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Neurochem Res. 2018 Oct;43(10):1905-1913. doi: 10.1007/s11064-018-2608-6. Epub 2018 Aug 7.

Luteolin Ameliorates Cognitive Impairments by Suppressing the Expression of Inflammatory Cytokines and Enhancing Synapse-Associated Proteins GAP-43 and SYN Levels in Streptozotocin-Induced Diabetic Rats.

Gu JX1,2, Cheng XJ1,2, Luo X1,2, Yang X1,2, Pang YP1,2, Zhang XF1,2, Zhang YY1,2, Liu Y3,4.

Author information

1
Jiangsu Key Laboratory of New Drug Research and Clinical Pharmacy, Xuzhou Medical University, Xuzhou, 221004, Jiangsu, China.
2
Department of Pathology, Xuzhou Medical University, Xuzhou, Jiangsu, China.
3
Jiangsu Key Laboratory of New Drug Research and Clinical Pharmacy, Xuzhou Medical University, Xuzhou, 221004, Jiangsu, China. cbpeliuyinew@163.com.
4
Department of Pathology, Xuzhou Medical University, Xuzhou, Jiangsu, China. cbpeliuyinew@163.com.

Abstract

Luteolin, a flavonoid isolated from Cirsium japonicum, has antioxidant, anti-inflammatory and neuroprotective activities. Our previous studies brought a prospect that luteolin benefited diabetic rats with cognitive impairments. In this study, we examined whether luteolin could suppress the inflammatory cytokines, thus increasing synapse-associated proteins in streptozotocin (STZ)-induced diabetes in rat models. The model rats underwent luteolin treatment for 8 consecutive weeks, followed by assessment of cognitive performances with MWM test. Nissl staining was employed to assess the neuropathological changes in the hippocampus and the effects of luteolin on diabetic rats. With animals sacrificed, expressions of inflammatory cytokines including interleukin-1β (IL-1β) and tumor necrosis factor-α (TNF-α) and synapse-associated proteins including growth-associated protein-43 (GAP-43) and synaptophysin (SYN) were determined. The results affirmed improvement of behavioral performances in the MWM test, downexpression of glycation end products (AGEs) in the plasma and the receptor for advanced glycation end products in the hippocampus, inhibition of IL-1β and TNF-α in both the hippocampus and plasma in diabetic rats. Furthermore, luteolin treatment upregulated the expressions of GAP-43 and SYN in the hippocampus. Thus, luteolin could ameliorate the cognitive dysfunctions in STZ-induced diabetic rat model.

KEYWORDS:

AGEs; Diabetes; Inflammation response; Luteolin; Memory; Synapse-associated proteins

PMID:
30088237
DOI:
10.1007/s11064-018-2608-6
[Indexed for MEDLINE]

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