Molecular Drug Metabolism and Toxicology Research Laboratories, Department of Biochemistry, College of Medicine, University of Ibadan, Ibadan, Nigeria.
J Food Biochem. 2021 Apr;45(4):e13660. doi: 10.1111/jfbc.13660. Epub 2021 Feb 24.
This study examined the protective effect of 6-Gingerol (6G) against lipopolysaccharide (LPS)-induced cognitive impairments, oxidative stress, neuroplasticity, amyloidogenesis, and inflammation. Male rats were allocated into six groups in this manner; Group I placed on normal saline only. Group II was treated for 7 days with LPS alone intraperitoneally at 250 µg/kg body weight (bw). Group III received 6G alone at 50 mg/kg bw orally for 14 days. Groups IV and V received 6G at 20 and 50 mg/kg bw for 7 days, respectively, and LPS for another 7 days to induce neurotoxicity. Group VI received 5 mg/kg bw of donepezil for 7 days and LPS for 7 days. Pretreatment with 20 and 50 mg/kg bw of 6G protected against LPS-mediated learning and memory function, and also locomotor and motor deficits. Besides, 20 and 50 mg/kg bw 6G mitigated LPS-induced alteration in markers of oxidative stress. Furthermore, induction of amyloidogenesis associated with disruption of histoarchitecture and high expression of interleukin 1β, inducible nitric oxide synthase, amyloid precursor protein (APP), β-secretase 1, and brain-derived neurotrophic factor by LPS was mitigated by the two doses of 6G in the rat hippocampus and cerebral cortex region of the brain. 6G pretreatment at the two doses mitigated LPS-mediated histopathological changes in the hippocampus and cerebral cortex of rats. Overall, our results demonstrate that the protective effect of 6G is mediated through the reversal of neurobehavioral deficit, oxidative stress, inflammation, and amyloidogenesis, thus making 6G a possible chemoprophylactic agent against brain injury as a result of LPS exposure. PRACTICAL APPLICATIONS: In the search for a holistic prevention of inflammation-associated neurodegeneration, nutraceuticals are becoming prominent. Hence, this study presents 6G, an active constituent of ginger, as a chemoprotective, antioxidant, and anti-inflammatory agent, which is able to ameliorate cognitive impairments, oxidative stress, neuroplasticity, amyloidogenesis, and inflammation in LPS-induced rat model of neuroinflammation.
本研究旨在探讨 6-姜酚（6G）对脂多糖（LPS）诱导的认知障碍、氧化应激、神经可塑性、淀粉样蛋白形成和炎症的保护作用。雄性大鼠被分为六组；第一组仅接受生理盐水处理。第二组大鼠腹腔内注射 LPS（250μg/kg 体重），连续处理 7 天。第三组大鼠连续 14 天经口给予 6G（50mg/kg 体重）。第四组和第五组大鼠分别连续 7 天经口给予 20 和 50mg/kg 体重的 6G，随后再腹腔内注射 LPS 7 天，以诱导神经毒性。第六组大鼠连续 7 天腹腔内注射 5mg/kg 体重的多奈哌齐和 LPS。20 和 50mg/kg 体重的 6G 预处理可防止 LPS 介导的学习和记忆功能障碍以及运动和运动功能障碍。此外，20 和 50mg/kg 体重的 6G 可减轻 LPS 诱导的氧化应激标志物的改变。此外，在大鼠海马和大脑皮质区域，6G 可减轻 LPS 诱导的与组织形态破坏相关的淀粉样蛋白形成，以及白细胞介素 1β、诱导型一氧化氮合酶、淀粉样前体蛋白（APP）、β-分泌酶 1 和脑源性神经营养因子的高表达。6G 预处理可减轻 LPS 介导的大鼠海马和大脑皮质的组织病理学变化。总的来说，我们的结果表明，6G 的保护作用是通过逆转神经行为缺陷、氧化应激、炎症和淀粉样蛋白形成来介导的，因此 6G 可能是一种针对 LPS 暴露导致脑损伤的化学预防剂。
在寻找炎症相关神经退行性变的整体预防方法时，营养保健品变得越来越突出。因此，本研究将 6G 作为一种化学保护剂、抗氧化剂和抗炎剂，展示了姜的一种活性成分，它能够改善 LPS 诱导的神经炎症大鼠模型中的认知障碍、氧化应激、神经可塑性、淀粉样蛋白形成和炎症。
