Brain-derived neurotrophic factor was utilized in the present study to treat cell injury models induced by aggregated β-amyloid（25 35）. Methylthiazolyldiphenyl-tetrazolium bromide assay and western blot analysis sh...Brain-derived neurotrophic factor was utilized in the present study to treat cell injury models induced by aggregated β-amyloid（25 35）. Methylthiazolyldiphenyl-tetrazolium bromide assay and western blot analysis showed that brain-derived neurotrophic factor provided neuroprotection against cellular apoptosis by suppressing the decline in β-amyloid（25 35）-induced cell activity and the increasing ratio of Bax/Bcl-2. After treating pheochromocytoma cells with tyrosine kinase receptor B receptor inhibitor K252a, brain-derived neurotrophic factor reverses the above- mentioned changes. The experimental findings suggested that brain-derived neurotrophic factor prevented β-amyloid peptide-induced cellular apoptosis by modulating Bax/Bcl-2 expression, and this effect was associated with binding to the specific tyrosine kinase receptor B receptor.展开更多
BACKGROUND： Studies have demonstrated that oxyhemoglobin （OxyHb） can induce brain cell apoptosis in vivo.OBJECTIVE： To observe the effects of exogenous nerve growth factor （NGF） on cerebral cortical neuronal Bcl...BACKGROUND： Studies have demonstrated that oxyhemoglobin （OxyHb） can induce brain cell apoptosis in vivo.OBJECTIVE： To observe the effects of exogenous nerve growth factor （NGF） on cerebral cortical neuronal Bcl-2 and Bax expression in mice with OxyHb-induced subarachnoid hemorrhage. DESIGN, TIME AND SETTING： A completely randomized grouping, controlled animal experiment was performed at the Experimental Center for Biomedicine, College of Medicine, Xi＇an Jiaotong University between February and April 2005. MATERIALS： Fifty-four healthy, male, adult, ICR mice were included in this study. Subarachnoid hemorrhage was induced by a subarachnoid injection of OxyHb in 48 mice. Mouse NGF was obtained from Xiamen Beidazhilu Bioengineering Co., Ltd., China.METHODS： All 54 mice were randomly divided into three groups： control （n = 6）, injury （n = 24）, and NGF （n = 24）. The NGF group received a subarachnoidal administration of OxyHb, immediately followed by a caudal vein injection of NGF （1 μg）. The injury group was injected with OxyHb, and subsequently with physiological saline. The control group only received intravenous physiological saline. MAIN OUTCOME MEASURES： At 1,6, 24, and 48 hours following subarachnoid hemorrhage induction, expression levels of Bcl-2 and Bax were detected by immunohistochemistry in the cerebral cortex 3 mm anterior and posterior to the injection site. RESULTS： At all time points following OxyHb injection, cerebral cortical Bax levels were significantly higher in the injured group than in the control and NGF groups （P 〈 0.01）. During the first 24 hours following OxyHb injection, cerebral cortical Bcl-2 levels were significantly lower in the injury group compared to the control group （P 〈 0.05 0.01）. Between 1 and 48 hours, Bcl-2 levels were significantly higher in the NGF group than in the injury group （P 〈 0.01 ）. CONCLUSION： Exogenous NGF can inhibit increased neuronal Bax expression and decreased Bcl-2 expression in the cerebral cortex of mice with OxyHb -induced subarachnoid hemorrhage.展开更多
The ventral tegmental area and the locus coeruleus are associated with psychological and physical dependence of opioid addiction. To date, very little is known about brain-derived neurotrophic factor （BDNF） and Bcl-...The ventral tegmental area and the locus coeruleus are associated with psychological and physical dependence of opioid addiction. To date, very little is known about brain-derived neurotrophic factor （BDNF） and Bcl-2 gene and protein changes following morphine addiction. The present study utilized immunohistochemistry and in situ hybridization techniques, which revealed that there were increased BDNF levels, but decreased Bcl-2 levels in the prefrontal cortex, locus coeruleus, hippocampus, and the ventral tegmental area during morphine-dependence formation and abstinence. However, the levels of BDNF remained unchanged, and Bcl-2 expression was increased in the nucleus accumbens. These results showed that BDNF and Bcl-2 are involved in the development of morphine dependence, and precipitation of abstinence syndrome.展开更多
<strong>Introduction:</strong> Type 2 diabetes is a major public health problem worldwide. This study aimed at identifying modifiable behavioral risk factors associated with biological factors in people at...<strong>Introduction:</strong> Type 2 diabetes is a major public health problem worldwide. This study aimed at identifying modifiable behavioral risk factors associated with biological factors in people at risk of type 2 diabetes which could be targeted in the design and implementation of appropriate interventions to prevent the disease. <strong>Methods:</strong> 180 subjects at risk of type 2 diabetes (aged 15 - 60 years) were identified and selected at random during a preliminary survey conducted in two groups of villages in northeastern Benin. The study took part on August 2017. Questionnaires were administered to consenting subjects;anthropometric measurements taken and blood samples withdrawn. Blood samples were subjected to biochemical testing according to standard protocols. <strong>Results:</strong> Data was obtained from 180 subjects at risk of type 2 diabetes. The average age of the subjects was 42.76 ± 11.30 years. Multivariate analysis showed inadequate dietary intake score, low physical activity and tobacco use as behavioral factors significantly associated with high waist circumference, high blood sugar, low HDL cholesterol, high triglyceride levels and high body fat percentage. <strong>Conclusion:</strong> There is a possible association between biological and behavioral risk factors.展开更多
BACKGROUND：In various retinal neurodegenerative animal models,ciliary neurotrophic factor （CNTF） exhibits prominent neuroprotective effects on retinal nerve cells.Bcl-2 is an anti-apoptotic protein.c-Jun is upregul...BACKGROUND：In various retinal neurodegenerative animal models,ciliary neurotrophic factor （CNTF） exhibits prominent neuroprotective effects on retinal nerve cells.Bcl-2 is an anti-apoptotic protein.c-Jun is upregulated and phosphorylated in the activated c-Jun N-terminal kinase pathway,which subsequently mediates apoptosis.However,the effect of CNTF on Bcl-2 and c-Jun expression in retinal nerve cells remains unclear.OBJECTIVE：To determine the dynamic changes in retinal nerve cell apoptosis,as well as bcl-2 and c-jun gene and protein expression,following a single dose of CNTF in a short period of time.DESIGN,TIME AND SETTING：A single-blind,randomized,controlled,in vitro experiment was performed at the Central Laboratory of Beijing Tongren Hospital from May 2008 to April 2009.MATERIALS：Neonatal bovine retinal nerve cells （Chinese Holstein）,recombinant human CNTF （PeproTech,Rocky Hill,NJ,USA）,rabbit polyclonal anti-Bcl-2 and c-Jun antibodies （Abeam,Cambridge,UK）,fluorescein isothiocyanate-conjugated annexin V/propidium iodide kit （BioVision,Mountain View,CA,USA）,real time polymerase chain reaction instrument （ABI,Foster City,CA,USA）,and flow cytometer （BD FACSCalibur,Franklin Lakes,NJ,USA）.METHODS：Neonatal bovine retinal cells from passage 2 were cultured for 3 days and incubated with,or without,50 ng/mL CNTF （control）.MAIN OUTCOME MEASURES：Cell apoptosis was detected via Annexin V-FITC/PI double-staining and flow cytometry.bcl-2 and c-jun mRNA and protein expression were detected by quantitative real time polymerase chain reaction and western blot analysis.RESULTS：The proportion of late-stage apoptotic cells was significantly decreased at 2,4,and 6 days after CNTF treatment compared with the control group （P 〈 0.01）.CNTF did not alter bcl-2 mRNA expression at the three time points,but significantly increased Bcl-2 protein expression at 2 and 4 days （P 〈 0.01）.c-jun mRNA expression was significantly decreased 4 days after CNTF treatment （P〈 0.01）.In addition,c-Jun protein expression was slightly increased at 4 days （P〈 0.01）,but decreased at 6 days,compared with the control group （P〈 0.05）.CONCLUSION：A single dose of CNTF （50 ng/mL） upregulated Bcl-2 protein and downregulated c-jun mRNA expression,followed by a parallel,but lagged,change in c-Jun protein production in cultured neonatal bovine retinal nerve cells.These results suggested that CNTF reduces retinal nerve cell apoptosis by modifying Bcl-2 and c-Jun expression.展开更多
BACKGROUND： Both animal experiments and clinical studies have shown that basic fibroblast growth factor （bFGF） and danshen （Salvia miltiorrhiza） can exhibit protective effects on ischemia-reperfusion cerebral inj...BACKGROUND： Both animal experiments and clinical studies have shown that basic fibroblast growth factor （bFGF） and danshen （Salvia miltiorrhiza） can exhibit protective effects on ischemia-reperfusion cerebral injury. OBJECTIVE： To test whether bFGF and danshen can protect cerebral injury induced by exposure to repeated, high, positive acceleration （＋Gz） in an animal model and to analyze the possible mechanisms. DESIGN, TIME AND SETTING： Randomized controlled animal study. The experiment was performed at the Research Center for Molecular Biology, Air-force General Hospital of Chinese PLA from April to August 2000. MATERIALS： A total of 20 clean grade, healthy, Sprague Dawley rats of both genders, weighing （200 ± 15） g, were provided by our experimental animal center. Rats were randomly divided into 5 groups： the control group, ＋Gz exposure group, bFGF group, danshen group, and saline group, with 4 animals per group. bFGF （Beijing Bailuyuan Biotechnology Co. Ltd.） and danshen solution （Shanghai Zhongxi Pharmaceutical Co. Ltd.） were used. METHODS： All rats were fixed on a rotary arm of a centrifugal apparatus （2 m in radius） with their heads oriented towards the center of the apparatus. Except for rats in the control group, the value of ＋Gz exposure was ＋14 Gz with an acceleration rate of 1.5 G/s. The peak force lasted for 45 seconds. ＋Gz exposure was performed three times with intervals of 30 minutes. Rats in the control group received the same ＋Gz procedure, but the G value was ＋1 Gz. Rats in bFGF group and danshen group were intraperitoneally injected with 100 μg/kg bFGF or 15 g/kg danshen solution, respectively, at 30 minutes prior to centrifugation and immediately after centrifugation. Rats in saline group were injected with the same volume of saline. Six hours after exposure, rats were decapitated. One hemisphere was preserved in liquid nitrogen for RNA extraction and the other was processed for apoptosis detection. MAIN OUTCOME MEASURES： mRNA levels of bcl-2 and p53 were measured by semi-quantitative reverse-transcription polymerase chain reaction. Apoptotic cell death was detected by terminal deoxynuleotidyl transferase-mediated dUTP nick end labeling. RESULTS： Changes in mRNA expression of bcl-2 and p53 and apoptotic cells were observed in rat brain six hours after repeated ＋Gz exposures, bFGF and danshen were able block the changes of bcl-2 and p53 expression and inhibit apoptotic cell death. CONCLUSION： The data suggest that apoptosis and changes in bcl-2 and p53 expression in the rat brain can be induced by repeated ＋Gz exposures. Apoptosis is, therefore, one of the molecular mechanisms of brain damage induced by repeated ＋Gz exposures, bFGF and danshen were of the equal potency in preventing brain injury induced by repeated ＋Gz exposures.展开更多
Objective:To study the expressions and clinical significances of PCNA, EGFR, Bcl-2 and Bax in thymoma. Methods: The expressions of EGFR, PCNA, Bcl-2 and Bax in 46 cases of thymoma and 11 cases of normal thymus were de...Objective:To study the expressions and clinical significances of PCNA, EGFR, Bcl-2 and Bax in thymoma. Methods: The expressions of EGFR, PCNA, Bcl-2 and Bax in 46 cases of thymoma and 11 cases of normal thymus were detected with S-P immunohistochemistry. The results were analyzed with the pathologic indexes. Results: The positive rates of EGFR, Bcl-2 and Bax in normal thymus were 18. 2%, 9. 1%,and 18.2% respectively, while in thymoma were 71.7%, 41.3%, and 15.2% separately. The expression of EGFR in thymoma was significantly correlated with Masaoka staging and Levine classification. The survival rate of EGFR negative patients was significantly higher thanthat of EGFR positive patients (P＜0. 01). PCNA labelling index was significantly higher in thymoma as (4.00±1.87)% than in normal thymus, (2.68±0. 62)% , which was significantly correlated with Levine classification. The expression of Bcl-2 in thymoma was also significantly correlated with Levine classification. The survival rate of Bcl-2 negative patients was significantly higher than that of Bcl-2 positive patients (P＜0. 01). The expression of PCNA, EGFR, Bcl-2and Bax in thymoma had no correlation with histologic type and myasthenia gravis (MG) (P＞0. 05). Conclusion: The expression of EGFR may be involved in the occurrence and development of thymoma. EGFR can be regarded as a supplementary predictor for Masaoka staging so as to predict the progression accurately.The expression of Bcl-2 may contribute to the occurrence of thymic carcinoma and Bcl-2 can be used as a biomarker identifying thymic carcinoma.展开更多
Melatonin, the principal secretory product of the pineal gland, functions as a potent antioxidant and free radical scavenger. Additionally, the antiapoptotic effect of melatonin has been observed both in vivo and in v...Melatonin, the principal secretory product of the pineal gland, functions as a potent antioxidant and free radical scavenger. Additionally, the antiapoptotic effect of melatonin has been observed both in vivo and in vitro. The aim of this study was to investigate the protective effects of melatonin against burn-induced injury in rat liver and whether these changes were associated with oxidative stress and changes in the expression of apoptosis related genes Bcl-2 and Bax. Melatonin (10 mg/kg, i.p.) was applied immediately after 30% of total body surface area (TBSA) burns of male Wistar rats. Malondialdehyde (MDA) as marker of oxidative stress and tumor necrosis factor (TNF-α) as inflammatory marker were assayed by biochemical methods. The hepatic apoptosis related genes Bcl-2 and Bax using light immunоchistochemistry were investigated, too. Hepatic TNF-α and MDA levels were increased significantly following severe burn. Thermal trauma increased the Bax expression without any changes of anti-apoptotic Bcl-2 protein in sinusoidal endothelial cells (SECs) of burn-treated animals compared with the control group animals as well as elevated ratio Bax/Bcl-2 suggesting the susceptibility of these cells to apoptosis. Melatonin significantly decreased the MDA and TNF-α levels in the liver tissue. It decreased also expression of Bax, increased expression of Bcl-2 and reduced Bax/Bcl-2 ratio. In conclusion, experimental data show that melatonin modulates the expression of Bcl-2 family proteins by increasing anti-apoptotic Bcl-2, inhibits apoptosis and restricts the burn-induced damage.展开更多
文摘Brain-derived neurotrophic factor was utilized in the present study to treat cell injury models induced by aggregated β-amyloid（25 35）. Methylthiazolyldiphenyl-tetrazolium bromide assay and western blot analysis showed that brain-derived neurotrophic factor provided neuroprotection against cellular apoptosis by suppressing the decline in β-amyloid（25 35）-induced cell activity and the increasing ratio of Bax/Bcl-2. After treating pheochromocytoma cells with tyrosine kinase receptor B receptor inhibitor K252a, brain-derived neurotrophic factor reverses the above- mentioned changes. The experimental findings suggested that brain-derived neurotrophic factor prevented β-amyloid peptide-induced cellular apoptosis by modulating Bax/Bcl-2 expression, and this effect was associated with binding to the specific tyrosine kinase receptor B receptor.
文摘BACKGROUND： Studies have demonstrated that oxyhemoglobin （OxyHb） can induce brain cell apoptosis in vivo.OBJECTIVE： To observe the effects of exogenous nerve growth factor （NGF） on cerebral cortical neuronal Bcl-2 and Bax expression in mice with OxyHb-induced subarachnoid hemorrhage. DESIGN, TIME AND SETTING： A completely randomized grouping, controlled animal experiment was performed at the Experimental Center for Biomedicine, College of Medicine, Xi＇an Jiaotong University between February and April 2005. MATERIALS： Fifty-four healthy, male, adult, ICR mice were included in this study. Subarachnoid hemorrhage was induced by a subarachnoid injection of OxyHb in 48 mice. Mouse NGF was obtained from Xiamen Beidazhilu Bioengineering Co., Ltd., China.METHODS： All 54 mice were randomly divided into three groups： control （n = 6）, injury （n = 24）, and NGF （n = 24）. The NGF group received a subarachnoidal administration of OxyHb, immediately followed by a caudal vein injection of NGF （1 μg）. The injury group was injected with OxyHb, and subsequently with physiological saline. The control group only received intravenous physiological saline. MAIN OUTCOME MEASURES： At 1,6, 24, and 48 hours following subarachnoid hemorrhage induction, expression levels of Bcl-2 and Bax were detected by immunohistochemistry in the cerebral cortex 3 mm anterior and posterior to the injection site. RESULTS： At all time points following OxyHb injection, cerebral cortical Bax levels were significantly higher in the injured group than in the control and NGF groups （P 〈 0.01）. During the first 24 hours following OxyHb injection, cerebral cortical Bcl-2 levels were significantly lower in the injury group compared to the control group （P 〈 0.05 0.01）. Between 1 and 48 hours, Bcl-2 levels were significantly higher in the NGF group than in the injury group （P 〈 0.01 ）. CONCLUSION： Exogenous NGF can inhibit increased neuronal Bax expression and decreased Bcl-2 expression in the cerebral cortex of mice with OxyHb -induced subarachnoid hemorrhage.
基金the Natural Science Foundation of Chongqing, No. 2005(54)
文摘The ventral tegmental area and the locus coeruleus are associated with psychological and physical dependence of opioid addiction. To date, very little is known about brain-derived neurotrophic factor （BDNF） and Bcl-2 gene and protein changes following morphine addiction. The present study utilized immunohistochemistry and in situ hybridization techniques, which revealed that there were increased BDNF levels, but decreased Bcl-2 levels in the prefrontal cortex, locus coeruleus, hippocampus, and the ventral tegmental area during morphine-dependence formation and abstinence. However, the levels of BDNF remained unchanged, and Bcl-2 expression was increased in the nucleus accumbens. These results showed that BDNF and Bcl-2 are involved in the development of morphine dependence, and precipitation of abstinence syndrome.
文摘<strong>Introduction:</strong> Type 2 diabetes is a major public health problem worldwide. This study aimed at identifying modifiable behavioral risk factors associated with biological factors in people at risk of type 2 diabetes which could be targeted in the design and implementation of appropriate interventions to prevent the disease. <strong>Methods:</strong> 180 subjects at risk of type 2 diabetes (aged 15 - 60 years) were identified and selected at random during a preliminary survey conducted in two groups of villages in northeastern Benin. The study took part on August 2017. Questionnaires were administered to consenting subjects;anthropometric measurements taken and blood samples withdrawn. Blood samples were subjected to biochemical testing according to standard protocols. <strong>Results:</strong> Data was obtained from 180 subjects at risk of type 2 diabetes. The average age of the subjects was 42.76 ± 11.30 years. Multivariate analysis showed inadequate dietary intake score, low physical activity and tobacco use as behavioral factors significantly associated with high waist circumference, high blood sugar, low HDL cholesterol, high triglyceride levels and high body fat percentage. <strong>Conclusion:</strong> There is a possible association between biological and behavioral risk factors.
基金the National Natural Science Foundation of China,No. 30973262
文摘BACKGROUND：In various retinal neurodegenerative animal models,ciliary neurotrophic factor （CNTF） exhibits prominent neuroprotective effects on retinal nerve cells.Bcl-2 is an anti-apoptotic protein.c-Jun is upregulated and phosphorylated in the activated c-Jun N-terminal kinase pathway,which subsequently mediates apoptosis.However,the effect of CNTF on Bcl-2 and c-Jun expression in retinal nerve cells remains unclear.OBJECTIVE：To determine the dynamic changes in retinal nerve cell apoptosis,as well as bcl-2 and c-jun gene and protein expression,following a single dose of CNTF in a short period of time.DESIGN,TIME AND SETTING：A single-blind,randomized,controlled,in vitro experiment was performed at the Central Laboratory of Beijing Tongren Hospital from May 2008 to April 2009.MATERIALS：Neonatal bovine retinal nerve cells （Chinese Holstein）,recombinant human CNTF （PeproTech,Rocky Hill,NJ,USA）,rabbit polyclonal anti-Bcl-2 and c-Jun antibodies （Abeam,Cambridge,UK）,fluorescein isothiocyanate-conjugated annexin V/propidium iodide kit （BioVision,Mountain View,CA,USA）,real time polymerase chain reaction instrument （ABI,Foster City,CA,USA）,and flow cytometer （BD FACSCalibur,Franklin Lakes,NJ,USA）.METHODS：Neonatal bovine retinal cells from passage 2 were cultured for 3 days and incubated with,or without,50 ng/mL CNTF （control）.MAIN OUTCOME MEASURES：Cell apoptosis was detected via Annexin V-FITC/PI double-staining and flow cytometry.bcl-2 and c-jun mRNA and protein expression were detected by quantitative real time polymerase chain reaction and western blot analysis.RESULTS：The proportion of late-stage apoptotic cells was significantly decreased at 2,4,and 6 days after CNTF treatment compared with the control group （P 〈 0.01）.CNTF did not alter bcl-2 mRNA expression at the three time points,but significantly increased Bcl-2 protein expression at 2 and 4 days （P 〈 0.01）.c-jun mRNA expression was significantly decreased 4 days after CNTF treatment （P〈 0.01）.In addition,c-Jun protein expression was slightly increased at 4 days （P〈 0.01）,but decreased at 6 days,compared with the control group （P〈 0.05）.CONCLUSION：A single dose of CNTF （50 ng/mL） upregulated Bcl-2 protein and downregulated c-jun mRNA expression,followed by a parallel,but lagged,change in c-Jun protein production in cultured neonatal bovine retinal nerve cells.These results suggested that CNTF reduces retinal nerve cell apoptosis by modifying Bcl-2 and c-Jun expression.
文摘BACKGROUND： Both animal experiments and clinical studies have shown that basic fibroblast growth factor （bFGF） and danshen （Salvia miltiorrhiza） can exhibit protective effects on ischemia-reperfusion cerebral injury. OBJECTIVE： To test whether bFGF and danshen can protect cerebral injury induced by exposure to repeated, high, positive acceleration （＋Gz） in an animal model and to analyze the possible mechanisms. DESIGN, TIME AND SETTING： Randomized controlled animal study. The experiment was performed at the Research Center for Molecular Biology, Air-force General Hospital of Chinese PLA from April to August 2000. MATERIALS： A total of 20 clean grade, healthy, Sprague Dawley rats of both genders, weighing （200 ± 15） g, were provided by our experimental animal center. Rats were randomly divided into 5 groups： the control group, ＋Gz exposure group, bFGF group, danshen group, and saline group, with 4 animals per group. bFGF （Beijing Bailuyuan Biotechnology Co. Ltd.） and danshen solution （Shanghai Zhongxi Pharmaceutical Co. Ltd.） were used. METHODS： All rats were fixed on a rotary arm of a centrifugal apparatus （2 m in radius） with their heads oriented towards the center of the apparatus. Except for rats in the control group, the value of ＋Gz exposure was ＋14 Gz with an acceleration rate of 1.5 G/s. The peak force lasted for 45 seconds. ＋Gz exposure was performed three times with intervals of 30 minutes. Rats in the control group received the same ＋Gz procedure, but the G value was ＋1 Gz. Rats in bFGF group and danshen group were intraperitoneally injected with 100 μg/kg bFGF or 15 g/kg danshen solution, respectively, at 30 minutes prior to centrifugation and immediately after centrifugation. Rats in saline group were injected with the same volume of saline. Six hours after exposure, rats were decapitated. One hemisphere was preserved in liquid nitrogen for RNA extraction and the other was processed for apoptosis detection. MAIN OUTCOME MEASURES： mRNA levels of bcl-2 and p53 were measured by semi-quantitative reverse-transcription polymerase chain reaction. Apoptotic cell death was detected by terminal deoxynuleotidyl transferase-mediated dUTP nick end labeling. RESULTS： Changes in mRNA expression of bcl-2 and p53 and apoptotic cells were observed in rat brain six hours after repeated ＋Gz exposures, bFGF and danshen were able block the changes of bcl-2 and p53 expression and inhibit apoptotic cell death. CONCLUSION： The data suggest that apoptosis and changes in bcl-2 and p53 expression in the rat brain can be induced by repeated ＋Gz exposures. Apoptosis is, therefore, one of the molecular mechanisms of brain damage induced by repeated ＋Gz exposures, bFGF and danshen were of the equal potency in preventing brain injury induced by repeated ＋Gz exposures.
文摘Objective:To study the expressions and clinical significances of PCNA, EGFR, Bcl-2 and Bax in thymoma. Methods: The expressions of EGFR, PCNA, Bcl-2 and Bax in 46 cases of thymoma and 11 cases of normal thymus were detected with S-P immunohistochemistry. The results were analyzed with the pathologic indexes. Results: The positive rates of EGFR, Bcl-2 and Bax in normal thymus were 18. 2%, 9. 1%,and 18.2% respectively, while in thymoma were 71.7%, 41.3%, and 15.2% separately. The expression of EGFR in thymoma was significantly correlated with Masaoka staging and Levine classification. The survival rate of EGFR negative patients was significantly higher thanthat of EGFR positive patients (P＜0. 01). PCNA labelling index was significantly higher in thymoma as (4.00±1.87)% than in normal thymus, (2.68±0. 62)% , which was significantly correlated with Levine classification. The expression of Bcl-2 in thymoma was also significantly correlated with Levine classification. The survival rate of Bcl-2 negative patients was significantly higher than that of Bcl-2 positive patients (P＜0. 01). The expression of PCNA, EGFR, Bcl-2and Bax in thymoma had no correlation with histologic type and myasthenia gravis (MG) (P＞0. 05). Conclusion: The expression of EGFR may be involved in the occurrence and development of thymoma. EGFR can be regarded as a supplementary predictor for Masaoka staging so as to predict the progression accurately.The expression of Bcl-2 may contribute to the occurrence of thymic carcinoma and Bcl-2 can be used as a biomarker identifying thymic carcinoma.
文摘Melatonin, the principal secretory product of the pineal gland, functions as a potent antioxidant and free radical scavenger. Additionally, the antiapoptotic effect of melatonin has been observed both in vivo and in vitro. The aim of this study was to investigate the protective effects of melatonin against burn-induced injury in rat liver and whether these changes were associated with oxidative stress and changes in the expression of apoptosis related genes Bcl-2 and Bax. Melatonin (10 mg/kg, i.p.) was applied immediately after 30% of total body surface area (TBSA) burns of male Wistar rats. Malondialdehyde (MDA) as marker of oxidative stress and tumor necrosis factor (TNF-α) as inflammatory marker were assayed by biochemical methods. The hepatic apoptosis related genes Bcl-2 and Bax using light immunоchistochemistry were investigated, too. Hepatic TNF-α and MDA levels were increased significantly following severe burn. Thermal trauma increased the Bax expression without any changes of anti-apoptotic Bcl-2 protein in sinusoidal endothelial cells (SECs) of burn-treated animals compared with the control group animals as well as elevated ratio Bax/Bcl-2 suggesting the susceptibility of these cells to apoptosis. Melatonin significantly decreased the MDA and TNF-α levels in the liver tissue. It decreased also expression of Bax, increased expression of Bcl-2 and reduced Bax/Bcl-2 ratio. In conclusion, experimental data show that melatonin modulates the expression of Bcl-2 family proteins by increasing anti-apoptotic Bcl-2, inhibits apoptosis and restricts the burn-induced damage.
