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中、重度辣味红甜椒可预防阿尔茨海默病糖尿病大鼠的记忆缺陷和肝胰岛素抵抗。

Red peppers with moderate and severe pungency prevent the memory deficit and hepatic insulin resistance in diabetic rats with Alzheimer's disease.

机构信息

Division of Metabolism and Functionality Research, Korean Food Research Institutes, Sungnam, South Korea.

Department of Food and Nutrition, Obesity/Diabetes Research Center, Hoseo University, 165 Sechul-Ri, BaeBang-Yup, Asan-Si, ChungNam-Do 336-795 South Korea.

出版信息

Nutr Metab (Lond). 2015 Mar 8;12:9. doi: 10.1186/s12986-015-0005-6. eCollection 2015.

DOI:10.1186/s12986-015-0005-6
PMID:25755673
原文链接:https://pmc.ncbi.nlm.nih.gov/articles/PMC4353669/
Abstract

BACKGROUND

Dementia induced by β-amyloid accumulation impairs peripheral glucose homeostasis, but red pepper extract improves glucose homeostasis. We therefore evaluated whether long-term oral consumption of different red pepper extracts improves cognitive dysfunction and glucose homeostasis in type 2 diabetic rats with β-amyloid-induced dementia.

METHODS

Male diabetic rats received hippocampal CA1 infusions of β-amyloid (25-35) (AD) or β-amyloid (35-25, non-plaque forming), at a rate of 3.6 nmol/day for 14 days (Non-AD). AD rats were divided into four dietary groups receiving either 1% lyophilized 70% ethanol extracts of either low, moderate and severe pungency red peppers (AD-LP, AD-MP, and AD-SP) or 1% dextrin (AD-CON) in Western diets (43% energy as fat).

RESULTS

The ascending order of control < LSP < MSP and SSP potentiated the phosphorylation of CREB and GSK and inhibited Tau phosphorylation in the hippocampus which in turn inhibited β-amyloid accumulation. The inhibition by MP and SP reduced the memory deficit measured by passive avoidance test and water maze test. Furthermore, the accumulation of β-amyloid induced glucose intolerance, although serum insulin levels were elevated during the late phase of oral glucose tolerance test (OGTT). All of the red pepper extracts prevented the glucose intolerance in AD rats. Consistent with OGTT results, during euglycemic hyperinulinemic clamp glucose infusion rates were lower in AD-CON than Non-AD-CON with no difference in whole body glucose uptake. Hepatic glucose output at the hyperinsulinemic state was increased in AD-CON. β-amyloid accumulation exacerbated hepatic insulin resistance, but all red pepper extract treatments reversed the insulin resistance in AD rats.

CONCLUSIONS

The extracts of moderate and severe red peppers were found to prevent the memory deficit and exacerbation of insulin resistance by blocking tau phosphorylation and β-amyloid accumulation in diabetic rats with experimentally induced Alzheimer's-like dementia. These results suggest that red pepper consumption might be an effective intervention for preventing age-related memory deficit.

摘要

背景

β-淀粉样蛋白积累引起的痴呆症会损害外周葡萄糖稳态,但红辣椒提取物可改善葡萄糖稳态。因此,我们评估了长期口服不同红辣椒提取物是否可以改善β-淀粉样蛋白诱导的痴呆症 2 型糖尿病大鼠的认知功能障碍和葡萄糖稳态。

方法

雄性糖尿病大鼠接受海马 CA1 内β-淀粉样蛋白(25-35)(AD)或β-淀粉样蛋白(35-25,非斑块形成)输注,速率为每天 3.6 nmol,持续 14 天(非 AD)。AD 大鼠分为四组,分别给予 Western 饮食中 1%冻干 70%乙醇低、中、高辣度红辣椒提取物(AD-LP、AD-MP 和 AD-SP)或 1%糊精(AD-CON)。

结果

对照组<LSP<MSP 和 SSP 依次增强了 CREB 和 GSK 的磷酸化,并抑制了海马中的 Tau 磷酸化,从而抑制了β-淀粉样蛋白的积累。MP 和 SP 的抑制作用降低了通过被动回避测试和水迷宫测试测量的记忆缺陷。此外,尽管在口服葡萄糖耐量试验(OGTT)的后期阶段血清胰岛素水平升高,但 MP 和 SP 的积累会引起葡萄糖不耐受。所有红辣椒提取物均预防了 AD 大鼠的葡萄糖不耐受。与 OGTT 结果一致,在正葡萄糖高胰岛素钳夹期间,AD-CON 的葡萄糖输注率低于 Non-AD-CON,全身葡萄糖摄取无差异。在高胰岛素状态下,肝葡萄糖输出增加 AD-CON。β-淀粉样蛋白积累加剧了肝胰岛素抵抗,但所有红辣椒提取物处理均逆转了 AD 大鼠的胰岛素抵抗。

结论

在实验性诱导的阿尔茨海默病样痴呆症糖尿病大鼠中,中等和高辣度红辣椒提取物可通过阻止 Tau 磷酸化和β-淀粉样蛋白积累来预防记忆缺陷和加剧胰岛素抵抗,从而发现这些提取物可预防记忆缺陷。这些结果表明,红辣椒的摄入可能是预防与年龄相关的记忆缺陷的有效干预措施。

https://cdn.ncbi.nlm.nih.gov/pmc/blobs/8442/4353669/011e8d5f2d91/12986_2015_5_Fig6_HTML.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/8442/4353669/5cd5eb90ad00/12986_2015_5_Fig1_HTML.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/8442/4353669/8b2ea1bdbc25/12986_2015_5_Fig2_HTML.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/8442/4353669/b6319c3137c3/12986_2015_5_Fig3_HTML.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/8442/4353669/5ccefd9dea90/12986_2015_5_Fig4_HTML.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/8442/4353669/018c309e048c/12986_2015_5_Fig5_HTML.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/8442/4353669/011e8d5f2d91/12986_2015_5_Fig6_HTML.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/8442/4353669/5cd5eb90ad00/12986_2015_5_Fig1_HTML.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/8442/4353669/8b2ea1bdbc25/12986_2015_5_Fig2_HTML.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/8442/4353669/b6319c3137c3/12986_2015_5_Fig3_HTML.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/8442/4353669/5ccefd9dea90/12986_2015_5_Fig4_HTML.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/8442/4353669/018c309e048c/12986_2015_5_Fig5_HTML.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/8442/4353669/011e8d5f2d91/12986_2015_5_Fig6_HTML.jpg

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