Amygdalin Attenuates Neuroinflammatory Injury via Down-Regulating Toll-Like Receptors-2/Toll-Like Receptors-4- Nuclear Factor Kappa-B Signaling Pathway in BV2
Tong Sun2, Jing-Jing Lu3, Bi-Xu Wang2, Xiao-Qing Ye2, Lan Li2, Fang-Mei Zhou2, Hai-Tong Wan4, Zhi-Shan Ding2★★ Corresponding author
- 1School of Medical Technology and Information Engineering, Zhejiang Chinese Medical University, China.
- 2College of Life Science, Zhejiang Chinese Medical University, Hangzhou 310053, Zhejiang, China.
- 3Zhejiang Chinese Medical University Hangzhou 310053, China.
CORRESPONDENCE
Zhi-Shan Ding
College of Life Science, Zhejiang Chinese Medical University, Hangzhou 310053, Zhejiang, China.
Received: 23-01-2022; Revised: 23-03-2022; Accepted: 03-08-2022.
Volume 18, Issue 80 · pp. 1096–1103 · PUBLISHED 23 November 2022 · DOI: 10.4103/pm.pm_32_22
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ABSTRACT
Objectives: The purpose of this study was to explore the anti‑inflammatory effect of amygdalin on lipopolysaccharide (LPS)‑induced neuron–microglia and its protective mechanism for toll‑like receptors (TLRs) signaling pathways. Materials and Methods: Griess, quantitative PCR, and flow cytometry were used to detect the influence of amygdalin on the release of inflammatory factors from BV2 mouse microglia (BV2 cells). The anti‑inflammatory pathway of amygdalin was further explored by western blotting. At the same time, the effect of amygdalin on LPS‑induced oxidative stress damage in BV2 cells was detected by WST‑8 and fluorescence probe. Results: After LPS induction, the pro‑inflammatory factors such as nitric oxide, interleukin‑6, tumor necrosis factor‑alpha, interleukin‑1β, and recombinant NLR Family, Pyrin Domain Containing Protein3 were significantly increased. However, the levels were reversed significantly after treatment with amygdalin. In addition, amygdalin significantly inhibited the increase of TLR4, TLR2, and its downstream signal myeloid differentiation primary response gene 88 and P‑NF‑κB p65 in BV2 cells induced by LPS. Amygdalin can also reverse the abnormal expression of LPS‑induced oxidative stress indexes such as cyclooxygenase‑2, reactive oxygen species, and superoxide dismutase. Conclusion: Amygdalin may reduce the LPS‑induced accumulation of pro‑inflammatory substances via the down‑regulating of the TLR2/TLR4‑nuclear factor kappa‑B signaling pathway.
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Sun, T., Lu, J., Wang, B., Ye, X., Li, L., Zhou, F., Wan, H., & Ding, Z. (2022). Amygdalin Attenuates Neuroinflammatory Injury via Down-Regulating Toll-Like Receptors-2/Toll-Like Receptors-4- Nuclear Factor Kappa-B Signaling Pathway in BV2. Pharmacognosy Magazine, 18(80), 1096–1103. https://doi.org/10.4103/pm.pm_32_22