Objective To study the role of Cysteine-rich 61 ( Cyr61/CNN1) in repair of combined injury by observing whether exogenous CCN1 promotes the proliferation and migration of radiation-injured L929 cells. Methods A radiation model of L929 cells was induced by ? ray at a dose of 4 Gy. The irradiated L929 cells were cultured in a medium containing 2 ml adenovirus plasmids of CCN1 or RFP at 37 ℃ in an atmosphere containing 5% CO2,which served as a CCN1 group and a RFP group,respectively. Irradiated L929 cells cultured in a blank control medium served as a blank control group. Effects of CCN1 on proliferation and migration of radiation-injured L929 cells were detected by MTT assay,plate colony formation assay,cell cycle analysis,and scratch test of wound healing. Results The proliferation and colony formation rates of L929 cells cultured in a medium containing CCN1 were significantly higher than in RFP and control groups [colony formation rate:( 34. 4 ?3. 6) % vs ( 24. 5 ?2. 9) % and ( 29. 5 ?3. 5) %,P

Objective To observe the effects of radiation on the growth and expression of cysteine-rich 61(Cyr61/CCN1) of L929 cells and investigate the relationship between CCN1 expression and radiation injury.Methods L929 cells were cultured and divided into 2 groups,cells irradiated with 4 Gy ?-irradiation as radio-group and untreated cells as control group.The cell proliferation was measured by MTT assay and plate colony formation testing.Flow cytometry was utilized to quantify the cell cycle distribution.CCN1 expression at protein and mRNA levels were determined by immunocytochemistry(ICC) and RT-PCR respectively.Results Significant inhibition of proliferation(P

Objective:To investigate the relationship between mitogen-activated protein kinase (MAPK) signaling pathway related signal molecules and the apoptosis of acute promyelocytic leukemia NB4 cells induced by puerariae radix flavones (PRF) and its significance.Methods:The cells were divided into control group [0.025% dimethyl sulfoxide (DMSO) to replace PRF] and 10, 30, 50 μg/ml PRF groups. The proliferation inhibition rate of NB4 cells exposed with PRF for 24, 48 and 72 hours was determined by methyl thiazolyl tetrazolium (MTT) method, and the nuclear morphology was determined by confocal laser scanning microscope after 48 hours. NB4 cells were divided into control group (adding 0.025% DMSO) and 10, 30 and 50 μg/ml PRF with or without 10 μmol/L c-Jun N-terminal kinase (JNK) inhibitor (SP600125) group, and the cells were treated for 48 hours and the changes in the expressions of MAPK pathway related proteins JNK, tumor necrosis factor α (TNF-α), extracellular signal-regulated kinase (ERK) and p38 MAPK were tested by Western blot.Results:10, 30 and 50 μg/ml PRF inhibited the proliferation of NB4 cells in 24, 48 and 72 hours, which was in time- and dose-dependent manners (all P < 0.05). The half-maximal inhibitory concentration (IC 50) at 24, 48 and 72 hours were (40.03±2.23) μg/ml, (22.92±1.72) μg/ml and (17.99±1.48) μg/ml, respectively. The confocal laser scanning microscope showed that NB4 cells displayed distinct apoptotic characteristics after PRF treatment. After co-cultivating NB4 cells with 10 μmol/L SP600125 and different concentrations of PRF for 48 hours, the expression of JNK1 in NB4 cells was suppressed ( P < 0.05), and the expressions of JNK2/3 and p38 MAPK decreased, but the differences were not statistically significant (both P > 0.05). The expressions of ERK1 and ERK2 gradually increased in the single-drug group, while the expression in the combined drug group decreased. The expression of TNF-α in the 50 μg/ml PRF+SP600125 group was down-regulated compared with the 50 μg/ml PRF single-drug group, while the expressions in the 10 and 30 μg/ml PRF+SP600125 groups were up-regulated compared with the 10 and 30 μg/ml PRF single-drug groups. Conclusion:10-50 μg/ml PRF may activate the MAPK signaling pathway through TNF-α. JNK, ERK1/2 and p38 MAPK interact with each other to activate pro-apoptotic related proteins and induce NB4 cells apoptosis.

Anemia, Aplastic ; drug therapy ; immunology ; Animals ; Antilymphocyte Serum ; immunology ; therapeutic use ; Calcineurin Inhibitors ; immunology ; therapeutic use ; Humans ; Immunoglobulins ; immunology ; therapeutic use ; Lymphocytes ; drug effects ; immunology ; Swine

Adult ; Female ; Humans ; Male ; Middle Aged ; Precursor Cell Lymphoblastic Leukemia-Lymphoma ; drug therapy ; Rhabdomyolysis ; chemically induced ; diagnosis ; Vindesine ; adverse effects ; therapeutic use