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KMID : 1034820160120040429
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Molecular & Cellular Toxicology
2016 Volume.12 No. 4 p.429 ~ p.436
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Dendropanax morbifera Leveille extract ameliorates memory impairments and inflammatory responses in the hippocampus of streptozotocin-induced type 1 diabetic rats
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Jung Hyo-Young
Chung Tae-Ho
Hwang In-Koo
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Abstract
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In this study, we investigated the effect of Dendropanax morbifera stem extract (DMS) on streptozotocin (STZ)-induced type 1 diabetic rats. The effect of DMS on memory function was assessed using the Morris water maze test. In addition, we investigated its effect on the microglial activation and subsequent release of pro-inflammatory cytokines such as tumor necrosis factor-α (TNF-α) and interleukin (IL)-1β in the hippocampus. Seven-week-old Wistar rats were exposed to 65 mg/kg STZ by intraperitoneal injection and 100 mg/kg of DMS was administered orally for 30 days. The administration of STZ significantly increased escape latency compared to the control group on all experimental days. Administration of DMS to STZ-treated rats significantly reduced the escape latency. Blood glucose levels significantly increased, while leptin levels significantly decreased in the STZ-treated rats compared to the control group. The administration of DMS to STZ-treated rats significantly ameliorated these changes in the levels of blood glucose and leptin. In addition, administration of DMS significantly increased the serum insulin levels in the STZ-treated rats, not in the control rats. Similarly, STZ treatment increased the morphological changes with hypertrophy of cytoplasm and processes in the hippocampal CA1 region, and significantly increased the levels of pro-inflammatory cytokines such as TNF-α and IL-1β levels in serum and hippocampal homogenates. Administration of DMS to STZ-treated rats significantly reduced the STZ-induced microglial activation and subsequent increase of TNF-α and IL-1β levels in the serum and hippocampal homogenates. These results indicate that DMS could prevent STZ-induced memory impairment by modulating the inflammatory responses in the hippocampus.
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KEYWORD
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Dendropanax morbifera, Hippocampus, Interleukin-1β, Microglia, Streptozotocin, Tumor necrosis factor-α
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