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Objective To explore the antioxidant mechanism ofhistone deacetylase 2 (HDAC2) regulating Nrf 2 acetylation in lipopolysaccharide (LPS)-induced type Ⅱ alveolar epithelial cell injury.Methods The experiment was divided into two parts.The first part was the routine culture of type Ⅱ alveolar epithelial cells of mice.The cells were stimulated with different concentrations of LPS (10 ng/ mL,100 ng/mL and 1 000 ng/mL).CCK-8 was used to detect the cell activity at 0 h,6 h,12 h,24 h and 48 h,respectively.The second part:Alveolar epithelial cells of type Ⅱ were cultured and divided into the normal control group (control group),LPS group,HDAC2 lentivirus interference group (siRNA-HDAC2 group) and HDAC2 lentivirus overexpression group (LV-HDAC2 group).The expression of HDAC2 and Nrf2 were detected by Western blot,the acetylation of Nrf2 was detected by immunoprecipitation,and the stability of nrf2 was detected after actinidone action.The activity of superoxide dismutase (SOD) and malondialdehyde (MDA) were detected by chemical colorimetry.SPSS 23.0 statistical software was used.LSD-t test was used for comparison between two groups,and one-way ANOVA test was used for comparison among multiple groups.Results Compared with the control group,the expression of HDAC2 protein in the LPS group increased (t=5.974,P=0.027),the acetylation level of Nrf2 decreased (t=7.223,P=0.002),the Nrf2 protein level increased (t=2.929,P=0.043),the protein stability of Nrf2 increased,the SOD activity decreased (t=121,P＜0.01),and the MDA content increased (t=10.45,P=0.000 5).Compared with the LPS group,Nrf2 acetylation level decreased in the LV-HDAC2 group (t=1 1.29,P=0.000 4),Nrf2 protein expression increased (t=3.194,P=0.033),Nrf2 protein stability increased,SOD activity increased (t=4.678,P=0.009),and MDA content decreased in the LV-HDAC2 group (t=5.417,P=0.005 6).While the opposite trend was observed in the siRNA-HDAC2 group.Conclusion After LPS stimulation,oxidative stress of type Ⅱ alveolar epithelial cells was aggravated.HDAC2 could decrease the level of Nrf2 acetylation,increase the expression of Nrf2 protein,and alleviate LPS-induced oxidative stress.
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Objecitive Under the fluorescent microscope ,we used fluorescein sodium fluorescence to determine glioma boundary ,thus gliomas removed through surgery more thoroughly .Mtehods We randomly se-lected 14 patients who were admitted in the First Hospital of JiLin University as the research objects ,patients with glioma were diagnosed as glioma according to the physical signs ,physical examination a,nd imaging findings before surgery.Diagnosed with glioma,intraoperative application of fluorescein sodium yellow fluorescence was deter -mined the tumor boundary ,and removal of the tumor ,according to the fluorescence intensity strength is different . The pathological diagnosis was to determine the boundary of fluorescent was accurate .Postoperative examined MRI was performed in order to make clear the excision of the tumor ,and the neurological condition of postoperative was observed.Results Glioma could be inspired by yellow fluorescence under fluorescent microscope .The normal brain tissue was not light .Postoperative pathological results showed that the fluorescent yellow area contained a lot of glioma cells,pale yellow fluorescence area found a small amount of glioma cells .Postoperative enhanced MRI scan had confirmed that application of fluorescein sodium could be more thoroughly resection of glioma ,postopera-tive dysfunction was reduced .Conclusion This method is prior to tumor boundary observasion without fluoresent staining and reducing the recurrence of the tumor and reducing the normal brain tissue damage ,and therefore,im-proving the quality of postoperative survival of patients .
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Objective To investigate the alteration of chaperonine hsp40 and its influence on delayed death of neurons in the CA1 region of hippocampus after transient cerebral ischemia. Method After transient global ischemia for 20 minutes, rat model was made. Following different lengths of reperfusion, all the 28 wistar rats were divided into sham-operation group,4 hour recovery group, 24 hour recovery group and 72 hour recovery group ( n = 7 rats in each group). Immunochemistry and laser scanning confocal microscopy were used to observe the distributional alteration of hsp40 in the neurons. Differential centrifuge and western blot assay were used to analyze the quantitative alteration of hsp40 and its redistribution in the neurons. Results Immunochemistry and laser scanning confocal microscopy showed the progressive reduction of hsp40 occurred at first in the cytosol, then in the nucleus until the death of all the neurons in the CA1 region died. Differential centrifuge and western blot assay showed the level of hsp40 decreased from 1.00 ± 0.21 to 0.23 ± 0.13 ( P ＜ 0.01 ) 24 hours after reperfusion; the quantity of hsp40 in the protein aggregates increased from 1.00±0.18 to 8.61 ± 1.89 (P ＜0.01 =24 h after reperfusion.Conclusions The reduction of hsp40 in the neurons of hippocampus CA1 region is an important role in protein aggregates formation.
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Objective To investigate the alteration of chaperone hsp40 and its effects on the dealyed neuron death in the CAI neurons after transient cerebral ischemia.Method Twenty-minute transient global ischemia rat model was used.Following different repeffusion period,all the 28 wistar rats were divided into sham-operation group ,4-hour recovery group,24-honr recovery group and 72-hour recovery gronp,7 ratsin in each group,Immunochemistry and laser scanning confocal microscopy were used to observe the distributional alteration of hsp40 in the neurons.Differential centrifuge and westemblot analysis were used to analyze the quantitative alteration of hsp40 and its redistribution in the neurons.Results lnanunechemistry and laser scanning confocal microscopy showedthe reduction of hsp40 first in cytosol,then in the nucleus until all the neurons in the CAI region died.Differential centrifuge and westemblot analysis showed the quantity of hsp40 decreased from (1.00_+0.21) to (0.23±0.13)(P<0.01) after 24-hour repeffusion;the quantity of hsp40 in the protein aggregates increased from (1.00±0.18) to(8.61±1.89)(P<0.01) after24-hour reperfusion.Conclusions The reduction of hsp40 in the neurons of hippocampus CA1 region is an important factor resulting in protein aggregates formation.
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Objective To explore the mechanism of ginsenoside-Rh2(G-Rh2) on inhibition of glioma by identifying differential proteins with proteomic technique. Methods The total proteins were extracted from SHG-44 cells treated with 32 ?mol?L-1 G-Rh2 for 72 h and the cells in control group,then were subjected to two-dimensional gel electrophoresis.Only spots with a fold change equal or above 1.5 and P
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Objective To observe the effects of Okinawa Habu apoxin protein-1 (OHAP-1) on the proliferation inhibition of rat C6 glioma cells and its mechanisms. Methods MTT colorimetric analysis was used to measure the inhibitory effect of OHAP-1 with different doses(2.5,5.0,and 10.0 mg?L-1) on C6 glioma cells .RT-PCR was used to evaluate the mRNA expressions of bcl-2 and bax genes.The activity of superoxide dismutase (SOD) and the level of maleicdialdehyde (MDA) in the C6 glioma cells were also examined. Results The proliferation of C6 glioma cells was significantly inhibited by different doses of OHAP-1(2.5,5.0,and 10.0 mg?L-1).The inhibitory rate were 49.77%,67.65%,and 76.42%,respectively.The inhibitory rate in 2.5,5.0, and 10.0 mg?L-1 groups were higher than that in control group(P
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Objective To investigate the possibility and mechanism of ~ 125 I in treatment of glioma. Methods SHG-44 glioma cells were cultivated in vitro, the inhibitory effect of ~ 125 I on SHG-44 cell proliferation was determined by MTT method. The stereotactic method was used to establish the rat intracranial glioma model. The MRI was performed at 1st week after implantation and ~ 125 I was implanted in the glioma area, the MRI was performed to measure the diameter of tumor 2 weeks after implantation. The rats were killed after 2 weeks ,PCNA gene experession was determined with immunohistological method both in control and experiment group.Results one week after implantation the glioma grew,the results of MTT method showed the growth of the SHG-44 was inhibited, ~ 125 I inhibited the expression of PCNA gene and enlonged the rat survival period. Conclusion ~ 125 I can inhibit the growth of glioma ,the mechanism may be concerned with its inhibitory effect on PCNA gene expression.
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Objective To compare the inhibitory effects of ginsenoside-Rh_2,elemene and adriamycin(AMD) on glioma cells cultivated in vitro.Methods MTT was used to detect the inhibitory effects of ginsenoside-Rh_2,elemene and AMD on glioma cell lines(C6,SHg-44,U251).The survival rate-time curves were established.The abilities of three drugs to induce apoptosis of three cells lines were determined by flow cytometry.(Results The) inhibitory effects of the three drugs on the growth of C6,SHg-44 and U-251 were dose-dependent and could be enhanced with dose increasing.The inhibitory effects of Rh_2 was stronger than that of AMD and elemene on three glioma cell lines.The inhibitory concentration of Rh_2 on three cell lines was significantly lower than that of AMD and elemene(P
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Objective To study the effects of quercetin(QUE) on proliferation of rat glioma C6 cell line in vitro.Methods The cells were divided into 5 treatment groups(10,25,50,75 and 100 ?mol?L~(-1) QUE),blank control and menstruum control group.The rat C6 cells were cultivated to 1?10~6?mL~(-1) in the RPMI 1640 medium,then added into 96 holes board with various doses of QUE by 3 holes per group,and MTT assay was used to observe the proliferation of the cells treated for 24,48 and 72 h.The change of cell cycle was also observed by flow cytometry(FCM) after the cells were treated with 50 and 100 ?mol?L~(-1) QUE for 48 h.The changes of the protein P53 and Bcl-2 of C6 cells treated with 50 ?mol?L~(-1) QUE for 48 h were detected by immunocytochemical methods.(Results With) the augmentation of QUE and the extension of the treated time,the C6 cell growth was inhibited,the A values decreased and the cell number in G_0/G_l phase was increased,the cell numbers in S and G_2/M phases were cut down,and the decreased expression of Bcl-2 protein and the increased expression of P53 protein were also observed after treatment with QUE.Conclusion Inhibitory effect of QUE on C6 cell line is proved to be dependent on the treated time of the drug and the dose of QUE,and the induced apoptosis of C6 cells is implemented by the means of up-regulation of P53 protein expression and down-regulation of Bcl-2 protein expression.
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<p><b>OBJECTIVE</b>To describe the transvenous catheterization technique for the treatment of cavernous sinus dural arteriovenous fistulas (CSdAVFs), including its indications, complications and efficacy.</p><p><b>METHODS</b>Eight patients with symptomatic CSdAVFs were treated by endovascular embolization with platinum coils, via the inferior petrosal sinus (IPS) in 6 patients, and via the Sylvian vein after surgical exposure in other 2 patients.</p><p><b>RESULTS</b>Complete angiographic resolution of the fistula was obtained in six patients immediately after the procedures, and a complete resolution of symptoms and signs was achieved in all patients. The residual fistulas in two patients disappeared completely in the follow-up angiography.</p><p><b>CONCLUSION</b>Transvenous embolization is a useful and safe approach in the management of CSdAVFs.</p>
Subject(s)
Aged , Aged, 80 and over , Female , Humans , Middle Aged , Cavernous Sinus , Congenital Abnormalities , Central Nervous System Vascular Malformations , Diagnostic Imaging , Therapeutics , Cerebral Angiography , Embolization, Therapeutic , MethodsABSTRACT
Objective To explore the CT and MR imaging characteristics of intracranial melanomas. Methods CT and MRI characteristics in five patients admitted to our hospital from June 1993 to June 2000 and diagnosed as intracranial melanomas were retrospectively analyzed. Results There were two cases of primary melanoma and three cases of secondary melanoma. All the cases were examined by CT. The lesions presented as high density in 4 cases, and low density in only 1 case. Four cases were examined by MRI. Short T 1 and short T 2 signals were found in 3 cases, and slightly long T 1 and short T 2 signal was found in 1 case. Conclusion There are some special characteristics of melanomas on the MR imaging, which are helpful to ensure the diagnosis and distinguish the primary melanomas from secondary melanomas.