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Curcumin abrogates cobalt-induced neuroinflammation by suppressing proinflammatory cytokines release, inhibiting microgliosis and modulation of ERK/MAPK signaling pathway
Journal of Chemical Neuroanatomy ( IF 2.8 ) Pub Date : 2024-02-28 , DOI: 10.1016/j.jchemneu.2024.102402
Rademene S. Oria , Godson E. Anyanwu , Johnson N. Nto , James O. Ikpa

Curcumin, a bioactive polyphenol derived from turmeric, has been reported to have anti-inflammatory properties. The current study investigated the anti-inflammatory effect of curcumin in the hippocampal subfields (CA1 and CA3) after exposure to cobalt (Co) and the impact of ERK protein. Twenty-eight albino Wistar rats were divided into four groups, each with seven randomly selected rats as follows: Control (distilled water), Cobalt (Co) only (40 mg/kg), 120 mg/kg or 240 mg/kg curcumin + Co (40 mg/kg). Treatment was via oral gavage for 28 days. We performed a biochemical investigation to determine the levels of proinflammatory cytokines (TNFα and IL-1β). Furthermore, we conducted an immunohistochemical evaluation to assess the expression of IBA1 by microglial cells and the immunoexpression of ERK protein in the hippocampus. Results revealed a significant (p<0.05) elevation in the tissue level of TNFα and IL-1β, an increase in the number of IBA1-positive microglia, and upregulation of ERK protein in the hippocampal subfields of the rats after exposure to cobalt-only. Nevertheless, pretreatment with curcumin restored these parameters to levels comparable to control. In conclusion, our results showed that curcumin abrogated the Co-induced neuroinflammation by suppressing the release of proinflammatory biomarkers, reducing microgliosis, and modulating the ERK/MAPK pathway.

中文翻译:

姜黄素通过抑制促炎细胞因子释放、抑制小胶质细胞增生和调节 ERK/MAPK 信号通路来消除钴诱导的神经炎症

姜黄素是一种从姜黄中提取的生物活性多酚,据报道具有抗炎特性。目前的研究调查了姜黄素在接触钴(Co)后海马亚区(CA1和CA3)的抗炎作用以及ERK蛋白的影响。将28只白化Wistar大鼠分为四组,每组随机选择7只大鼠,如下:对照(蒸馏水)、仅钴(Co)(40 mg/kg)、120 mg/kg或240 mg/kg姜黄素+钴(40 毫克/千克)。治疗是通过口服强饲法进行28天。我们进行了生化研究以确定促炎细胞因子(TNFα 和 IL-1β)的水平。此外,我们进行了免疫组织化学评估,以评估小胶质细胞 IBA1 的表达和海马 ERK 蛋白的免疫表达。结果显示,仅接触钴后,大鼠海马亚区的 TNFα 和 IL-1β 组织水平显着升高(p<0.05),IBA1 阳性小胶质细胞数量增加,ERK 蛋白上调。然而,姜黄素预处理将这些参数恢复到与对照相当的水平。总之,我们的结果表明姜黄素通过抑制促炎生物标志物的释放、减少小胶质细胞增生和调节 ERK/MAPK 通路来消除 Co 诱导的神经炎症。
更新日期:2024-02-28
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