732 cell line was treated with different temperature, cisplatin alone and 43 degrees C +cisplatin for 1 h, respectively and the in vitro cytotoxic effect was observed with MTT assay. The cell cycle and the apoptotic rate were analyzed with flow cytometry (FCM); the cellular apoptosis was observed also with electron microscope.

RESULTThe cytotoxicity index increase markedly as the temperature elevated or the concentration of cisplatin increased. While treated with 43 degrees C hyperthermia and cisplatin simultaneously, the cytotoxicity index increased to 72.37%;the cell cycle of the treated OS-732 cells line was changed with marked increase in S phase and decreasing in G(2)/M phase. The apoptotic rate increased markedly with the highest of 56.47%. Electron microscope showed the characteristic apoptotic alterations.

CONCLUSIONHyperthermia with cisplatin enhance cytotoxicity on osteosarcoma OS-732 cell line and the induced cell apoptosis may be one of the mechanisms of enhanced cytotoxicity by thermo-chemotherapy.

Antineoplastic Agents ; pharmacology ; Apoptosis ; drug effects ; Bone Neoplasms ; pathology ; therapy ; Cell Line, Tumor ; Cisplatin ; pharmacology ; Combined Modality Therapy ; DNA Damage ; Flow Cytometry ; Humans ; Hyperthermia, Induced ; Osteosarcoma ; pathology ; therapy

Carcinoma, Non-Small-Cell Lung ; diagnosis ; metabolism ; China ; Consensus ; Humans ; Immunohistochemistry ; In Situ Hybridization, Fluorescence ; Lung Neoplasms ; diagnosis ; metabolism ; Oncogene Proteins, Fusion ; metabolism ; Polymerase Chain Reaction ; Receptor Protein-Tyrosine Kinases ; metabolism

Animals ; Cellular Reprogramming ; Dentate Gyrus ; cytology ; Fibroblasts ; cytology ; Mice ; Neural Stem Cells ; cytology ; transplantation ; Swine