Research of the intracellular transmission mechanism of the information concerning stress response

PDE-III抑制剂米力农可抑制缺血-再灌注期间肝组织中cAMP降解。由于这种作用，在再灌注过程中血清转氨酶的升高被米力农治疗有效地抑制。关于这种有益作用的机制，窦灌注率的改善和白细胞-内皮细胞的相互作用显着减少。还检查了另一种PDE-III抑制剂Olprinone和腺苷酸环化酶刺激剂NKH 477。两者均能抑制再灌注时转氨酶水平。在Olprinone 2 γ组中，ALT释放为1725 IU/l。该值为对照的一半。但是，全身血压有下降到100 mmHg以下的趋势。NKH 477对血压的影响在0.1 - 1.0 γ之间是轻微的，并且0.2 γ的NKH 477可以将ALT抑制到1615 IU/l。当它们同时给药时，ALT降至1434 IU/l。虽然增加肝脏组织的能力 ...更多信息 2 γ Olprinone中的cAMP大于0.2 γ NKH 477，对ALT抑制和血压的最终效果表明NKH 477比Olprinone更适合临床使用。在应激反应过程中，NF-κ B是参与细胞内信息传递的重要分子之一。由于PDTC据说抑制NF-κ B的活化，我们检查了PDTC给药对缺血-再灌注损伤的影响。有趣的是，PDTC诱导HO-1在肝组织中，并制定了显着的窦扩张，可能是由于分子CO的增加。因此，PDTC可以产生缺血耐受的肝脏像PDE-III抑制剂。由于PDE-III抑制剂没有正弦扩张效应，PDE-III抑制剂和PDTC之间的信号转导似乎完全不同，尽管两者都是显著的耐受诱导剂。这些事实表明了与生物体对逆境的防御系统有关的分子信息的复杂性和多样性。少

A PDE-III inhibitor, Milrinone, could suppress cAMP degradation in the liver tissue during ischemia-reperfusion. Owing to this effect, serum transaminase increase during reperfusion was effectively suppressed by the Milrinone treatment.Concerning the mechanism for this beneficial effect, sinusoidal perfusion rate was improved and the leukocytes-endothelial interaction was significantly decreased. Another PDE-III inhibitor, Olprinone, and adenylate cyclase stimulator, NKH477, were also examined. Both of which could suppress the transaminase level during reperfusion. In Olprinone 2 gamma group, ALT release was 1725 IU/l. This value was as half as control. However, the systemic blood pressure was tended to decline below 100 mmHg. The effect of NKH477 on the blood pressure was mild with the dose between 0.1-1.0 gamma, and 0.2 gamma of NKH477 could suppress ALT to 1615 IU/l. When they were simultaneously administered, ALT decreased to 1434 IU/l. Although the power to increase the liver tiss … More ue cAMP was greater in 2 gamma Olprinone than 0.2 gamma NKH477, final effects on ALT suppression and blood pressure suggested that NKH477 is better for clinical use than Olprinone. However, further study is necessary.In the process of stress response, NF-kappaB is one of the most important molecules concerning intracellular information transmission. Since the PDTC is said to suppress the activation of NF-kappaB, we examined the effects of PDTC administration on ischemia-reperfusion injury. Interestingly, PDTC induced HO-1 in the liver tissue and developed remarkable sinusoidal dilatation, probably due to an increase of molecular CO. Consequently, PDTC could produce ischemic tolerance of the liver like PDE-III inhibitors. Since the PDE-III inhibitor had no sinusoidal dilatation effect, signal transduction seemed to be completely different between PDE-III inhibitor and PDTC, although both of which are significant tolerance inducer. These facts indicate the complexity and multiplicity of the molecular information relating to defense system of organism to the stress. Less