Helicid reverses lipopolysaccharide‐induced inflammation and promotes GDNF levels in C6 glioma cells through modulation of prepronociceptin,Chemistry & Biodiversity

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Helicid reverses lipopolysaccharide‐induced inflammation and promotes GDNF levels in C6 glioma cells through modulation of prepronociceptin
Chemistry & Biodiversity ( IF 2.3 ) Pub Date : 2020-06-17 , DOI: 10.1002/cbdv.202000063
Yuanxiang Zhang ₁ , Di Luan ₂ , Yanhao Liu ₁ , Hongjin Li ₁ , Jian Dong ₁ , Xiaotong Zhang ₁ , Lili Yuan ₂ , Zhengling Zhong ₃ , Lan Jiang ₄ , Xuyi Li ₅ , Mingquan Ye ₁ , Jiucui Tong _{1,

3}

Affiliation

Helicid suppresses inflammatory factors and protects nerve cells in the hippocampus of rats with depression, but the mechanisms underlying its protective effects are unclear at present. In this investigation, we conducted gene silencing, Helicid intervention and rescue experiments to explore the protective actions of PNOC, the prepronociceptin gene known to regulate inflammatory processes, and Helicid on a C6 cell model of inflammation induced by LPS. Collective data from Western blots, ELISA, immunofluorescence and flow cytometry experiments showed that PNOC silencing or administration of Helicid led to reduced inflammatory factor levels, oxidative stress and expression of glial fibrillary acidic protein (GFAP), along with increased glial cell lines‐derived neurotrophic factor (GDNF) expression. Furthermore, expression of p‐Akt in the Akt signaling pathway was increased. Interestingly, overexpression of PNOC in the Helicid treatment group partially reversed the Helicid‐induced changes in the above biochemical indexes. Our collective results provide strong evidence of Helicid‐mediated regulation of the Akt signaling pathway through PNOC to improve cell inflammation and oxidative stress.

中文翻译：

Helicid 通过调节前原伤害感受素逆转脂多糖诱导的炎症并提高 C6 神经胶质瘤细胞中的 GDNF 水平

Helicid抑制抑郁症大鼠海马的炎症因子并保护神经细胞，但其保护作用的机制目前尚不清楚。在这项研究中，我们进行了基因沉默、Helicid 干预和拯救实验，以探索 PNOC、已知调节炎症过程的前原感受素基因和 Helicid 对 LPS 诱导的 C6 炎症细胞模型的保护作用。来自蛋白质印迹、ELISA、免疫荧光和流式细胞术实验的集体数据表明，PNOC 沉默或 Helicid 的施用导致炎症因子水平、氧化应激和神经胶质纤维酸性蛋白 (GFAP) 的表达降低，以及神经胶质细胞系衍生的神经营养蛋白增加。因子 (GDNF) 表达。此外，Akt 信号通路中 p-Akt 的表达增加。有趣的是，在 Helicid 治疗组中 PNOC 的过度表达部分逆转了 Helicid 诱导的上述生化指标的变化。我们的集体结果提供了强有力的证据，证明 Helicid 介导的 Akt 信号通路通过 PNOC 调节以改善细胞炎症和氧化应激。

更新日期：2020-06-17

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