Compound 2 was dissolved bax pathway in DMSO St and then added dropwise to a w Ssrigen suspension of GO. DOX Cl in deionized water was added and the pH was adjusted to 8 using triethylamine and the final mixture was stirred for 24 h. The mixture was filtered through a 450 nm filter and the residue was dispersed in demineralised water to the ultrasonic DMSO and to eliminate free DOX. Then the suspension at 4000 rpm for 5 min on unsolved Centrifuged to remove ste porphyrin and chunks of GO. Procedure was repeated nine times to obtain a suspension of 2/DOX/GO, the resulting complex was stored at 4 8C. Cytotoxicity tsexperimente Cells of mouse osteoblasts and building rmutterhalskrebs October 1 f were cultured in Dulbecco’s modified Eagle’s medium containing 10% fetal calf serum and grown K gentamicin in 24-well plates for 24 h erg complements. Cells were treated with DOX, 1/2/DOX/GO, 1 / 2/DOX/GOFA, DOX/2/GO 1/2/GO and incubated for 4 h.
Then all cells were closely involved in cell medium Che’s transfer. After incubation for a further 24 h and 48 h, the Lebensf Ability of the cells compared with a test-cell number was measured. The experience of the animal model: All experiments were approved and in accordance with the Code of China’s national animal welfare science experiments. The experience has also been evaluated by the Ethics Committee of Animal Experiments Commission Nankai University t. Four-week-old female BALB / c were naked folic Acid deficiency Chow w Fed during the entire experimental period. HeLa tumor models were generated by subcutaneous injection of HeLa cells in DMEM 5106 in the left bar of each mouse. When tumor volume reached 50 100 mm 3, the Mice were divided into three groups. Two groups of M nozzles Were with 200 ml of DOX or 1/2/DOX/GO injected via the tail vein every four days. The doses were set to 1 mgkg1 DOX. The tumor volumes were measured using a caliper every 4 d and using the following formula: v0.52. The relative tumor volume were calculated as V/V0. Statistical analysis was performed using the Student t test. Differences were considered statistically significant when the P value was 0.0 and keeps the cells of lung cancer when these cancer cells that are resistant to doxorubicin, have been selected. Furthermore, inhibited the epidermal growth factor f is the expression of the TG2 Promotes apoptosis by doxorubicin in breast cancer cells induced.
Au inhibits Addition, the suppression of expression by siRNA-mediated fibronectin TG2 sion Zelladh And survival of the cell in doxorubicin-resistant cells. These observations suggest that the protein level of TG2 plays a role, increases ht The survival of cancer cells treated with doxorubicin. Doxorubicin oxygen free radicals generated, and a previous study showed that latent TG2 is activated in altretamine response to oxidative stress. Thus, we assumed that activation of TG2 doxorubicin may be a prerequisite for the survival of cancer cells under conditions doxorubicintreatment. In this study, we found that doxorubicin induces sustained activation of TG2 by at least three different signaling pathways and that the sustained activity of t Of TG2 is essential for the survival of doxorubicin-treated cells. Materials and Methods Cell culture and treatment of wild-type and TG2 null mouse embryo.