The aim of the study is to explore the effectiveness of radical gastrectomy with modified gastric bypass surgery in treating gastric cancer patients with type 2 diabetes mellitus (T2DM). A total of 93 patients with gastric cancer and T2DM were treated in our hospital and enrolled in this study. Patients in group A (n = 30) had a body mass index (BMI) of >28 kg/m(2). Radical total gastrectomy and modified esophagojejunal Roux-en-y anastomosis were performed on 13 patients, and radical distal subtotal gastrectomy and gastric remnant jejunal Roux-en-y anastomosis were performed on 17 patients. The data from groups B, C, and D were derived from 63 patients with gastric cancer and diabetes who were admitted to our hospital from January 2005 to July 2012. All patients underwent radical gastrectomy (including 21 cases of gastric cancer surgery with Billroth I anastomosis, 25 cases of radical gastrectomy with Roux-en-Y anastomosis and BMI >28 kg/m(2), and 17 cases with BMI <28 kg/m(2)). The BMI, fasting blood glucose (FBG), meal after the 2-hour glucose (2 h PBG), C-peptide (C-P), and glycosylated hemoglobin (HbAIC) data were collected before and 6 and 12 months after surgery. In groups A and D, BMI, FBG, 2 h PBG, C-P, and HbAIC at the 6th and 12th post-operative months were significantly lower than those before the surgery. In group B, BMI, FBG, 2 h PBG, C-P, and HbAIC at the 6th and 12th post-operative months did not decrease significantly, when compared with the pre-operative levels. In group C, BMI, FBG, 2 h PBG, C-P, and HbAIC at the 6th and 12th post-operative months decreased but showed no statistical significance. However, in comparison, groups A C showed significant differences after the surgeries. Radical gastrectomy combined with modified gastric bypass surgery is effective in treating patients with gastric cancer with type 2 diabetes, although this requires further investigation.
Abstract. There is growing evidence indicating that autophagy plays a protective role in liver ischemia/reperfusion (IR) injury. Heme oxygenase-1 (HO-1) can also prevent liver IR injury by limiting inflammation and inducing an anti-apoptotic response. Autophagy also plays a crucial role in liver IR injury. The aim of the present study was to investigate the role of HO-1 in liver IR injury and the association between HO-1, autophagy and apoptotic pathways. IR simulation was performed using buffalo rat liver (BRL) cells, and HO-1 activity was either induced by hemin (HIR group) or inhibited by zinc protoporphyrin (ZnPP) (ZIR group). In the HIR and ZIR group, the expression of HO-1 and autophagy-related genes [light chain 3-Ⅱ (LC3-Ⅱ)] was assessed by RT-qPCR and the protein expression of caspases, autophagy-related genes and genes associated with apoptotic pathways (Bax) was detected by western blot anlaysis. The results of RT-PCR revealed the genetically decreased expression of HO-1 and autophagy-related genes in the ZIR group. Similar results were obtained by western blot analysis and immunofluorescence. An ultrastructural analysis revealed a lower number of autophagosomes in the ZIR group; in the HIR group, the number of autophagosomes was increased. The expression of Bax and cytosolic cytochrome c was increased, while that of Bcl-2 was decreased following treatment of the cells with ZnPP prior to IR simulation; the oppostie occurred in the HIR group. Cleaved caspase-3, caspase-9 and poly(ADPribose) polymerase (PARP) protein were activated in the IR and ZIR groups. The disruption of mitochondrial membrane potential was also observed in the ZIR group. In general, the downregulation of HO-1 reduced autophagy and activated the mitochondrial apoptotic pathway.
Abstract. The aim of the present study was to investigate the association between the mitogen-activated protein kinase (MAPK) signal transduction pathway and multidrug resistance in hepatocellular carcinoma cells. A Cell Counting Kit-8 assay was used to determine the drug sensitivity of HepG2 and HepG2/ADM hepatocellular carcinoma cell lines in combination with the MAPK/extracellular-signal-regulated kinase kinase (MEK) inhibitor U0126. Flow cytometry was used to analyze the rate of apoptosis. The reverse transcription-quantitative polymerase chain reaction (RT-qPCR) was used to determine P-glycoprotein (P-gp) and multidrug resistance-associated protein 1 (MRP1) mRNA expression following treatment with various concentrations of U0126. P-gp and MRP1 expression levels were measured using Western blot analysis. The half-maximal inhibitory concentration was markedly decreased in combination with U0126. RT-qPCR results demonstrated that the expression of multidrug resistance 1 (MDR1) and MRP1 in HepG2/ADM cells was increased 5.37-and 6-14-fold compared with that in HepG2 cells. Furthermore, the expression levels in HepG2/ADM cells were decreased following U0126 treatment in a dose-dependent manner. The expression of P-gp and MRP1 in HepG2/ADM cells was increased 2.68-and 2.76-fold compared with that in HepG2 cells. Furthermore, the expression levels in HepG/ADM cells were decreased following U0126 treatment in a dose-dependent manner. The results of the present study indicate that the MEK inhibitor U0126 enhances sensitivity to chemotherapeutic drugs by downregulating P-gp and MRP1 expression in resistant hepatocellular carcinoma cells. The combination of MEK inhibitor and conventional chemotherapeutic drugs may provide novel therapeutic prospects for the treatment of drug-resistant hepatocellular carcinoma.
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