人参通过激活抗氧化/BDNF保护机制和抑制促炎细胞因子/NF-KB信号通路,在缺氧应激小鼠中表现出类似适应原的活性

James Olukayode Oni , Divine Oluwaferanmi Oyenekan , Yetunde Olamide Olayemi , Osarugue Christabel Irabor , Precious Ogbuji , McCarthy Oritseweyinmi Tova , Paul Ademola Adeleke , Gbemisayo Adetomiwa Abbas , Solomon Umukoro
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引用次数: 0

摘要

缺氧应激对脑细胞造成严重损伤,引起各种神经病理并发症。人参在中医中被广泛用作健康生活的补品,因为它具有适应/恢复活力的特性,并可缓解慢性压力相关疾病,包括眩晕、抑郁、短期记忆丧失和缺乏注意力或警惕性。本研究探讨了人参商业产品(Ginsomin)在低氧-缺氧应激雄性瑞士小鼠中的适应原特性及其作用机制。将小鼠(20 ~ 22 g)分为5组(n = 6), 1组(非应激对照组)和2组(应激对照组)给予蒸馏水,3 ~ 5组给予人参(10、50、100 mg/kg),连续口服7 d。2 ~ 5组缺氧应激20 min,持续6 d,第7天评估缺氧惊厥潜伏期。随后评估神经行为变化(运动功能、记忆、焦虑、猝厥、抑郁和肌肉力量)。测定血糖和皮质酮水平,以及丙二醛、亚硝酸盐、抗氧化谱、促炎细胞因子(肿瘤坏死因子- α和白细胞介素-6)、谷氨酸、脑源性神经营养因子(BDNF)和核因子κB (NF-κB)的脑含量。测定大鼠脑乙酰胆碱酯酶、caspase-3、髓过氧化物酶、核因子2-相关因子2 (NFr-2)和谷氨酸脱羧酶(GAD)活性。人参减轻应激小鼠缺氧惊厥和神经行为缺陷。它降低了血浆皮质酮和葡萄糖水平,降低了丙二醛、亚硝酸盐、促炎细胞因子、NF-kB、caspase-3、乙酰胆碱酯酶、谷氨酸和髓过氧化物酶的脑含量。人参处理小鼠的大脑抗氧化谱增加;GAD、BDNF和NFr-2含量与应力控制的关系。讨论。研究结果表明,人参通过多种分子机制,通过抑制皮质酮介导的氧化和炎症/凋亡信号通路,激活GAD、BDNF和NFr-2应激保护性防御系统,显示出类似于适应原的特性。综上所述,这些发现进一步证实了其在缓解常见老年慢性应激相关疾病中的适应原样特性。
本文章由计算机程序翻译,如有差异,请以英文原文为准。

Ginseng exhibits adaptogenic-like activity in mice exposed to hypoxic-anoxic stress through activation of antioxidant/BDNF protective mechanisms and inhibition of pro-inflammatory cytokines/NF-KB signaling pathways

Ginseng exhibits adaptogenic-like activity in mice exposed to hypoxic-anoxic stress through activation of antioxidant/BDNF protective mechanisms and inhibition of pro-inflammatory cytokines/NF-KB signaling pathways

Introduction

Hypoxic-anoxic stress causes severe injury to the brain cells resulting in various neuropathological complications. Ginseng is widely used in Traditional Chinese Medicine (TCM) as a tonic for healthy living due to its adaptogenic/rejuvenating properties and in mitigating chronic stress-related diseases including vertigo, depression, short-term memory loss, and lack of attention or vigilance. This study evaluates the adaptogenic-like properties of Panax ginseng commercial product (Ginsomin) and the biochemical mechanisms underlying its action in male Swiss mice exposed to hypoxic-anoxic stress.

Methods

. The mice (20–22 g) were distributed into five groups (n = 6). Groups 1 (non-stress control) and 2 (stress-control) received distilled water while groups 3–5 had ginseng (10, 50, and 100 mg/kg), orally for seven days. Groups 2 to 5 were subjected to hypoxic stress for 20 min for six days prior to assessment of the latency to anoxic convulsion on day 7. The neurobehavioral changes (motor functions, memory, anxiety, catalepsy, depression, and muscle strength) were evaluated afterwards. Blood glucose and corticosterone levels alongside brain contents of malondialdehyde, nitrites, antioxidant profiles, pro-inflammatory cytokines (tumor necrosis factor–alpha and interleukin-6), glutamate, brain derived neurotrophic factor (BDNF), and nuclear factor kappa B (NF-κB) were determined. The brain acetylcholinesterase, caspase-3, myeloperoxidase, nuclear factor erythroid 2-related factor 2 (NFr-2) and glutamic acid decarboxylase (GAD) activities were evaluated.

Results

. Ginseng attenuated the anoxic convulsion and neurobehavioral deficits in stressed-mice. It reduced plasma corticosterone and glucose levels, and decreased the brain contents of malondialdehyde, nitrites, pro-inflammatory cytokines, NF-kB, caspase-3, acetylcholinesterase, glutamate and myeloperoxidase. Ginseng-treated mice had increased brain antioxidant profiles; GAD, BDNF, and NFr-2 contents relative to stress-control.

Discussion

. The results of the study showed that ginseng demonstrated adaptogenic-like properties by attenuating neurobehavioral deficits in mice exposed to hypoxic-anoxic stress via multiple molecular mechanisms, relating to inhibition of corticosterone-mediated oxidative and inflammatory/apoptotic signaling pathways, and activation of GAD, BDNF and NFr-2 stress-protective defense systems. Taken together, these findings further confirm its adaptogenic-like properties in alleviating common geriatric chronic stress-related diseases in Chinese medicines.
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