Endo Y
Eur J Pharmacol. 1983 Aug 5;91(4):493-9. doi: 10.1016/0014-2999(83)90175-9.
The administration of an Escherichia coli lipopolysaccharide (LPS), or an endotoxin into mice produced a variation in tissue serotonin (5HT) levels within 4.5 h. 5HT levels in the kidney and lung were decreased by the higher doses of LPS, but those in the liver and spleen were increased even by lower doses of the agent. The increase in liver 5HT was most marked. Such variations in 5HT levels were also produced by the administration of concanavalin A. In vitro experiments using extracts from livers of LPS-treated and non-treated mice indicated that there was no difference in the 5HT formation from 5-hydroxytryptophan between the two groups, but that 5HT formation from tryptophan was higher in the LPS-treated mice. The LPS-induced 5HT increase in liver was suppressed by p-chlorophenylalanine (an inhibitor of tryptophan hydroxylase), actinomycin D, cycloheximide and dexamethasone, but not by Ro 4-4602 (an inhibitor of aromatic amino acid decarboxylase), pargyline (an inhibitor of monoamine oxidase) and indomethacin. A possible mechanism of the 5HT increase in the liver is discussed on the basis of these results.
给小鼠注射大肠杆菌脂多糖(LPS)或内毒素后,4.5小时内组织中血清素(5HT)水平会发生变化。高剂量的LPS会降低肾脏和肺中的5HT水平,但低剂量的该制剂就能使肝脏和脾脏中的5HT水平升高。肝脏中5HT的升高最为明显。注射伴刀豆球蛋白A也会产生5HT水平的这种变化。使用LPS处理和未处理小鼠肝脏提取物进行的体外实验表明,两组之间由5-羟色氨酸生成5HT的过程没有差异,但LPS处理小鼠中由色氨酸生成5HT的过程更高。对氯苯丙氨酸(色氨酸羟化酶抑制剂)、放线菌素D、环己酰亚胺和地塞米松可抑制LPS诱导的肝脏中5HT升高,但罗4-4602(芳香族氨基酸脱羧酶抑制剂)、帕吉林(单胺氧化酶抑制剂)和吲哚美辛则不能。基于这些结果,讨论了肝脏中5HT升高的可能机制。