Purpose:To study the reversal effects on multidrug resistance in multidrug-resistent bladder cell lines BIU-87/ADM. Methods:The degree of drug-resistence was detected by MTTmethod; the concentration of ADM in cells BIU-87 and BIU-87/ADM was detected after the cells were treated by carvedilol and ADM. Results:Pretreatment by carvedilol increased the concentration of ADM in BIU-87/ADM cells, ,and the concentration was much higher than that in those cells treated by ADM only. Conclusions:Carvedilol can enhance the cytotoxic effect of ADM,and can reverse the multidrug resistance in bladder cancer lines BIU-87/ADM.

Purpose:To study the expression of TopoⅡ gene in multidrug resistant cells of human bladder cancer. Methods:The degree of drug resistance was detected by MTT method ;the expression of TopoⅡ gene in cell lines BIU 87/ADM and BIU 87 was detected with reverse transcriptase polymerase chain reaction. Results:The cell lines BIU 87/ADM were 56.4 times more resistant to ADM than the cell lines BIU 87;the expression of TopoⅡ gene was poorly positive in BIU 87/ADM but strongly positive in BIU 87 cells. Conclusions: The decreased expression of TopoⅡ gene in BIU 87/ADM cells might contribute to the development of multidrug resistance of human bladder cancer.

AIM: The aim of this study was to determine the relationship between PAI-1,TIMP-1 gene expression and renal tubulointerstitial fibrosis(TIF) of ureteral obstruction ,and the interfering effects of hepatocyte growth factor (HGF) treatment. METHODS: Sixty rats were divided into normal control, sham operation,unilateral ureteral obstruction(UUO),and rhHGF treated groups (received 0 5 mg?kg -1 ?d -1 HGF for twenty-one days), and were sacrificed at postoperative day 3, 7, 14, 21. The levels of PAI-1, TIMP-1 mRNA were measured by RT-PCR. MMP2 and MMP9 activities were detected by substrate zymography, and renal fibrosis was assessed by measuring tissue hydroxyproline. RESULTS: Compared to controls, expression levels of PAI-1,TIMP-1 mRNA were significantly increased in UUO rats, and this was accompanied by decreased activities of MMP2 and MMP9 and increase in tissue hydroxyproline content. HGF treatment significantly decreased expressions of PAI-1, TIMP-1 mRNA, increased MMP2 and MMP9 activities,and decreased tissue hydroxyproline content in the obstructive kidney. CONCLUSIONS: These results indicate that the increases in PAI-1, TIMP-1 mRNA expression may be the major cause of sustained decreased matrix degradation during the development of tubulointerstitial fibrosis after unilateral ureteral obstruction. rhHGF efficiently ameliorates renal tubulointerstitial injury by the reduction of PAI-1,TIMP-1 mRNA expression, and increasing MMP2, MMP9 activities. [

Objective To investigate the association between multi-drug resistant 1 (MDR1) gene C3435T and T129C polymorphism with refractory epilepsy in children. Methods A total of 260 children including 60 refractory epilepsy, 100 drug-responsive epilepsy, and 100 healthy children were enrolled. The genotypes for MDR1 polymorphisms were determined by polymerase chain reaction-restriction fragment length polymorphism analysis.The distribution of genotypes and allele frequencies of the three groups were compared. Results The distribution of TT/TC/CC genotypes and T/C allele frequencies of C3435T showed no signiifcant difference between drug-resistant patients and drug-responsive patients or normal control group (P>0.05). Drug-resistant patients were more likely to have the TC genotype and the C allele at T129C when compared with the drug-responsive patients and the normal control group (P<0.05). Conclusions T129C polymorphism of the MDR1 gene was associated with refractory epilepsy in children.

Recent studies have suggested that long-term application of anti-angiogenic drugs may impair oral mucosal wound healing. This study investigated the effect of sunitinib on oral mucosal healing impairment in mice and the therapeutic potential of Bifidobacterium breve (B. breve). A mouse hard palate mucosal defect model was used to investigate the influence of sunitinib and/or zoledronate on wound healing. The volume and density of the bone under the mucosal defect were assessed by micro-computed tomography (micro-CT). Inflammatory factors were detected by protein microarray analysis and enzyme-linked immunosorbent assay (ELISA). The senescence and biological functions were tested in oral mucosal stem cells (OMSCs) treated with sunitinib. Ligated loop experiments were used to investigate the effect of oral B. breve. Neutralizing antibody for interleukin-10 (IL-10) was used to prove the critical role of IL-10 in the pro-healing process derived from B. breve. Results showed that sunitinib caused oral mucosal wound healing impairment in mice. In vitro, sunitinib induced cellular senescence in OMSCs and affected biological functions such as proliferation, migration, and differentiation. Oral administration of B. breve reduced oral mucosal inflammation and promoted wound healing via intestinal dendritic cells (DCs)-derived IL-10. IL-10 reversed cellular senescence caused by sunitinib in OMSCs, and IL-10 neutralizing antibody blocked the ameliorative effect of B. breve on oral mucosal wound healing under sunitinib treatment conditions. In conclusion, sunitinib induces cellular senescence in OMSCs and causes oral mucosal wound healing impairment and oral administration of B. breve could improve wound healing impairment via intestinal DCs-derived IL-10.
Animals ; Mice ; Interleukin-10 ; Bifidobacterium breve ; Up-Regulation ; Angiogenesis Inhibitors ; Sunitinib ; X-Ray Microtomography ; Administration, Oral ; Wound Healing ; Antibodies, Neutralizing