Objective To analyze the upstream region of radiation-induced junB gene. Methods Four plasmids containing 250 bp, 590 bp, 900 bp and 1650 bp, and CAT reporter gene were constructed separately and introduced to L8704 c...Objective To analyze the upstream region of radiation-induced junB gene. Methods Four plasmids containing 250 bp, 590 bp, 900 bp and 1650 bp, and CAT reporter gene were constructed separately and introduced to L8704 cells. The cells were irradiated with 2 Gy X-rays and incubated at different intervals. Total RNA was extracted from the cells and fluctuation of the CAT mRNA level was assessed by the RNA ratio of CAT/β-actin measured by quantitative Northern blot hybridization. Results CAT mRNA expression containing 900 bp and 1560 bpjunB promoter remarkably and rapidly increased, and reached its peak 30min after 2 Gy X-my irradiation. Conclusions 590-900 bp fragments located in the upstream region of junB gene play an important role in the early process of cells against radiation.展开更多
BACKGROUND: Ischemia/reperfusion is the main cause of hepatic damage in liver transplantation. Immediate early genes (IEGs) encode proteins can regulate expression of cellular response genes after injury, and is assoc...BACKGROUND: Ischemia/reperfusion is the main cause of hepatic damage in liver transplantation. Immediate early genes (IEGs) encode proteins can regulate expression of cellular response genes after injury, and is associated with tissue repair and cell apoptosis. The purpose of this re- search was to investigate the effects of preconditioning on expression of immediate early genes c-fos and c-jun follow- ing hepatic ischemia/reperfusion (IR) and its roles in cellu- lar regeneration and apoptosis. METHODS: Ninety-six Wistar rats were randomly divided into IR group and hepatic ischemic preconditioning (IPC) group, and each group was further divided into eight sub- groups (n =6). The model of partial liver ischemia/reper- fusion was used. The rats were subjected to 60-minute liver ischemia, preceded by 10-minute preconditioning. After 0-, 0.5-, 1-, 2-, 4-, 8-, 12-, 24-hour reperfusion, the se- rum and liver tissue in each group were collected to detect the level of serum ALT/AST, liver histopathology, expres- sion of c-fos, and c-jun mRNA. Flow cytometer was used to detect Ki67 and Sub-G1 as the quantity indicators of cell regeneration and apoptosis respectively. RESULTS: Compared with IR group, IPC group showed a significantly lower ALT/AST level in 0. 5-hour sub-group to 8-hour sub-group (P<0.05). Ki67 elevated significantly at 0.5, 1, 2 hours, but decreased significantly at 24 hours ( P < 0 . 05). Ap index decreased significantly after 1-hour reperfusion(P<0.05). Expressions of c-fos and c-jun mR- NA were low, especially c-jun at 0.5, 1 and 2 hours after reperfusion. CONCLUSION: Ischemic preconditioning can protect liver cells against ischemia/reperfusion injury, and this protec- tive effect may be related to influence transcription levels of c-fos and c-jun.展开更多
为了探讨甲基汞对大鼠大脑皮层损伤的分子机制,应用免疫组织化学方法研究了甲基汞暴露后(对照组为w=0.009的生理盐水,暴露组浓度分别为0.05、0.5、5μg/g;取样时间分别为20、60、240、1 440 m in),大鼠大脑皮层即刻早期基因c-FOS蛋白表...为了探讨甲基汞对大鼠大脑皮层损伤的分子机制,应用免疫组织化学方法研究了甲基汞暴露后(对照组为w=0.009的生理盐水,暴露组浓度分别为0.05、0.5、5μg/g;取样时间分别为20、60、240、1 440 m in),大鼠大脑皮层即刻早期基因c-FOS蛋白表达变化.结果表明,大鼠脑c-FOS蛋白表达优先于汞的蓄积,甲基汞对大鼠大脑皮层c-FOS蛋白表达与其浓度之间有一定的剂量-效应关系;c-FOS参与了甲基汞对大鼠大脑皮层损伤毒性过程,即刻早期基因c-FOS可以作为甲基汞神经毒性检测评价效应指标.展开更多
基金This project was supported by Japanese Research Development Corporation (JRDC).
文摘Objective To analyze the upstream region of radiation-induced junB gene. Methods Four plasmids containing 250 bp, 590 bp, 900 bp and 1650 bp, and CAT reporter gene were constructed separately and introduced to L8704 cells. The cells were irradiated with 2 Gy X-rays and incubated at different intervals. Total RNA was extracted from the cells and fluctuation of the CAT mRNA level was assessed by the RNA ratio of CAT/β-actin measured by quantitative Northern blot hybridization. Results CAT mRNA expression containing 900 bp and 1560 bpjunB promoter remarkably and rapidly increased, and reached its peak 30min after 2 Gy X-my irradiation. Conclusions 590-900 bp fragments located in the upstream region of junB gene play an important role in the early process of cells against radiation.
文摘BACKGROUND: Ischemia/reperfusion is the main cause of hepatic damage in liver transplantation. Immediate early genes (IEGs) encode proteins can regulate expression of cellular response genes after injury, and is associated with tissue repair and cell apoptosis. The purpose of this re- search was to investigate the effects of preconditioning on expression of immediate early genes c-fos and c-jun follow- ing hepatic ischemia/reperfusion (IR) and its roles in cellu- lar regeneration and apoptosis. METHODS: Ninety-six Wistar rats were randomly divided into IR group and hepatic ischemic preconditioning (IPC) group, and each group was further divided into eight sub- groups (n =6). The model of partial liver ischemia/reper- fusion was used. The rats were subjected to 60-minute liver ischemia, preceded by 10-minute preconditioning. After 0-, 0.5-, 1-, 2-, 4-, 8-, 12-, 24-hour reperfusion, the se- rum and liver tissue in each group were collected to detect the level of serum ALT/AST, liver histopathology, expres- sion of c-fos, and c-jun mRNA. Flow cytometer was used to detect Ki67 and Sub-G1 as the quantity indicators of cell regeneration and apoptosis respectively. RESULTS: Compared with IR group, IPC group showed a significantly lower ALT/AST level in 0. 5-hour sub-group to 8-hour sub-group (P<0.05). Ki67 elevated significantly at 0.5, 1, 2 hours, but decreased significantly at 24 hours ( P < 0 . 05). Ap index decreased significantly after 1-hour reperfusion(P<0.05). Expressions of c-fos and c-jun mR- NA were low, especially c-jun at 0.5, 1 and 2 hours after reperfusion. CONCLUSION: Ischemic preconditioning can protect liver cells against ischemia/reperfusion injury, and this protec- tive effect may be related to influence transcription levels of c-fos and c-jun.
文摘为了探讨甲基汞对大鼠大脑皮层损伤的分子机制,应用免疫组织化学方法研究了甲基汞暴露后(对照组为w=0.009的生理盐水,暴露组浓度分别为0.05、0.5、5μg/g;取样时间分别为20、60、240、1 440 m in),大鼠大脑皮层即刻早期基因c-FOS蛋白表达变化.结果表明,大鼠脑c-FOS蛋白表达优先于汞的蓄积,甲基汞对大鼠大脑皮层c-FOS蛋白表达与其浓度之间有一定的剂量-效应关系;c-FOS参与了甲基汞对大鼠大脑皮层损伤毒性过程,即刻早期基因c-FOS可以作为甲基汞神经毒性检测评价效应指标.
