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首页> 外文期刊>Neurochemistry International: The International Journal for the Rapid Publication of Critical Reviews, Preliminary and Original Research Communications in Neurochemistry >Lectin from Canavalia brasiliensis (ConBr) protects hippocampal slices against glutamate neurotoxicity in a manner dependent of PI3K/Akt pathway
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Lectin from Canavalia brasiliensis (ConBr) protects hippocampal slices against glutamate neurotoxicity in a manner dependent of PI3K/Akt pathway

机译：来自巴西小叶芥的凝集素（ConBr）以依赖PI3K / Akt途径的方式保护海马切片免受谷氨酸神经毒性

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摘要

The excitotoxicity induced by excessive activation of the glutamatergic neurotransmission pathway is involved in several neuropathologies. In this sense, molecules that prevent the release of glutamate or the excessive activation of its receptors can be useful in preventing the neuronal cell death observed in these diseases. Lectins are proteins capable of reversible binding to the carbohydrates in glycoconjugates, and some have been used in the study and purification of glutamate receptors. ConBr is a mannose/glucose-binding lectin purified from Canavalia brasiliensis seeds. In the present study, we aimed to evaluate the neuroprotective activity of ConBr against glutamate-induced excitotoxicity. Hippocampal slices were isolated from adult male mice and incubated for 6 h in Krebs saline/DMEM buffer alone (control), in the presence of glutamate or glutamate plus ConBr. The phosphorylation of Akt and mitogen activated protein kinases (MAPKs) such as ERK1/2, p38MAPK and JNK1/2/3 was evaluated with western blotting. The results indicate that glutamate provoked a reduction in the hippocampal slice viability (-25%), diminished the phosphorylation of Akt and augmented p38MAPK and ERK1 phosphorylation. No changes were observed in the phosphorylation of JNK1/2/3 or ERK2. Notably, ConBr, through a mechanism dependent on carbohydrate interaction, prevented the reduction of cell viability and Akt phosphorylation induced by glutamate. Furthermore, in the presence of the PI3K inhibitor LY294002, ConBr was unable to reverse glutamate neurotoxicity. Taken together, our data suggest that the neuroprotective effect of ConBr against glutamate neurotoxicity requires oligosaccharide interaction and is dependent on the PI3K/Akt pathway.
机译：由谷氨酸能神经传递途径的过度激活引起的兴奋性毒性涉及几种神经病理学。从这个意义上讲，阻止谷氨酸释放或受体过度活化的分子可用于预防在这些疾病中观察到的神经元细胞死亡。凝集素是能够与糖缀合物中的碳水化合物可逆结合的蛋白质，其中一些已用于谷氨酸受体的研究和纯化。 ConBr是一种甘露糖/葡萄糖结合凝集素，是从巴西蚕豆种子中纯化的。在本研究中，我们旨在评估ConBr对谷氨酸诱导的兴奋性毒性的神经保护活性。从成年雄性小鼠中分离海马切片，并在存在谷氨酸或谷氨酸加ConBr的情况下，在单独的Krebs盐水/ DMEM缓冲液（对照）中孵育6小时。用蛋白质印迹法评估了Akt和有丝分裂原活化蛋白激酶（MAPK）（如ERK1 / 2，p38MAPK和JNK1 / 2/3）的磷酸化。结果表明，谷氨酸引起海马切片活力的降低（-25％），减少了Akt的磷酸化，增强了p38MAPK和ERK1的磷酸化。在JNK1 / 2/3或ERK2的磷酸化中未观察到变化。值得注意的是，ConBr通过依赖于碳水化合物相互作用的机制阻止了谷氨酸诱导的细胞活力降低和Akt磷酸化。此外，在PI3K抑制剂LY294002存在下，ConBr不能逆转谷氨酸的神经毒性。综上所述，我们的数据表明，ConBr对抗谷氨酸神经毒性的神经保护作用需要寡糖相互作用，并且依赖于PI3K / Akt途径。

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