ABSTRACT
<p><b>OBJECTIVE</b>To study the effects of immunoglobulin on the neuronal expression of IL-1beta and IL-1ra and the neuronal death at hippocampus in rats with convulsion induced by pentylenetetrazol.</p><p><b>METHODS</b>The epilepsy model was established by injecting intraperitoneally pentylenetetrazol (PTZ) into Wistar rats. Forty-five rats were randomly divided into three groups, normal control group, PTZ plus intravenous immunoglobulin (PTZ-IVIG); PTZ plus normal saline (PTZ-NS). Neuronal death was assessed by light microscopy with the hematoxylin-eosin (HE) staining and with in situ terminal deoxynucleotidyl transferase dUTP nick-end labeling (TUNEL). IL-1beta and IL-1ra expressions were examined by histochemistry.</p><p><b>RESULTS</b>The ratio of IL-1beta/IL-1ra at hippocampal CA(1) region in PTZ-IVIG group (0.5 +/- 0.1) was significantly lower than that in PTZ-NS group (1.9 +/- 0.5, t = 12.9, P < 0.05). Apoptotic cell numbers at the hippocampal CA(1) region were significantly decreased in the PTZ-IVIG group, compared to PTZ-NS group (t = 27.1, P < 0.05). The numbers of positive cells were 16.4 +/- 3.3/1000 microm(2) in the former and 41.7 +/- 3.5/1000 microm(2) in the latter. Necrotic cell numbers at the hippocampal CA(1) region were significantly decreased in the PTZ-IVIG group (19.0 +/- 2.6/1000 microm(2)), compared to PTZ-NS group (42.3 +/- 4.9/1000 microm(2), t = 20.9, P < 0.05).</p><p><b>CONCLUSION</b>Immunoglobulin could inhibit neuronal death induced by convulsion and its possible mechanism might be the regulation of IL-1 system in neurons.</p>
Subject(s)
Animals , Rats , Apoptosis , Hippocampus , Allergy and Immunology , Metabolism , Immunoglobulins, Intravenous , Pharmacology , Interleukin 1 Receptor Antagonist Protein , Metabolism , Interleukin-1beta , Metabolism , Neurons , Pentylenetetrazole , Rats, Wistar , Seizures , Allergy and Immunology , MetabolismABSTRACT
<p><b>OBJECTIVE</b>To clarify if programmed cell death mechanisms induced by seizures take part in the necrotic process of neurons.</p><p><b>METHODS</b>Seizure was induced by pilocarpine (P) in Sprague-Dawley adult rats which were allowed to recover for 24 or 72 hours before perfusion-fixation. Neuronal death was assessed by light microscopy with the hematoxylin-eosin (HE) staining and with in situ terminal deoxynucleotidyl transferase dUTP nick-end labeling (TUNEL). Bax and Bcl-2 protein expression were examined by histochemistry.</p><p><b>RESULTS</b>Twenty-four and 72 hours after seizures, neuronal death in hippocampus CA1 region was morphologically necrotic. TUNEL-positive and morphologically necrotic cells increased in the hippocampal CA1 region at 72 hours after seizures, there was significant difference compared with controls (P < 0.001). Bax expression was also increased in the hippocampal CA1 region at 72 hours after seizures (P < 0.001), but Bcl-2 expression did not increase, while Bcl-2/Bax ratio decreased.</p><p><b>CONCLUSION</b>Seizures induced late-onset neuronal necrosis was accompanied by programmed cell death mechanisms.</p>