Institute of Nutrition, Mahidol University, Salaya, Phuttamonthon, Nakhon Pathom, 73170, Thailand.
Department of Biochemistry, Faculty of Medicine, Chiang Mai University, Chiang Mai, 50200, Thailand.
J Ethnopharmacol. 2022 Oct 5;296:115440. doi: 10.1016/j.jep.2022.115440. Epub 2022 Jun 4.
Phikud Navakot (PN), a mixture of nine herbal plants, is an ancient Thai traditional medicine used for relieving circulatory disorders and dizziness. PN has also shown anti-inflammatory effects in rats with acute myocardial infarction. Moreover, phytochemical-inhibiting neuroinflammation, including gallic acid, vanillic acid, ferulic acid, and rutin were detected in PN extract; however, the anti-neuroinflammatory activity of PN extract and its components in a coculture system of microglia and neuronal cells is limited.
To investigate the anti-neuroinflammatory activities of PN on lipopolysaccharide (LPS)-induced inflammation in a coculture system of microglia and neuronal cells.
ELISA and qRT-PCR were used to assess cytokine expression. The phosphorylation of mitogen-activated protein kinases (MAPKs) was determined by Western blotting. Microglia-mediated neuroinflammation was evaluated using a BV-2 microglia-N2a neuron transwell co-culture.
PN extract and its component, gallic acid, decreased LPS-induced the mRNA expression of interleukin-6 (IL-6) and inducible nitric oxide synthase (iNOS), as well as IL-6 protein levels in both microglial monoculture and coculture systems. This was accompanied by a reduction in neurodegeneration triggered by microglia in N2a neurons with increased neuronal integrity markers (βIII tubulin and tyrosine hydroxylase (TH)). These effects were caused by the ability of PN extract to inhibit extracellular signal-regulated protein kinases 1 and 2 (ERK1/2) activation.
This is the first study to show that PN extract inhibits neurodegeneration in LPS-activated BV-2 microglia by targeting ERK signaling activity.
Phikud Navakot（PN）是由九种草药混合而成的一种古老的泰式传统药物，用于缓解循环障碍和头晕。PN 还显示出对急性心肌梗死大鼠的抗炎作用。此外，在 PN 提取物中检测到抑制神经炎症的植物化学物质，包括没食子酸、香草酸、阿魏酸和芦丁；然而，PN 提取物及其成分在小胶质细胞和神经元细胞共培养体系中的抗炎活性有限。
研究 PN 在小胶质细胞和神经元细胞共培养体系中对脂多糖（LPS）诱导炎症的抗炎活性。
采用 ELISA 和 qRT-PCR 检测细胞因子表达，Western blot 检测丝裂原活化蛋白激酶（MAPKs）磷酸化。采用 BV-2 小胶质细胞-N2a 神经元 Transwell 共培养评估小胶质细胞介导的神经炎症。
PN 提取物及其成分没食子酸降低了 LPS 诱导的小胶质细胞和共培养体系中白细胞介素-6（IL-6）和诱导型一氧化氮合酶（iNOS）的 mRNA 表达，以及 IL-6 蛋白水平。这伴随着小胶质细胞在 N2a 神经元中触发的神经退行性变减少，神经元完整性标志物（βIII 微管蛋白和酪氨酸羟化酶（TH））增加。这些作用是由 PN 提取物抑制细胞外信号调节蛋白激酶 1 和 2（ERK1/2）激活的能力引起的。
这是第一项表明 PN 提取物通过靶向 ERK 信号活性抑制 LPS 激活的 BV-2 小胶质细胞中的神经退行性变的研究。
