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Mechanisms of interleukin-1beta-induced GDNF release from rat glioma cells

机译:从大鼠胶质瘤细胞中白细胞介素-1beta诱导的GDNF释放机制

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We investigated the mechanisms of the IL-1beta-induced GDNF release from rat C6 glioma cells. IL-1beta stimulated GDNF release and induced the phosphorylation of IkappaB, p38 MAP kinase, p44/p42 MAP kinase, SAPK/JNK and STAT3. The IL-1beta-stimulated levels of GDNF were suppressed by wedelolactone, SB203580, PD98059 or JAK inhibitor I. On the contrary, SP600125 failed to reduce the IL-lbeta-effect. These results strongly suggest that IL-1(3 stimulates GDNF release through the pathways of IkappaB-NFkappaB, p38 MAP kinase, p44/p42 MAP kinase and JAK-STAT3, but not through the SAPK/JNK pathway in glioma cells.
机译:我们研究了IL-1Beta诱导的GDNF释放的机制来自大鼠C6胶质瘤细胞。 IL-1BETA刺激GDNF释放并诱导IKAPPAB,P38 MAP激酶,P44 / P42 MAP激酶,SAPK / JNK和Stat3的磷酸化。通过Wedelolone,SB203580,PD98059或Jak抑制剂I抑制了IL-1Beta刺激的GDNF水平。相反,SP600125未能降低IL-Lbeta效应。这些结果强烈表明IL-1(3通过Ikappab-NFKappab,P38 Map激酶,P44 / P42 Map激酶和Jak-Stat3促进GDNF释放,但不是通过胶质瘤细胞中的SAPK / JNK途径。

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