Anthocyanins from Lycium ruthenicum Murr. Ameliorated D-Galactose-Induced Memory Impairment, Oxidative Stress, and Neuroinflammation in Adult Rats

Anthocyanins from Lycium ruthenicum Murr. Ameliorated D-Galactose-Induced Memory Impairment, Oxidative Stress, and Neuroinflammation in Adult Rats
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来自黑果枸杞的花青素。

DOI:
10.1021/acs.jafc.8b06402
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发表时间:
2019-03-20
影响因子:
6.1
通讯作者:
Suo, Yourui
Suo, Yourui
中科院分区:
农林科学1区
文献类型:
--
作者:
Chen, Shasha;Zhou, Haonan;Suo, Yourui

文献摘要

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枸杞穆尔(LR)是一种多年生灌木,常用作营养食品和药物。在此,我们从LR中鉴定出12种花色苷,其中矮牵牛素衍生物占总花色苷含量的约97%。此外,花青素发挥神经保护作用的潜在机制在D-半乳糖(D-gal)处理的大鼠进行了探讨。行为学结果表明,花色苷缓解D-半乳糖诱导的记忆障碍。此外,花青素减少晚期糖基化终末产物受体(receptor for advanced glycation end products,EDP),抑制D-半乳糖引起的氧化应激。花青素抑制小胶质细胞增生和星形胶质细胞增生,并减少核因子κ B(NF-κ B)、白细胞介素-1-β(IL-1 β)、环氧合酶-2(考克斯-2)和肿瘤坏死因子-α(TNF-α)的过度表达。此外,花青素降低C-jun N-末端激酶(p-JNK),caspase-3水平,和B细胞淋巴瘤2相关的X蛋白/B细胞淋巴瘤2(Bax/Bcl 2)的比例。因此,来自LR的花青素减轻由D-半乳糖引起的记忆障碍、神经炎症和神经变性,可能通过JNK/NF-κ B/JNK途径,代表用于预防和治疗神经变性疾病的有希望的、安全的候选物。
Lycium ruthenicum Murr. (LR) is a perennial shrub commonly used as a nutritional food and medicine. Herein, we identified 12 anthocyanins from LR, with petunidin derivatives constituting approximately 97% of the total anthocyanin content. Furthermore, the potential mechanism of anthocyanins exerting neuroprotective effects in D-galactose (D-gal)-treated rats was explored. Behavioral results showed that anthocyanins relieved D-gal-induced memory disorder. Additionally, anthocyanins reduced receptor for advanced glycation end products (RAGE) and suppressed oxidative stress caused by D-gal. Anthocyanins suppressed microgliosis and astrocytosis and reduced the overexpression of nuclear factor kappa B (NF-kappa B), interleukin-1-beta (IL-1 beta)cyclooxygenase-2 (COX-2), and tumor necrosis factor-alpha (TNF-alpha). Moreover, anthocyanins lowered C-jun N-terminal kinase (p-JNK), caspase-3 levels, and the B-cell lymphoma 2-associated X protein/B-cell lymphoma 2 (Bax/Bcl2) ratio. Thus, anthocyanins from LR attenuated memory disfunction, neuroinflammation, and neurodegeneration caused by D-gal, possibly through the RAGE/NF-kappa B/JNK pathway, representing a promising, safe candidate for prevention and therapy of neurodegenerative diseases.