ABSTRACT
Objective To evaluate the short-term efficacy and quality of life of primary hepatocellular carcinoma patients after radiotherapy and pregabalin treatment for neuropathic pain with bone metastasis. Methods 32 patients with primary hepatocellular carcinoma bone metastases were treated with radiotherapy combined with pregabalin treatment.Then, we prospectively studied the analgesic efficacy for neuropathic pain and quality of life, used the brief pain inventory and douleur neuropathique 4 questionnaire (DN4) to evaluate pain at baseline, one and two months after radiotherapy, assessed pain response using the international consensus endpoint definition of bone metastasis, and used European Organization for Research and Treatment of Cancer Research and Treatment Quality of Life Questionnaire (EORTC QLQ-C30) and bone metastasis module (QLQ-BM22) for quality of life assessment. Results One and two months after radiotherapy, the average DN4 score of neuropathic pain decreased, and the objective pain relief rates were 62.8% and 68.6%, respectively.The physical, emotional, social, and role functional scores of EORTC QLQ-C30 functional scale significantly increased in the first month after radiotherapy.Symptom scale of pain (P=0.015), insomnia (P=0.035), and loss of appetite (P=0.022) improved, and fatigue was aggravated (P < 0.05).Two months after radiotherapy, the mean overall health score and all functional scale scores significantly increased than those at baseline.The scores of all symptom scales decreased, except fatigue, constipation, and financial difficulties (P < 0.05).In addition, pain responders showed significant improvement in emotional function (P=0.025) and physical function (P=0.029) in the functional scale and in pain (P=0.014) and fatigue (P=0.035) in the symptom scale.The QLQ-BM22 score showed that the painful sites (P=0.021) and pain characteristics (P=0.04) of the responders significantly improved compared with those of nonresponders two months after radiotherapy. Conclusion Radiotherapy combined with pregabalin can relieve neuropathic pain caused by bone metastasis from primary hepatocellular carcinoma and greatly improve the quality of life, particularly in pain responders.
ABSTRACT
Objective To explore the possible protective effect of hyperbaric oxygen (HBO) on cognitive deficits induced by amyloid β25-35 (Aβ25-35) and neuronal apoptosis in the hippocampi of rats with Alzheimer's disease (AD).Methods The animal AD model was established in 24 Sprague-Dawley rats by bilateral hippocampal injection of Aβ25-35.Twelve rats were injected with normal saline as controls,and another 12 served as normal controls.After the injection,the model rats were further divided into a model group and a treatment group.All the rats were housed with normal feeding for 2 weeks and then those in the treatment groups received a total of 2 courses of HBO treatment (10 days each with an interval of 3 days in between).The other groups were left with no treatment.After the treatment,the rats' learning and memory ability were tested using Morris' water maze test,and any neuronal changes were observed using TUNEL staining.The expression of mRNA and Bcl-2 and Bax proteins in the hippocampus were detected using a RT-PCR and Western blotting.Results HBO significantly improved the learning and memory impairment and alleviated neuronal apoptosis in the hippocampus compared against the control group.In addition,HBO treatment significantly increased the mRNA and protein expression of Bcl-2 and down-regulated the expression of Bax.Conclusion HBO treatment can prevent learning and memory impairment induced by Aβ25-35 peptides,which might be mediated by inhibiting neuronal apoptosis in the hippocampus.
ABSTRACT
Objective To study the role of deleted in liver cancer-1 (DLC-1) gene main domains on the regulation of human colon cancer HT29 cell proliferation.Methods Subcloning recombinant plasmid vectors with Rho GTPase activating protein (RhoGAP),sterile alpha motif (SAM) or steroidogenic acute regulatory-related lipid-transfer (START) domains of DLC-1 gene knockout were constructed and transfected into human colon cancer cell HT29.Wild HT29 cell group (control group),pcDNA3.1-HT29 cell group (vector group) and pcDNA3.1-HT29-DLC-1 cell group (whole DLC-1 gene transfected group) were set as control.The change of cell proliferation was detected by methylthiazolyldiphenyl-tetrazolium bromide (MTT) assay and colony formation test.The cell apoptosis was analyzed by flow cytometry.The activity of RhoA protein was detected by pull-down assay.The differences between the groups were analyzed by the analysis of variance.Results At 48 hours after the successful transfection,compared with control group and vector group,cells proliferation and the activity of RhoA protein were significantly suppressed in whole DLC-1 gene transfected group (F=146.36,698.08,both P＜0.05) and early cell apoptosis increased (F=294.08,P＜0.05).Compared with control group and vector group,there was no significant difference in cell proliferation ability,cell apoptosis and the activity of RhoA protein activity in RhoGAP knockout transfected cells (F=0.99,0.049,5.769,all P＞0.05).Compared with whole DLC-1 gene transfected group,the suppression of cell proliferation was more significant in SAM knockout transfected cells (F=31.00,P＜0.05),the activity of RhoA protein down regulated (F=92.57,P＜0.05) and apoptosis increased (F=130.44,P＜0.05).Compared with whole DLC-1 gene transfected group,the ability of cell proliferation increased (F=15.47,P＜0.05),apoptosis cell decreased (F＝110.23,P＜0.05) and the activity of RhoA protein up regulated (F=199.39,P＜0.05) in START knockout transfected cells.Conclusions The role of DLC-1 gene in the suppression of cell proliferation in HT29 cells was RhoGAP-dependent.SAM domain may be the self suppression domain for endogenous RhoGAP activity.START domain may take effect through enhancing RhoGAP domain.
ABSTRACT
Objective To investigate the effect of hyperbaric oxygen(HBO)combined with 5-fluorouracil (5-FU)chemotherapy on colon carcinoma Lovo cells.Methods Lovo ceils were exposed to 0.20 MPa HBO combined with 5-FU at different concentrations.The cell cycle was monitored with flow cytometry,and cell proliferation was detected using a methylthiazol tetrazolium test(MTT).Results ①After exposure to HBO,phase accumulation of Lovo cells was significantly higher than in the control group,and the accumulation of Lovo cells exposed to HBO after 24 h was significantly higher than at 12 and 48 hours.②There was difference between HBO(0.20 MPa,post 24 h)+ 5-FU(≤8 pM)group and 5-FU(≤8 μM,12 h)group on the inhibition of cells proliferation(P ＜0.05),and significan difference could be seen between the two groups after treatment for 48 h(P ＜ 0.01); ③There was no significant difference between HBO + 5-FU group and 5-FU group treatment with the concentration(16,32,64 μM)of 5-FU(P ＞ 0.05)for 12 h ;however,the difference could be seen after treatment for 48 h between the two groups(P ＜ 0.05).Conclusion The lethal effect on Lovo cells of 5-FU can be enhanced by exposure to 0.20 MPa HBO,especially with low concentrations of 5-FU.
ABSTRACT
Objective To investigate the effects of hyperbaric oxygen (HBO) on the expression of hypoxia inducible factor-1α (HIF-1α) mRNA and vascular endothelial growth factor (VEGF) mRNA in colon adenocarcinoma cells. Methods SW480 colon cancer cells were divided into a control group and an HBO group, which was in turn divided into various subgroups according to the various HBO pressures (0.15 MPa, O. 20 MPa, 0.25 MPa) and exposure times (12, 24 and 36 h) tested. The expression of HIF-1α and VEGF mRNA was evaluated with RT-PCR after the various treatments. Results The expression of HIF-1α mRNA was lower in the SW480 cells than in the controls after exposure to 0.25 MPa HBO for 12 h. No expression of HIF-1α mRNA was detected after exposure to 0.25 MPa HBO for 24 h. The expression of VEGF mRNA was lower after exposure to 0.25 MPa HBO for 36 h than in the controls. Conclusion Absence of HIF-1α mRNA expression and decreased expression of VEGF mRNA in SW480 can be observed after exposure to 0.25 MPa HBO for 24 h, suggesting that HBO may inhibit the formation of tumor blood vessels through down-regulating the expression of these mRNAs.