| The retina is very easy to be subjected to ischemia reperfusion injury (IRI) because of its special vascular supply. Mechanical ocular trauma can cause retinal IRI by vascular spasm, constriction or rupture, fibrous tissue traction and secondary glaucoma, etc. Free radicals, calcium ion overloading, excited amino acids and leukocyte infiltration were proved to be closely related to IRI. But the beginning agent of these mechanisms is not clear. Nuclear factor-kappaB (NF- K B) is a major transcriptive regulator which can regulate the transcription and expression of a series of genes. It had been proved that NF-KB played an important role in the beginning of IRI of myocardium, brain, liver, while its effect in retinal IRI is unknown. Monosialoganglioside(GM-l) is a kind of nerve protectant, it contributes to neuron survival on several ways: block excited amino acids and free radicals, reduce cell edema and calcium ionelevation, increase the effects of neurotrophic factors. Many experimental and clinical investigations had indicated its good protection on nerve system diseases and IRI. But there is no report of GM-1 in ophthalmology in our country. We selected morphological observation and measurement , transmission electron microscopy and immunohistochemistry SP method to study the activation of NF-nB and protection of GM-1 in rat retinal IRI.125 healthy adult Wistar rats free from eye disease were devided randomly into 4 groups: normal-control group, IRI group , NS group and GM-1 group. Except for the normal-control group(5 rats), each animal received completely retinal ischemia by increasing intraocular pressure for 60 minutes. According to the surviving time after reperfusion, the last 3 groups were sub-devided into 8 timepoints: Oh(only ischemia), Ih, 3h, 6h, 12h, 24h, Id, 3d and Id. There were 5 rats in each timepoint. The NS group and GM-1 group were given NS 3ml/kg or GM-1 3ml/kg(30mg/kg) intraperitonially 12h, Ih before and immediately after ischemia, while other 2 groups received no treatment. The eyes were enucleated , fixed, embedded and sectioned. The morphological change of retina was studied by light microscopy. Mean thickness of the inner retinal layers(MTIRL) was measured by using ocular micrometer. Ultrastructural changes of cell injury or apoptosis was observed under transmission electron microscope. The expression and activation of NF- K B was detected by routineimmunohistochemistry SP method. Results1. HE stain indicated: (1)in IRI and NS group, inner retina was edema after 60 minutes ischemia and reperfusion from Oh-12h. Pycnosis nuclei appeared during 12h-24h. The gradually lost of cells and atrophy of inner retina could be seen after 3 days. (2) GM-1 group had the lighter edema and atrophy which indicated the protection of GM-1. There was no change in outer layer retina.2. Mean thickness of the inner retinal layers: (l)MTIRL in normal retina was (75.25+3.82) urn. In IRI and NS group, inner retina began thicker after ischemia(P<0.05). Between Ih and 12h after reperfusion, MTIRL was thickend significantly(P<0.01) and reached the peak level in 6h. It had no difference between normal and 24h after reperfusion(P>0.05) , and extensively decreased after 3d (P<0.01), and was more severe on 7d(P<0.01). (2)GM-1 group: MTIRL was larger than normal after ischemia(P<0.05). It became thicker significantly after reperfusion from Ih to 12h(P<0.01). No significant difference was found between GM-1 group and IRI or NS group(P>0.05) from Oh to 3h, but remarkably decreased 6h to 12h after reperfusion(P<0.01). In 24h and 3d, MTIRL of GM-1 group were at the normal level(P>0.05). Although in 7d, the inner retina was thinner than normal(P<0.01), it was still thicker than the former 2 groups(P<0.01).3. Transmission electron microscopy indicated: (l)after ischemia, the IRI group only had slightly mitochondriadilation. 6h after reperfusion, mitochondria swelled notably, endoplasmic reticulum expanded, synaptic vesicle in nerve fiber disappear...
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