Objective To investigate the expression of presenilin-2(PS2) and glutathione S transferase π(GSTπ) and their role in the prognosis and therapy of infiltrating ductal breast carcinoma. Methods The expression of PS2 and GSTπ in tumor tissues from 210 patients with infiltrating ductal breast carcinoma confirmed by pathologic examination and treated with modified radical mastectomy was examined by using LSAB immunohistochemical method. Results The expression rate of PS2 was 49.5%(104/210) and the expression rate of GSTπ was 48.1%(101/210). The grade of the postoperative 5-year survival rate and 10-year survival rate in four groups of 210 patients, from high to low, was the group 1 (PS2 positive expression/GSTπ negative expression), the group 2 (PS2 positive expression/GSTπ positive expression), the group 3 (PS2 negative expression/GSTπ negative expression) and the group 4 (PS2 negative expression/GSTπ positive expression). Conclusion The prognosis of the group 1 is the best, the group 2 better, the group 3 good and the group 4 the worst. The results suggest that reasonable use of endocrinotherapy and chemotherapy in infiltrating ductal breast carcinoma is necessary.
Objective To study the protective effect of glutamine on the intestinal mucosal antioxidation in endotoxemic rats. Methods Twenty-eight male Wistar rats were randomly divided into three groups, group A:parenteral nutrition supplemented with glutamine, group B:TPN without glutamine,and group C:normal control. Endotoxemia was induced by continous intravenous infusion of lipopolysaccharide(LPS) at a dose of 2 mg/kg per day throughout the 5-day study period. The mucosal protein、DNA、ATP、SOD、MDA、GSH、sIgA were determined. Results The mucosal protein、DNA、ATP、SOD、GSH and sIgA content in endotoxic rats were markedly decreased, MDA was increased as compared with normal control(P＜0.05). The former indices in group A were improved and MDA content was decreased as compared with group B(P＜0.05). Conclusion Glutamine can improve gut energy metabolism, decrease the extent of mucosal injury of free radicals, and give an protective effect on the mucosal probably by increasing GSH.
Objective To investigate the effects of glutathione (GSH) on survival of the random skin flap in rats and the probable mechanism that contribute to this effect. Methods Twenty SD rats with 200-250 g in weight, were randomly divided into the experimental group and control group(n=10). Random flap of 8 cm×2 cm in size was made on the back of each rat with the pedicel on the angular of the scapular. GSH(250 mg/kg) and NS of the same dose were injected into the abdominal cavity of rats in the experimental groupand the control group immediately after the operative, 1st and 2nd days respectively. The rats were killed on the 7th day after the operation. The tissue pathology, the survival rate of the flap, the superoxide dismutase(SOD) activity and malonyldialdehyde (MDA) level were compared between two groups. Results The mean survival rate of the flap on the 7th day in the experimental group（56.77%±10.67%） was higher than that in the control group(40.16%±7.12%)(Plt;0.05).SOD activity in experimental group （306.06±84.87 U/mgprot）was higher than that in the control group （224.79±27.12 U/mgprot）, while MDA level （3.835±0.457 nmol/mgprot）was lower than that in the control group (6.127±0.837 nmol/mgprot)(Plt;0.05). Histological observation showed that the neutrophil infiltration was less in experimental group than that in the control group; that the experimental group was surperior to the control group in angiogenesis, fibroblasts, fair cells and cuaneous gland. Conclusion The intraperitoneal use of GSH may promote the survival rate of the random flaps and the possible mechanism for improvement may lies in that the GSH can reduce the level of oxygen free radical and lipidperoxidation,and lessen neutrophil infiltration.
PURPOSE: To probe the effect of taurine on lipid peroxidation,surperoxide dismutase(SOD) and glutathione peroxidase(GSH-Px)in retina in vitro. METHODS: The animal eye cups were put into media(divided into four groups:control,model,taurine and beta;-carotene) respectively,and incubated at 37deg;C in a humidified atmosphere of 5% CO2/95% air. After 24h or 48h ,the retinas were taken out from the media and the SOD,GSH-Px ,protein and malondialdehyde(MDA) were examined. RESULTS:Taurine could inhibite lipid peroxidation in retina ,decrease MDA level ,could not protect GSH-Px activity in retina. The effect of taurine on SOD activity in retina was also uncertain. CONCLUSION:Taurine can inhibit lipid peroxidation in retina in vitro,but the mechanism of that has nothing to do with the effect of taurine on SOD activity and GSH-Px activity. （Chin J Ocul Fundus Dis,1996,12: 183-185 ）
Objective To evaluate the effectiveness and safety of reduced glutathione in the treatment of acute renal failure. Methods Twenty-three patients with acute renal failure were divided into the treatment group (n=10) and the control group (n=13) by simple randomisation. Patients in the treatment group received intravenous reduced glutathione 1200 mg daily. Patients in the control group were not treated with reduced glutathione. The therapeutic course for both groups was 4 weeks. Serum creatinine and urea nitrogen were determined before treatment as well as at the end of each of the 4 weeks. Proximal and distal renal tubular functions were evaluated at the end of the treatment. The time when clinical symptoms were improved was recorded and adverse drug reactions were monitored. Results The durations of nausea and vomiting as well as the oliguria stage were shorter in the treatment group than in the control group. The serum creatinine level in the treatment group decreased more markedly than that in the control group. At the end of the treatment, the renal tubular function was better in the treatment group than in the control group. Conclusion Reduced glutathione contributes to the early recovery of renal function in patients with acute renal failure. However, more high-quality and large-scale randomized controlled trials are needed.
ObjectiveTo evaluate the effect of ZnPP Ⅸ on the expressions of heme oxygenase-1 (HO-1) and glutathione-Stransferase-π （GST-π） and the chemosensitivity of drug-resistant hepatic carcinoma cell line Bel/Fu, and explore it’s possibility to reverse drug-resistance and the relevant regulating mechanism. Methods①MTT assay was adopted to detect the drug sensitivity for adriamycin, mitomycin, and 5-fluorouracil of Bel/Fu cell after ZnPP Ⅸ being induced for 24 h. ②RTPCR was carried out to detect the expressions of HO-1 and GST-π mRNA after Bel/FU cells being treated with different concentrations ZnPP Ⅸ for 24 h. ResultsAfter Bel/Fu cells being treated with ZnPP Ⅸ for 24 h, the 50% inhibiting concentration (IC50) for drugs was decreased dramatically （Plt;0.05）. Meanwhile, the expressions of HO-1 and GST-π mRNA in the treated cells also decreased dose-dependently (Plt;0.01). ConclusionsZnPP Ⅸ can increase the chemosensitivity of Bel/FU cells by down-regulation of HO-1 and GST-π expression. ZnPP Ⅸ is a potential agent to reverse multidrug resistance of hepatic carcinoma cells.
ObjectiveTo study the effect of rotenone on rat substantia nigra dopamine (DA) in the nervous system and oxidative stress parameters (malondialdehyde and glutathione), the influence of rotenone on DA neurons toxic effect and its pathogenesis. MethodsThis study applied back subcutaneous injection of rotenone in rats [1.0 mg/(kg·d)], and used immunocytochemistry technique to detect changes in the expression of tyrosine kinase (TH) in 10 rats of the control group and 10 rats of the experimental group. Spectrophotometry was used to detect the change of oxidative stress parameters in rats (malondialdehyde and glutathione). ResultsDA neurons in rats had various degrees of damage. The TH immune response strength of rats in the substantia nigra and striatum decreased significantly. The number of immune response nigra TH positive neurons was significantly less in the experimental group than in the control group (P< 0.01). Spectrophotometer method was used to detect the midbrain nigra of glutathione, which was significantly less in the experimental group than in the control group (P<0.01). Malondialdehyde in the experimental group was significantly higher (P<0.01). ConclusionRotenone has obvious neurotoxicity, and can lead to the damage of DA neurons and obvious oxidative stress injury in rats, which provides an experimental basis for the pathogenesis of Parkinson's disease, and at the same time provides new targets for the treatment.
Objective To investigate the effects of glutathione S-transferase M5 (GSTM5) on the inflammation in human bronchial epithelial 16HBE cells and its possible molecular mechanisms. Methods Acute lung injury cell model was constructed with 16HBE cells induced by tumour necrosis factorα (TNF-α, 10 ng/mL). The cells were devided into a control group, a TNF-α group (TNF-α), a GSTM5 group (GSTM5+TNF-α), a negative control group (negative control plasmid+TNF-α). GSTM5-GFP plasmid and negative control plasmid were respectively transfected to the cells of the GSTM5 group and the negative control group using Lipofectamine2000. The contents of interleukin-6(IL-6), IL-8, IL-10 in the cell supernatant were measured by ELISA.The expression of nuclear factor-κB (NF-κB) mRNA was detected by RT-PCR, and the expression of NF-κB, phospho-NF-κB, p38, phospho-p38 protein were detected by Western blot. Results The GSTM5-GFP eukaryotic expression vector was successfully constructed and transfected successfully confirmed by fluorescence microscope. The contents of IL-6, IL-8, IL-10 in the TNF-α-induced cell supernatant were significantly higher than those in the control group(P < 0.05), and the contents of IL-6, IL-8, IL-10 in the GSTM5 group were lower than those in the TNF-α group (P < 0.05)with statistically significant difference. At the same time, the total NF-κB mRNA, phospho -NF-κB and phospho-p38 protein were increased in TNF-α stimulated cells compared with the control group (P < 0.05), while the GSTM5 group was lower than that in the TNF-α group and the negative control group (P < 0.05). Conclusion Overexpression of GSTM5 inhibits the phosphorylation of p38MAPK and NF-κB and down-regulates the inflammation of TNF-α-induced human bronchial epithelial 16HBE cells.
ObjectiveTo systematically review the association between glutathione S-transferase pi (GSTP1) Ile105Val (A/G) and the risk of cutaneous melanoma. MethodWe searched PubMed, EMbase, CNKI and WanFang Data to identify case-control studies which investigated the association between GSPT1 Ile105Val (A/G) polymorphism and the risk of cutaneous melanoma from their inception to June 31th 2016. Two reviewers independently screened literature, extracted data and assessed the risk of bias of included studies. Then meta-analysis was performed by using RevMan 5.3 software. ResultsA total of 4 case-control studies involving 978 cutaneous melanoma cases and 796 controls were included. The results showed that: the GSPT1 Ile105Val (A/G) polymorphism was significantly associated with the risk of cutaneous melanoma in the dominant model (GG+GA vs. AA: OR=1.22, 95%CI 1.01 to 1.48, P=0.04), but no significant association was found in the recessive model, heterozygote model, and homozygote model (GG vs. CA+AA: OR=1.18, 95%CI 0.86 to 1.60, P=0.30; GA vs. AA: OR=1.20, 95%CI 0.98 to 1.47, P=0.08; GG vs. AA: OR=1.28, 95%CI 0.92 to 1.77, P=0.14). ConclusionCurrent evidence shows, The GSTP1 Ile105Val (A/G) polymorphism is associated with the risk of cutaneous melanoma. Due to limited quantity and quality of the included studies, more high-quality large-scale studies are needed to verify the above conclusion.
ObjectiveTo establish a cell inflammation model induced by tumor necrosis factor-α (TNF-α) in human bronchus epithelial cells, and investigate the effects of glutathione S-transferase mu 5 (GSTM5) on the inflammation and oxidative stress. Methods16HBE cells were treated with TNF-α (10 ng/mL, 24 h) in the absence or presence of the constructed GSTM5 eukaryotic expression vector (1 μg/mL). The concentration of malondialdehyde (MDA) and total antioxidation capacity (T-AOC) were detected by colorimetric method. The survival rate of cells was assessed by the methyl thiazolyl tetrazolium (MTT) assay. The transcription level of NADPH oxidase-1 (NOX1), NOX2, NOX3, NOX4, NOX5, dual oxidase-1 (DUOX1) and DUOX2 were evaluated by RT-PCR. Western blot was performed to investigate the protein levels of NOX1 and NOX2. ResultsTNF-α simulation significantly increased the level of MDA in cells, and decreased the level of T-AOC and survival rate of 16HBE. When transfected with the GSTM5 eukaryotic expression vector, the concentration of MDA significantly decreased (P < 0.05), and the activation of T-AOC increased dramatically (P < 0.05). Consequently, the survival rate of 16HBE in the GSTM5 group improved (P < 0.05). The 16HBE cells transfected with the constructed GSTM5 eukaryotic expression vector had a lower transcription and protein levels of NOX1 and NOX2 (all P < 0.01). There were no significant changes in the mRNA expressions of NOX3, NOX4, NOX5, DUOX1 or DUOX2. ConclusionGSTM5 may down-regulate the transcription level of NOX1 and NOX2 to reduce the inflammation and oxidative stress induced by TNF-α.