Early intervention with gastrodin reduces striatal neurotoxicity in adult rats with experimentally-induced diabetes mellitus

Early intervention with gastrodin reduces striatal neurotoxicity in adult rats with experimentally-induced diabetes mellitus
复制标题

天麻素的早期干预可降低实验性糖尿病成年大鼠的纹状体神经毒性

DOI:
10.3892/mmr.2019.9954
复制
发表时间:
2019-04-01
影响因子:
3.4
通讯作者:
Zou, Ying-Ying
Zou, Ying-Ying
中科院分区:
医学4区
文献类型:
--
作者:
Qi, Yu-Han;Zhu, Rui;Zou, Ying-Ying

文献摘要

被引文献

相似文献

Glutamate-induced excitotoxicity in the striatum has an important role in neurodegenerative diseases. It has been reported that diabetes mellitus (DM) induces excitotoxicity in striatal neurons, although the underlying mechanism remains to be fully elucidated. The present study aimed to investigate the effect of gastrodin on DM-induced excitotoxicity in the striatal neurons of diabetic rats. Adult Sprague-Dawley rats were divided into control, diabetic, and gastrodin intervention groups. Diabetes in the rats was induced with a single intraperitoneal injection of streptozotocin (65 mg/kg). In the gastrodin groups, the rats were gavaged with 60 or 120 mg/kg/day gastrodin for 6 weeks, 3 weeks following the induction of diabetes. Pathological alterations in the striatum were assessed using hematoxylin and eosin (H&E) staining. The protein expression levels of phosphorylated (p)-extracellular signal-regulated kinase (ERK)1/2, p-mitogen-activated protein kinase kinase (MEK)1/2, tyrosine receptor kinase B (TrKB) and brain-derived neurotrophic factor (BDNF) in the striatal neurons were evaluated by western blotting and double immunofluorescence. Additionally, the extracellular levels of glutamate were measured by microanalysis followed by high-pressure-liquid-chromatography. In diabetic rats, striatal neuronal degeneration was evident following H&E staining, which revealed the common occurrence of pyknotic nuclei. This was coupled with an increase in glutamate levels in the striatal tissues. The protein expression levels of p-ERK1/2, p-MEK1/2, TrKB and BDNF in the striatal tissues were significantly increased in the diabetic rats compared with those in the normal rats. In the gastrodin groups, degeneration of the striatal neurons was ameliorated. Furthermore, the expression levels of glutamate, p-ERK1/2, p-MEK1/2, TrKB and BDNF in the striatal neurons were decreased. From these findings, it was concluded that reduced neurotoxicity in striatal neurons following treatment with gastrodin may be attributed to its suppressive effects on the expression of p-ERK1/2, p-MEK1/2, BDNF and TrKB.