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
目的检测过敏性猝死豚鼠血清IgE含量在不同时间段的变化规律,为过敏性猝死的法医学鉴定寻找客观指标。方法64只豚鼠随机分为0,12,24,48 h 4个时间段,每个时间段又进一步分为实验组和对照组。采用ELISA夹心法检测不同时间段血清IgE含量...目的检测过敏性猝死豚鼠血清IgE含量在不同时间段的变化规律,为过敏性猝死的法医学鉴定寻找客观指标。方法64只豚鼠随机分为0,12,24,48 h 4个时间段,每个时间段又进一步分为实验组和对照组。采用ELISA夹心法检测不同时间段血清IgE含量。结果实验组与对照组相比较P<0.001,实验组豚鼠血清IgE含量显著升高;实验组各时间段相比较P>0.05,4个时间段豚鼠血清IgE含量无明显变化。结论过敏性猝死豚鼠与对照组相比较血清IgE含量显著升高,48 h内实验组豚鼠血清IgE含量无明显变化,血清IgE含量升高可作为鉴定过敏性猝死的指标。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.
文摘目的检测过敏性猝死豚鼠血清IgE含量在不同时间段的变化规律,为过敏性猝死的法医学鉴定寻找客观指标。方法64只豚鼠随机分为0,12,24,48 h 4个时间段,每个时间段又进一步分为实验组和对照组。采用ELISA夹心法检测不同时间段血清IgE含量。结果实验组与对照组相比较P<0.001,实验组豚鼠血清IgE含量显著升高;实验组各时间段相比较P>0.05,4个时间段豚鼠血清IgE含量无明显变化。结论过敏性猝死豚鼠与对照组相比较血清IgE含量显著升高,48 h内实验组豚鼠血清IgE含量无明显变化,血清IgE含量升高可作为鉴定过敏性猝死的指标。
文摘目的:探讨脑死亡状态下胰腺及小肠组织中蛋白激酶C(protein kinase C,PKC)水平的变化.方法:巴马小型猪10只,随机平均分为脑死亡组及对照组.用颅内加压法建立脑死亡模型,脑死亡后6,12和24 h点活检部分胰腺和小肠组织行电镜观察,并用RT-PCR和免疫组化法检测PKC-αmRNA和蛋白的表达情况.结果:脑死亡组胰腺和小肠组织中PKC-αmRNA均表达,并随着脑死亡时间的增加表达亮度增高,而在对照组胰腺和小肠组织中PKC-αmRNA无表达.脑死亡组PKC-α蛋白在胰腺和小肠组织中的表达显著高于对照组,并且6、12、24 h间也有显著差异(0.6209±0.031 vs 0.381±0.038 vs 0.151±0.0108;P<0.05).对照组PKC-α蛋白在胰腺及小肠细胞胞质内表达,仅见少量阳性细胞.电镜下,脑死亡组胰腺及小肠组织形态学变化明显重于对照组.结论:脑死亡状态下胰腺及小肠组织中PKC-αmRNA和蛋白表达水平明显升高,这可能与脑死亡状态下胰腺及小肠的组织损伤有关.
