Avaliação da proteína acídica fibrilar glial como marcador da injúria por isquemia-reperfusão hepática / Evaluation of glial fibrillar acidic protein as a marker of hepatic ischemia-reperfusion

OBJETIVO: Avaliar a expressão da Proteína Acídica Fibrilar Glial após a injúria por isquemia-reperfusão. MÉTODOS: vinte e quatro ratos foram distribuídos em quatro grupos: Controle, submetidos à anestesia e biópsia hepática; Simulação, injeção de heparina através da veia cava e dissecção do pedículo hepático superior, biópsia após 24 horas; Isquemia 30 minutos, mesmo procedimento do grupo Simulação, acrescido de clampeamento do pedículo hepático superior por 30 minutos; Isquemia 90 minutos, mesmo procedimento do grupo Isquemia 30 minutos, porém com período de clampeamento de 90 minutos. Após 24 horas de observação, os animais foram submetidos à laparotomia e seus fígados avaliados macroscopicamente, microscopicamente, por coloração de Hematoxilina-Eosina (HE) e submetidos à análise da expressão da GFAP por Western Blotting. RESULTADOS: Não se observou diferença no aspecto macroscópico dos fígados entre os diferentes grupos experimentais, tendo todos evidenciado morfologia normal. A análise por HE não evidenciou diferenças significativas, no que diz respeito à morfologia lobular. Por outro lado, nos grupos isquemia, foram encontrados infiltrados neutrofílicos e pequenas áreas de necrose. A expressão de GFAP foi semelhante em todos os grupos, seja qualitativamente quanto quantitativamente. CONCLUSÃO: A expressão da Proteína Acídica Fibrilar Glial não se alterou em nosso modelo de isquemia-reperfusão.

OBJECTIVE: To evaluate the expression of Glial Fibrillary Acidic Protein (GFAP) after ischemia-reperfusion injury. METHODS: twenty four rats were divided into four groups: Control, submitted to anesthesia and liver biopsy; Sham, receiving injection of heparin through the vena cava and hepatic pedicle dissection, with liver biopsy after 24 hours; Ischemia-30, the same as Sham group, plus hepatic pedicle clamping for 30 minutes; and Ischemia-90, the same procedure of Ischemia-30 group, but with clamping period of 90 minutes. After 24 hours of observation, the animals underwent laparotomy and we evaluated their livers macroscopically, microscopically by hematoxylin-eosin (HE) and analyzed the expression of GFAP by Western Blotting. RESULTS: There was no difference in the gross appearance of the livers between the different experimental groups, all having demonstrated normal morphology. HE analysis showed no significant differences with respect to lobule morphology. On the other hand, in the ischemia groups we observed neutrophilic infiltrates and small areas of necrosis. GFAP expression was similar in all groups, either qualitatively and quantitatively. CONCLUSION: The expression of Glial Fibrillary Acidic Protein did not change in our model of ischemia-reperfusion.

Gamma-ray irradiation stimulates the expression of caveolin-1 and GFAP in rat spinal cord: a study of immunoblot and immunohistochemistry

We studied the expression of caveolin-1 in the spinal cords of rats using 60Co gamma-ray irradiation (single dose of 8 Gray (Gy)) in order to determine the possible involvement of caveolin-1 in the tissues of the central nervous system after irradiation. Spinal cords sampled at days 1, 4, and 9 post-irradiation (PI) (n = 5 per each time point) were analyzed by Western blot and immunohistochemistry. Western blot analysis showed that the expression of caveolin-1 was significantly increased at day 1 PI (p < 0.05), and returned to the level of normal control rats on days 4 and 9 PI. Immunohistochemistry showed that caveolin-1 immunoreactivity was enhanced in some glial cells, vascular endothelial cells, and neurons in the spinal cords. The increased expression of glial fibrillary acidic protein (GFAP), a marker for an astroglial reaction, was consistent with that of caveolin-1. In addition, caveolin-1 was co-localized in hypertrophied GFAP-positive astrocytes. Taking all these facts into consideration, we postulate that irradiation induces the increased expression of caveolin-1 in cells of the central nervous system, and that its increased expression in astrocytes may contribute to hypertrophy of astrocytes in the spinal cord after irradiation. The precise role of caveolin-1 in the spinal cords should be studied further.

Effects of ischemia and anoxia on cell activation and cell cycle of cultured astrocytes in vitro / 华中科技大学学报（医学）（英德文版）

To examine the effects of ischemia and anoxia on cell activation and cell cycle of astrocytes in vitro, the cell cycles and the proliferation of astrocytes in different time points after ischemia and anoxia were studied by flow cytometry and BrdU labeling and the expression of GFAP and cyclin D1 was detected by the fluorescence immunochemistry. After ischemia and anoxia in vitro, the astrocytes in S phase were significantly increased as compared with those in the normal group and the proliferating ability of the astrocytes was highest 6 h after the treatment as revealed by BrdU pulse labeling, but the astrocytes in S phase and proliferating ability were decreased after 6 h. At the early stages of ischemia and anoxia, the positive staining intensity of GFAP was increased, peaked at 6th h, while 12 h after the ischemia and anoxia, the positive staining intensity of GFAP became weak, and the expression of cyclin D1 was gradually increased after the ischemic and anoxic damage. It is concluded that astrocytes are activated to proliferate and enter new cycle events by ischemia and anoxia, and cyclin D1 is implicated in the proliferation and repair of astrocytes. The cell cycle events are closely associated with the proliferation and activation of astrocytes.

Gliofibroma: A Case Report and Review of the Literature

Gliofibroma is a rare astrocytic tumor, composed of a glial component ranging from benign to high grade of malignancy and a consistently benign mesenchymal component. Its exact biological behavior is not fully known. In addition, histogenesis and prognostic factors are also still debatable. We herein present a rare case of gliofibroma in a 25-yr-old male with seizure. A computed tomographic scan of the brain showed a 1.5 cm-sized, enhancing mass with calcification. Histologically, the tumor consisted of glial fibrillary acidic protein (GFAP)-positive glial cells admixed with a mesenchymal component and extensive collagen lay down. The glial cells displayed variable cellularity, but without mitosis or necrosis. Since the MIB-1 labeling index was up to 35.8% in the cellular areas of the glial component, it could be considered to be a predictor of worse prognosis.