Abstract
BackgroundCurcuma longa L. is a well-known medicinal plant that has been used for its anti-cancer, neuroprotective, and hepatoprotective effects. However, the neuroprotective effect of fermented C. longa (FCL) has not been reported. Therefore, in this study, the effectiveness of FCL for the regulation of memory dysfunction was investigated in two brain cell lines (rat glioma C6 and murine microglia BV2) and scopolamine-treated mice.MethodsC. longa powder was fermented by 5% Lactobacillus plantarum K154 containing 2% (w/v) yeast extract at 30 °C for 72 h followed by sterilization at 121 °C for 15 min. The protective effects of fermented C. longa (FCL) on oxidative stress induced cell death were analyzed by MTT assay in C6 cells. The anti-inflammatory effects of FCL were investigated by measuring the production of nitric oxide (NO) and prostaglandin E2 (PGE2) as well as the expression levels of inducible NO synthase (iNOS) and cyclooxygenase-2 (COX-2) in LPS-stimulated BV2 cells. The step-through passive avoidance test, Morris water maze test, acetylcholinesterase (AChE) activity, and expression of cAMP response element-binding protein (CREB) and brain-derived neurotropic factor (BDNF) were employed to determine the effects of FCL on scopolamine-induced memory deficit in mice. The contents of curcuminoids were analyzed through LC/MS.ResultsPretreatment with FCL effectively prevented the cell death induced by oxidative stress in C6 cells. Moreover, FCL inhibited the production NO and PGE2 via the inhibition of iNOS and COX-2 expression in BV2 cells. FCL significantly attenuated scopolamine-induced memory impairment in mice and prevented scopolamine-induced AChE activity in the hippocampus. Additionally, FCL reversed the reduction of CREB and BDNF expression. The curcuminoids content in FCL was 1.44%.ConclusionFCL pretreatment could alleviate scopolamine-induced memory impairment in mice, as well as oxidative stress and inflammation in C6 and BV2 cells, respectively. Thus, FCL might be a useful material for preventing impairment of learning and memory.
Highlights
Curcuma longa L. is a well-known medicinal plant that has been used for its anti-cancer, neuroprotective, and hepatoprotective effects
Neuroprotective effects of fermented C. longa (FCL) in tert-buryl hydroperoxide (t-BHP) and H2O2-treated C6 cells To examine the protective potential of FCL against oxidative stress in vitro, its inhibitory effects on t-BHP- and H2O2-induced cell death were measured in C6 glial cells
Previous studies have confirmed that pCREB and brain-derived neurotropic factor (BDNF) are key molecules involved in memory formation, and that activation of cAMP response element-binding protein (CREB) transcriptional activity regulates BDNF expression to induce cognitive function [38, 39]. These findings indicated that the CREB signaling pathway is involved in memory enhancement, and that down-regulation of CREB activation leads to deficits in long-term memory
Summary
Curcuma longa L. is a well-known medicinal plant that has been used for its anti-cancer, neuroprotective, and hepatoprotective effects. In this study, the effectiveness of FCL for the regulation of memory dysfunction was investigated in two brain cell lines (rat glioma C6 and murine microglia BV2) and scopolamine-treated mice. Cognitive impairment, declining learning ability and memory, are common symptoms in age-related neurodegenerative diseases including Alzheimer’s disease (AD), Parkinson’s disease, and stroke. Glial cells, including astrocytes and microglial cells, play critical roles in supporting and protecting neurons. When glial cells (e.g., rat glioma C6, microglial BV2) are activated by free radicals, inflammatory process is initiated, resulting in the death of neuronal cells by the production of pro-inflammatory and neurotoxic factor such as inducible nitric oxide synthase (iNOS), cyclooxygenase-2 (COX-2), and several cytokines [3, 4]. C6 and BV2 cells have been extensively used as cell models of neurotoxicity to investigate responses to proinflammatory cytokines, lipopolysaccharide (LPS), and oxidative stress for searching new drug candidates [5, 6]
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