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Alterations in Hippocampal Oxidative Stress Expression of AMPA Receptor GluR2 Subunit and Associated Spatial Memory Loss by Bacopa monnieri Extract (CDRI-08) in Streptozotocin-Induced Diabetes Mellitus Type 2 Mice

机译:链脲佐菌素诱导的2型糖尿病小鼠海马Bacopa monnieri提取物(CDRI-08)的海马氧化应激AMPA受体GluR2亚基的表达和相关的空间记忆丧失的变化。

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摘要

Bacopa monnieri extract has been implicated in the recovery of memory impairments due to various neurological disorders in animal models and humans. However, the precise molecular mechanism of the role of CDRI-08, a well characterized fraction of Bacopa monnieri extract, in recovery of the diabetes mellitus-induced memory impairments is not known. Here, we demonstrate that DM2 mice treated orally with lower dose of CDRI-08 (50- or 100 mg/kg BW) is able to significantly enhance spatial memory in STZ-DM2 mice and this is correlated with a significant decline in oxidative stress and up regulation of the AMPA receptor GluR2 subunit gene expression in the hippocampus. Treatment of DM2 mice with its higher dose (150 mg/kg BW or above) shows anti-diabetic effect in addition to its ability to recover the spatial memory impairment by reversing the DM2-induced elevated oxidative stress and decreased GluR2 subunit expression near to their values in normal and CDRI-08 treated control mice. Our results provide evidences towards molecular basis of the memory enhancing and anti diabetic role of the Bacopa monnieri extract in STZ-induced DM2 mice, which may have therapeutic implications.
机译:Bacopa monnieri提取物与动物模型和人类各种神经系统疾病引起的记忆障碍的恢复有关。但是,尚不清楚CDRI-08(Bacopa monnieri提取物的一部分)在恢复糖尿病引起的记忆障碍中的作用的确切分子机制。在这里,我们证明经口服CDRI-08(50或100 mg / kg BW)剂量较低的DM2小鼠能够显着增强STZ-DM2小鼠的空间记忆能力,这与氧化应激和上调海马AMPA受体GluR2亚基基因的表达。用较高剂量(150 mg / kg BW或更高)治疗DM2小鼠,除具有通过逆转DM2诱导的氧化应激升高和附近GluR2亚基表达降低而恢复空间记忆障碍的能力外,还具有抗糖尿病作用。正常和CDRI-08处理的对照小鼠中的数值。我们的结果提供了证据,表明Bacopa monnieri提取物在STZ诱导的DM2小鼠中具有增强记忆和抗糖尿病作用的分子基础,这可能具有治疗意义。

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