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Objective@#To explore the clinical value of magnetic resonance T2-mapping imaging in the diagnosis of early intervertebral disc degeneration in obese people.@*Methods@#From January 2018 to June 2019, 30 obese volunteers and 30 healthy volunteers with normal weight underwent T2-mapping scan, while their routine MRI examination showed no abnormalities were slected.The T2 value of nucleus pulposus in both two groups were measured and compared.@*Results@#The T2 values of nucleus pulposus of intervertebral disc of lumbar 1-2, lumbar 2-3, lumbar 3-4, lumbar 4-5 and lumbar 5-sacral 1 in the control group were (108.17±10.87)ms, (113.93±11.54)ms, (126.65±10.22)ms, (118.62±8.86)ms and (111.61±10.65)ms, respectively, which of nucleus pulposus in different segments was statistically significant(F=14.28, P<0.001). The T2 values of nucleus pulposus of intervertebral disc of lumbar 1-2, lumbar 2-3, lumbar 3-4, lumbar 4-5, lumbar 5-sacral 1 in the simple obesity group were (104.90±7.67)ms, (101.10±6.61)ms, (112.65±5.75)ms, (98.27±6.18)ms, (89.82±6.34)ms, respectively, , which of nucleus pulposus in different segments was statistically significant(F=49.52, P<0.001). There were statistically significant differences in the T2 values of nucleus pulposus of intervertebral disc of lumbar 2-3, lumbar 3-4, lumbar 4-5, lumbar 5-sacral 1 between the two groups(t=5.283, 6.535, 10.327, 9.626, all P<0.001).@*Conclusion@#Magnetic resonance T2-mapping can detect early changes in tissue composition of intervertebral disc degeneration.Therefore, magnetic resonance T2-mapping imaging technology can provide an important reference for the early diagnosis of intervertebral disc degeneration in obese people.
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Objective To explore the clinical value of magnetic resonance T 2 -mapping imaging in the diagnosis of early intervertebral disc degeneration in obese people.Methods From January 2018 to June 2019, 30 obese volunteers and 30 healthy volunteers with normal weight underwent T 2 -mapping scan,while their routine MRI examination showed no abnormalities were slected.The T2 value of nucleus pulposus in both two groups were measured and compared.Results The T2 values of nucleus pulposus of intervertebral disc of lumbar 1-2,lumbar 2-3,lumbar 3-4,lumbar 4-5 and lumbar 5-sacral 1 in the control group were (108.17 ±10.87)ms,(113.93 ± 11.54)ms,(126.65 ±10.22) ms,(118.62 ±8.86) ms and (111.61 ±10.65) ms,respectively,which of nucleus pulposus in different segments was statistically significant (F＝14.28,P＜0.001).The T2 values of nucleus pulposus of intervertebral disc of lumbar 1-2,lumbar 2-3,lumbar 3 -4,lumbar 4-5,lumbar 5 -sacral 1 in the simple obesity group were (104.90 ±7.67)ms,(101.10 ±6.61) ms,(112.65 ±5.75) ms,(98.27 ±6.18)ms,(89.82 ± 6.34)ms,respectively,,which of nucleus pulposus in different segments was statistically significant (F＝49.52,P＜0.001).There were statistically significant differences in the T 2 values of nucleus pulposus of intervertebral disc of lumbar 2-3,lumbar 3-4,lumbar 4 -5,lumbar 5 -sacral 1 between the two groups (t＝5.283,6.535,10.327, 9.626,all P＜0.001).Conclusion Magnetic resonance T2 -mapping can detect early changes in tissue composition of intervertebral disc degeneration.Therefore,magnetic resonance T2 -mapping imaging technology can provide an important reference for the early diagnosis of intervertebral disc degeneration in obese people .
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Objective To investigate the effects and its possible mechanisms of tiopronin (TIP) on interleukin-2 (IL-2) immunotherapy of human leukemia KG-1 cells transplanted in nude mice.Methods KG-1 cells (1 x 107/ml) in logarithmic growth phase were injected subcutaneously into the groin of the left hind leg of the 45 5-week-old nude mice.When the subcutaneous tumor diameter was about 8 mm,nude mice were randomly divided into three groups (n =15):Control group (intraperitoneal injection of phosphate buffer),IL-2 group (hypodermic injection of IL-2),IL-2 + TIP group (hypodermic injection of IL-2 and intraperitoneal injection of TIP).The therapeutic effect of TIP combined with IL-2 on human leukemia KG-1 cells transplanted in nude mice was observed.The number of nature killer (NK) cells in peripheral blood of nude mice was detected by flow cytometry.Nitrate reductase assay was used to detect reactive nitric metabolite (RNM) levels in peripheral blood of nude mice.Enzyme linked immunosorbent assay (ELISA) was used to detect the levels of tumor necrosis factor-β (TNF-β) and interferon-γ (IFN-γ) in peripheral blood of nude mice.Terminal-deoxynucleoitidyl transferase mediated nick end labeling (TUNEL) assay was used to analyze apoptosis.Results Both IL-2 and IL-2 + TIP could inhibit the growth of transplanted tumor.Compared with IL-2 group [(54.32 ± 4.32) ％],the tumor inhibition rate of IL-2 + TIP group was (90.15 ± 3.75)％,and its inhibition of tumor growth was more obvious (t =11.893,P ＜ 0.001).The tumor weights of Control group,IL-2 group and IL-2 + TIP group were (0.95 ± 0.05)g,(0.58 ± 0.03)g and (0.27 ± 0.07)g,and there was statistically significant difference among the three groups (F =52.716,P ＜ 0.001).Compared with IL-2 group,the tumor weight of IL-2 + TIP group was significantly reduced (P =0.008).The number of NK cells in IL-2 + TIP group was (0.658 ±0.157)/L,which was significantly higher than (0.452 ±0.124)/L of IL-2 group (P =0.021).The concentration of RNM in IL-2 + TIP group was (42.92 ± 4.68)μmol/ml,which was significantly lower than (163.38 ± 5.49)μmol/ml in IL-2 group (P =0.007).The concentrations of TNF-β and IFN-γin IL-2 + TIP group were (247.68 ± 8.24) pg/ml and (185.61 ±7.58) pg/ml,which were significantly higher than (97.48 ± 7.28)pg/ml (P =0.021) and (70.62 ± 8.47)pg/ml (P =0.015) in IL-2 group.The apoptotic rate of tumor cells in IL-2 + TIP group was (47.38±4.25)％,which was significantly higher than (21.41 ±2.79)％ in IL-2 group (P ＜0.001).Conclusion TIP can increase the sensitivity of leukemia cells to IL-2 immunothe-rapy by removing RNM,promoting NK cells activity and increasing NK cells-induced tumor cell apoptosis.
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Objective To investigate the effect of Tiopronin (TIP) on interleukin (IL)-2 immunotherapy of human leukemia KG-1 cells and its possible mechanism.Methods KG-1 ceils in logarithmic growth phase were randomly divided into KG-1 + IL-2 group and KG-1 + IL-2 + TIP group.Methyl thiazolyl tetrazolium (MTI) assay and colony formation assay were used to detect the sensitivity and proliferation of KG-1 cells.The changes of reactive nitric metabolites (RNM) were detected with nitrate reductase method.The production of tumor necrosis factor (TNF)-3 and interferon (IFN)-γ,was detected with enzyme linked immunosorbent assay (ELISA).The expression of CD3ξ was detected with Western blot and real time polymerase chain reaction (RT-PCR).Results IL-2 and IL-2 + TIP could inhibit the growth of KG-1 cells.The inhibitory rate of KG-1 + IL-2 + TIP group was significantly higher than that of KG-1 + IL-2 group,and the sensitivity of KG-1 cells to IL-2 was 6.2 times higher.Both IL-2 and IL-2 + TIP group inhibited the colony formation of KG-1 cells.Compared to KG-1 + IL-2 group,KG-1 + IL-2 + TIP group inhibited the colony formation of KG-1 cells by 3.5 times.The RNM production of KG-1 + IL-2 group was (158.26 ± 3.82) μmol/ml,which was significantly higher than (45.18 ± 4.29) μ mol/ml of KG-1 + IL-2 + TIP group (P ＜ 0.05).The levels of TNF-β and IFN-γin KG-1 + IL-2 + TIP group were (253.28 ± 7.84) pg/ml and (181.25 ±6.41) pg/ml,which was significantly higher than (98.45 ±6.43) pg/ml and (68.74 ±8.26) pg/ml of KG-1 +IL-2 group (P＜0.05).The expression of CD3ξ in KG-1 +IL-2 +TIP group was significantly higher than that in KG-1 + IL-2 group.Conclusions Tiopronin can promote NK/T cell activity and increase the sensitivity of leukemia KG-1 cells to IL-2 by eliminating reactive nitrogen metabolites.
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Objective To investigate the effect of E1A gene on the radiosensitivity of human nasopharyngeal carcinoma cells and its possible mechanism. Methods The E1A gene was transfected into nasopharyngeal carcinoma CNE-2R cells by adenovirus vector. The expression of E1A gene was detected by RT-PCR. Untransfected CNE-2R cells(PBS group)and CNE-2R cells transfected with empty vector Ad-β-gal(Ad-β-gal group)and E1A(Ad-E1A group)were given 0 Gy,2 Gy,4 Gy,6 Gy,8 Gy 6 MV X-ray irradiation. The changes in radiosensitivity of CNE-2R cells were determined by colony-forming assay. Flow cytometry was used to analyze cell apoptosis in each group. The expression of NF-κB, CK2α, Bcl-2, and cleaved caspase-3 was measured by Western blot. Results RT-PCR confirmed that the E1A gene was transfected into CNE-2R cells and stably expressed. The Ad-E1A group had a significantly lower plating efficiency than the PBS group and the Ad-β-gal group(P<0.05). The Ad-E1A group had significantly lower cell survival rate at 2 Gy irradiation than the PBS group and the Ad-β-gal group(0.217 vs. 0.602, P<0.05;0.217 vs. 0.585, P<0.05). The Ad-E1A group had a significantly higher α/β value than the PBS group and the Ad-β-gal group(24.680 vs. 5.268, P<0.05;24.680 vs. 5.132, P<0.05). Flow cytometry results showed that irradiation alone could promote the apoptosis of CNE-2R cells,when combined with E1A gene,the apoptosis rate was significantly increased(P<0.05). Western blot results showed that E1A gene down-regulated the expression of NF-κB/p65,CK2α,and Bcl-2 and up-regulated the expression of cleaved caspase-3. Conclusions E1A gene can enhance the radiosensitivity of nasopharyngeal carcinoma cells by inhibiting the expression of CK2 to block the NF-κB signaling pathway and promoting cell apoptosis.
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Objective:To study the inhibitory effect of E1A gene on the growth of tumors in nude mice implanted with nasopharygeal carcinoma CNE2 cells and its promotion effect on the racliosensitivity of CNE2-implanted tumors, and to investigate the related mechanism. Methods: E1A gene was transfected into CNE2 cells using adenovirus system, and sta-ble E1A positive clones were established. The inhibitory effect of E1A on tumor formation-ability of CNE2 cells was ob-served in nude mice. The efficacy of E1A gene therapy with or without radiotherapy against CNE2 cell-implanted tumors was evaluated. The effect of E1A gene therapy on the expression of P53 was detected by RT-PCR. Results: CNE2 cells stably transfected with E1A gene (CNE2-Ad-E1A) were successfully established. The tumor formation time was later and tumor size was smaller in CNE2-Ad-E1A cell-implanted mice compared with those in CNE2 cell- and CNE2-Ad-β-gal cell-implanted mice (CNE2 cells stably transfected with Ad-β-gal). Radiotherapy, E1A gene therapy and E1A gene + radio-therapy all suppressed the growth of implanted tumors, with the tumor suppression rates being (60.32±5.34) %, (70.53±6.12) %, and (97.15±4.87) % , respectively. E1A gene therapy significantly increased the expression of P53 gene in tumor tissues. Conclusion: E1A can inhibit the growth of tumors in mice implanted with nasopharygeal carcinoma cells, and enhance its sensitivity to radiotherapy, which may be related to the increased expression of P53 gene in tumor tissues.
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Objective To study the effect of E1A gene on the radiosensitivity of nasopharyngeal carcinoma (NPC) cells and its mechanism. Methods Ad-E1A gene was transfected into human NPC cells (CNE2), then the positive clones (CNE2-Ad-E1A) were identified by RT-PCR. CNE2 cells, CNE2 cells transfected with Ad-β-gal (CNE2-Ad-β-gal) and CNE2-Ad-E1A cells were irradiated with 0 Gy,2 Gy,4 Gy,6 Gy and 8 Gy respectively using 6 MV X-ray. Clone forming assays were carried out, cell survival curves were drawn and the sensitivity enhancing ratio (SER) was calculated. The redistributions of cell cy-cle were analyzed by flow cytometry. RT-PCR was used to detect the expression of wtp53. Results RT-PCR confirmed that E1A gene had been integTated into positively transfected cells and stably expressed. Cell survival curves showed that the SER of D0,Dq and SF_2 value was 1.37, 1.95 and 1.46 in CNE2-Ad-E1A cells. The D_0,D_q and SF_2 value was 1.57 Gy,1.82 Gy, 0.89 in CNE-2 cells and 1.53 Gy,1.78 Gy,0.82 in CNE2-Ad-β-gal cells, respectively. The G_2/M arrest was shown in CNE2-Ad-E1A cells. Moreover, the expression of wtp53 gene was markedly enhanced in Ad-E1A-CNE2 cells. Conclusions E1A gene can ef-fectively enhance the radiosensitivity of human NPC cells, which may be associated the enhancement of wt-p53 expression and G_2/M arrest.
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OBJECTIVE@#To determine the effect of Ad-E1A gene therapy on the radiosensitivity of nasopharyngeal carcinoma cell by downregulating the expression of VEGF in vitro.@*METHOD@#The human nasopharyngeal carcinoma CNE-2Z cell lines were investigated. The recombinant adenovirus vector containing E1A gene was used for this study. After CNE-2Z cells was treated with PBS, Ad-beta-gal and Ad-E1A for 48 h, the three groups were irradiated in different doses at 0, 2.4, 6, 8 and 10 Gy, the cytotoxicity was determined by MTT assay and cell cycle was analysis by flow cytometry. The VEGF expression were evaluated by RT-PCR assay and immunocytochemical analysis.@*RESULT@#Significant cell deaths by IR were observed in a dose dependent manner in the three group CNE-2Z cells. After transduction of the E1A gene into CNE-2Z cells, the sensitivity of these cells to radiation was enhanced than the PBS treated group and Ad-beta-gal treated group. Cell growth inhibition in Ad-E1A group by IR was strongly enhanced than Ad-beta-gal treated group and PBS treated group. RT-PCR assay and immunocytochemical analysis showed VEGF expression was downregulated in Ad-E1A treated group.@*CONCLUSION@#E1A gene therapy can effectively enhance the nasopharyngeal carcinoma cell sensitivity to the radiotherapy by down-regulating VEGF expression. These findings may pave the way for efficient radiation-gene therapy to NPC in future.
Subject(s)
Humans , Adenoviridae , Genetics , Cell Line, Tumor , Gene Expression Regulation, Neoplastic , Genetic Therapy , Genetic Vectors , Nasopharyngeal Neoplasms , Genetics , Metabolism , Radiotherapy , Radiation Tolerance , Vascular Endothelial Growth Factor A , MetabolismABSTRACT
Objective To investigate the effect of El A gene on the radiosensitivity of human laryngeal carcinoma cells and its correlated mechanisms. Methods The Ad-E1A and Ad-β-gal were amplifieated in Hek293 cells, extracted by freezing (-80℃) and thawing(37℃) repeatedly (3 times) , purificated by the method of density gradient of CsC1 and titrated by plaque assay method. Then they were transfected into human laryngeal carcinoma cells (Hep-2) and authenticated by RT-PCR. The radiosensitivity of Hep-2 cells transfeeted with or without El A were studied by cell surviral curve. Finally we investigated the correlated mechanisms including cell apoptosis studied by flow cytometry and VEGF content studied by RT-PCR. Resuits The radiosensitivity of Hep-2 cells transfected with El A was intensified, Do and Dq were lowered and α was increased. Flow cytometry showed that the apoptosis rate of cells with E1A or with El A and radiotherapy was increased. The VEGF content of the cells transfeeted with E1 A or treated by radiotherapy was decreased, which reached the lowest level when the cells were treated with the both mathods. Conclusions E1 A gene can intensify the radiosensitivity and contribute to the apoptosis of human laryngeal carcinoma cells. El A gene and radiotherapy can markedly decrease the VEGF content.
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Objective:To study the inhibitory effect of E1A gene on the growth of tumors in nude mice implanted with nasopharygeal carcinoma CNE2 cells and its promotion effect on the radiosensitivity of CNE2-implanted tumors,and to investigate the related mechanism.Methods: E1A gene was transfected into CNE2 cells using adenovirus system,and stable E1A positive clones were established.The inhibitory effect of E1A on tumor formation-ability of CNE2 cells was observed in nude mice.The efficacy of E1A gene therapy with or without radiotherapy against CNE2 cell-implanted tumors was evaluated.The effect of E1A gene therapy on the expression of P53 was detected by RT-PCR.Results: CNE2 cells stably transfected with E1A gene(CNE2-Ad-E1A)were successfully established.The tumor formation time was later and tumor size was smaller in CNE2-Ad-E1A cell-implanted mice compared with those in CNE2 cell-and CNE2-Ad-?-gal cell-implanted mice(CNE2 cells stably transfected with Ad-?-gal).Radiotherapy,E1A gene therapy and E1A gene+radiotherapy all suppressed the growth of implanted tumors,with the tumor suppression rates being(60.32?5.34)%,(70.53?6.12)%,and(97.15?4.87)%,respectively.E1A gene therapy significantly increased the expression of P53 gene in tumor tissues.Conclusion: E1A can inhibit the growth of tumors in mice implanted with nasopharygeal carcinoma cells,and enhance its sensitivity to radiotherapy,which may be related to the increased expression of P53 gene in tumor tissues.