ABSTRACT
Nip2 mRNA expression of hippocampus was clarified in the postnatal, adult and aging rat. We observed the change of Nip2 mRNA expression in the ischemic rat hippocampus at 3, 6, 24 and 72 hours after reperfusion. And we investigated the relation between Nip2 and apoptosis after ischemic insults. The Rats were killed 2, 4, 7 days after birth and normal adult rats and aged rat were killed. Male F344 rats were subjected to transient middle cerebral artery occlusion. Reperfusion was achieved by withdrawing the filament after 90 min minutes, and rats were sacrificed 3, 6, 24, 72 hours after reperfusion. Hippocampal sections were stained for TUNEL using ApopTag kit following the protocol provided by the manufacturer, and stained with 2, 3, 5 -triphenyl tetrazolium chloride and cresyl violet We used quantitative reverse transcription and polymerase chain reaction to characterise changes in the mRNA expression of Nip2 in the rat models of transient focal ischemia and postnatal, adult and aged rat. Nip2 mRNA expression were increased in the rat of postnatal development and aging more than these of adult. After reperfusion, marked increase of Nip2 mRNA was observed after 3 and 6 hours. After that time mRNA expression of Nip2 was decreased gradually. The TUNEL staining detected DNA fragmentation in neurons of the entorhinal cortex, forcep major corpus callosum and secondary visual cortex at 24 hours. And TTC staining results showed the whitish infact changes of hippocampal CA1 region and lateral habenular nucleus. We hypothesize that the overexpression of Nip2 is concerned with sensitivity to the ischemic insult at postnatal period and aging period. And, early apoptotic events after cerebral ischemic insults relate to Nip2 mRNA overexpression.
Subject(s)
Adult , Animals , Humans , Male , Rats , Aging , Apoptosis , CA1 Region, Hippocampal , Corpus Callosum , DNA Fragmentation , Entorhinal Cortex , Habenula , Hippocampus , In Situ Nick-End Labeling , Infarction, Middle Cerebral Artery , Ischemia , Models, Animal , Neurons , Parturition , Polymerase Chain Reaction , Rats, Inbred F344 , Reperfusion , Reverse Transcription , RNA, Messenger , Surgical Instruments , Viola , Visual CortexABSTRACT
Tenascin is suggested the one of cause of vitiligo by interfering melanocyte adhesion and migration. The distribution and expression levels of tenascin were examined by semiquantitative immunohistochemistry on skin biopsies from vitiligo patients with varying area of photodamage. The level of tenascin on adult skin is severely restricted but we had observed the increase on vitiligo skin lesions. Although it is uncertain that the increased tenascin expression is the cause or the result of disease, vitiligo and increased tenascin expression is thought to be related each other. This study has shown that tenascin increased on photodamaged vitiligo skin lesions. So we shoud consider choosing phototherapy to vitiligo.