ABSTRACT
Objective To explore the expressions of interleukin (IL)-17A and its receptor IL-17RA in different degrees of malignant gliomas. Methods Fifty patients with glioma were collected in this study. Accordance to the World Health Organization Classification System, patients were classified by malignancy grade, including gradeⅠ(n=12), gradeⅡ(n=18), gradeⅢ(n=13) and gradeⅣ(n=7). The glioma tissue and peripheral blood samples of patients were obtained for detecting the expression levels of IL-17A and IL-17RA mRNA by using immunohistochemistry, quantitative real-time PCR. Western blot assay was used to detect expressions of IL- 17A and IL- 17RA in both the macroscopic (immunohistochemistry) and molecular levels (mRNA and protein). Results Immunohistochemical staining showed that the expression levels of IL-17A and its receptor IL-17RA increased with the increase of the malignant degree of gliomas. The mRNA levels of IL-17A and IL-17RA receptors in peripheral blood were up-regulated with the increasing malignancy grade of glioma (F=8.96, P<0.05;F=10.34, P<0.05). The mRNA levels of IL-17A and IL-17RA in glioma tissues were up-regulated with the increasing malignancy grade of glioma (F=11.21, P<0.05;F=14.11, P<0.05). The protein levels of IL-17A and IL-17RA in peripheral blood and glioma tissues were also up-regulated with the increasing malignancy grade of glioma (in peripheral blood:F=9.90, P<0.05;F=11.80, P<0.05;and in gliomas tissues:F=8.15, P<0.05;F=14.46, P<0.05). Conclusion The expressions of IL-17A and IL-17RA receptor are positively correlated with malignancy grade of glioma. These results provide some reference for clinical diagnosis of malignant gliomas.
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Objective To investigate the effects of fasudil on expressions of Bcl-2 and Bax in cerebral cortex of model rats with subarachnoid hemorrhage (SAH). Methods Thirty rats were divided into sham operation group, SAH group and SAH+fasudil group, 10 rats in each group. Double injection of blood into occipital cistern method was used for SAH model in SAH group and SAH+fasudil group. In the sham operation group, the blood injection was instead by normal saline. In the SAH+fasudil group, at 30 min after the second injection of blood, rats were administrated with intraperitoneal injection of fasudil at a dose of 3 mg/kg. The general situation, neurological score, TUNEL staining for cortex cell apoptosis, immune histochemical staining and Western blotting assay for Bcl-2 and Bax protein expression were compared 24 h after the operation between the three groups. Results Compared with the sham operation group, rats in SAH group and SAH +fasudil group appeared obvious neurological deficits. The neurological score was significantly lower in SAH group ( 2.68 ± 0.31) than that of sham operation group (5.00±0.00). The neurological score was significantly higher in SAH+fasudil group (3.27 ± 0.35) compared with that of SAH group (2.68 ± 0.31, P<0.05). There was obvious cell apoptosis in SAH group and SAH+fasudil group, and the apoptosis was less in SAH+fasudil group than that of SAH group (P<0.05). The level of Bcl-2 expression was significantly lower in SAH group than that of sham operation group, and Bax expression was significantly higher in SAH group than that of sham operation group (P<0.05). The level of Bcl-2 expression was significantly higher in SAH+fasudil group than that of SAH group, but Bax expression was significantly lower in SAH+fasudil group than that of SAH group (P<0.05). Conclusion Fasudil can improve the neurological damage in rats with SAH, which may be related with the regulation of apoptosis related proteins Bcl-2 and Bax.
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Objective:To observe the change of BDNF level expression in experimental in hippocampal and habenular nucles in experimental depression rats.Methods:The depression model of rats was established by chronic unpredictable mild stress. Openfield test was performed to detect the behavior of rats. Immunohistochemistry was used to observe the changes of BDNF level.Results:Compared to the control group,the number of depressed animals was much less than that of normal animals.Conclusion:The level of BDNF decrease significantly in experimental depressive model of rats.