BACKGROUND: Brain-dead donors are the main sources for organ transplantation, but many studies show that brain-death affects the organ's function after transplantation. This study was undertaken to investigate liv...BACKGROUND: Brain-dead donors are the main sources for organ transplantation, but many studies show that brain-death affects the organ's function after transplantation. This study was undertaken to investigate liver injury after brain-death in BA-Ma mini pigs and the protective effects of breviscapine on hepatic function and on PKC-alpha mRNA and its protein expression. METHODS: Fifteen BA-Ma mini pigs were equally divided into 3 groups at random: brain-dead (group B), breviscapine pretreated (group P), and control (group Q. The brain-dead model was established by increasing intracranial pressure in a modified, slow and intermittent way. At 3, 6, 12, 18 and 24 hours after the initial brain-death, the levels of serum AST, ALT, TNF-alpha, IL-1 beta, and IL-6 were determined. The changes in hepatic tissues were assessed, and the expression of PKC-alpha and PKC-alpha mRNA was detected by immunohistochemistry and RTPCR, respectively. RESULTS: The levels of AST and ALT in groups B and P began to increase 12 hours after brain-death, while the values in group P were lower than those in group B (P<0.05). The levels of IL-1 beta, IL-6, and TNF-alpha in groups B and P at 3, 6, 12 and 18 hours were lower than those in group B (P<0.05). At 6, 12 and 24 hours, the expressions of PKC-a mRNA and PKC-a protein in group P were lower than those in group B (P<0.05). The degree of injury to hepatic cells in group P was milder than that in group B. CONCLUSIONS: Breviscapine inhibits the degree of PKC-alpha mRNA transcription and its protein translation, decreases the release of inflammatory factors, and thus alleviates hepatic injury during brain-death.展开更多
目的:探讨"脾虚生痰"所致巴马小型猪冠心病的发病机制及从脾论治方药的作用效应与机制。方法:采用隔日游泳+高脂饲料+冠状动脉结扎法复制"脾虚生痰"型冠心病巴马小型猪模型,连续10周,随机分为模型组、益气健脾组、...目的:探讨"脾虚生痰"所致巴马小型猪冠心病的发病机制及从脾论治方药的作用效应与机制。方法:采用隔日游泳+高脂饲料+冠状动脉结扎法复制"脾虚生痰"型冠心病巴马小型猪模型,连续10周,随机分为模型组、益气健脾组、益气健脾祛痰组及益气健脾化瘀祛痰组,10只/组;10只正常组动物不结扎冠状动脉和不游泳。给药24周后,观察心肌缺血区组织学病变和超微结构变化,PCR法检测NF-κB、IL-6、TNF-α和水通道蛋白1(AQP1)m RNA表达水平,蛋白免疫印迹法检测p38MAPK和AQP1的蛋白表达水平。结果:与正常组比较,模型组NF-κB、IL-6、TNF-α和AQP1 m RNA表达水平显著升高(P<0.05);p38MAPK和AQP1蛋白表达显著升高(P<0.05)。与模型组比较,各给药组上述指标表达水平均显著降低(P<0.05)。结论:益气健脾方加减可减轻缺血区心肌组织炎性反应和水肿的发生,从而改善"脾虚生痰"所致巴马小型猪冠心病症状。展开更多
基金This study was supported by a grant from the Distinguished Innovation of Henan Province (0421002500).
文摘BACKGROUND: Brain-dead donors are the main sources for organ transplantation, but many studies show that brain-death affects the organ's function after transplantation. This study was undertaken to investigate liver injury after brain-death in BA-Ma mini pigs and the protective effects of breviscapine on hepatic function and on PKC-alpha mRNA and its protein expression. METHODS: Fifteen BA-Ma mini pigs were equally divided into 3 groups at random: brain-dead (group B), breviscapine pretreated (group P), and control (group Q. The brain-dead model was established by increasing intracranial pressure in a modified, slow and intermittent way. At 3, 6, 12, 18 and 24 hours after the initial brain-death, the levels of serum AST, ALT, TNF-alpha, IL-1 beta, and IL-6 were determined. The changes in hepatic tissues were assessed, and the expression of PKC-alpha and PKC-alpha mRNA was detected by immunohistochemistry and RTPCR, respectively. RESULTS: The levels of AST and ALT in groups B and P began to increase 12 hours after brain-death, while the values in group P were lower than those in group B (P<0.05). The levels of IL-1 beta, IL-6, and TNF-alpha in groups B and P at 3, 6, 12 and 18 hours were lower than those in group B (P<0.05). At 6, 12 and 24 hours, the expressions of PKC-a mRNA and PKC-a protein in group P were lower than those in group B (P<0.05). The degree of injury to hepatic cells in group P was milder than that in group B. CONCLUSIONS: Breviscapine inhibits the degree of PKC-alpha mRNA transcription and its protein translation, decreases the release of inflammatory factors, and thus alleviates hepatic injury during brain-death.
文摘目的:探讨"脾虚生痰"所致巴马小型猪冠心病的发病机制及从脾论治方药的作用效应与机制。方法:采用隔日游泳+高脂饲料+冠状动脉结扎法复制"脾虚生痰"型冠心病巴马小型猪模型,连续10周,随机分为模型组、益气健脾组、益气健脾祛痰组及益气健脾化瘀祛痰组,10只/组;10只正常组动物不结扎冠状动脉和不游泳。给药24周后,观察心肌缺血区组织学病变和超微结构变化,PCR法检测NF-κB、IL-6、TNF-α和水通道蛋白1(AQP1)m RNA表达水平,蛋白免疫印迹法检测p38MAPK和AQP1的蛋白表达水平。结果:与正常组比较,模型组NF-κB、IL-6、TNF-α和AQP1 m RNA表达水平显著升高(P<0.05);p38MAPK和AQP1蛋白表达显著升高(P<0.05)。与模型组比较,各给药组上述指标表达水平均显著降低(P<0.05)。结论:益气健脾方加减可减轻缺血区心肌组织炎性反应和水肿的发生,从而改善"脾虚生痰"所致巴马小型猪冠心病症状。
