Send to

Choose Destination
Molecules. 2019 Sep 12;24(18). pii: E3317. doi: 10.3390/molecules24183317.

Anti-Inflammatory Effect of Erinacine C on NO Production Through Down-Regulation of NF-κB and Activation of Nrf2-Mediated HO-1 in BV2 Microglial Cells Treated with LPS.

Author information

Department of Nutrition, Master Program of Biomedical Nutrition, Hungkuang University, Taichung City 43302, Taiwan.
Department of Food Nutrition and Health Biotechnology, Asia University, Taichung City 41354, Taiwan.
Department of Medical Laboratory Science and Technology, Central Taiwan University of Science and Technology, Taichung City 40601, Taiwan.
Grape King Bio Ltd., Taoyuan City 324, Taiwan.
Department of Food Science, Nutrition, and Nutraceutical Biotechnology, Shih Chien University, Taipei City 104, Taiwan.
Institute of Food Science and Technology, National Taiwan University, Taipei City 10617, Taiwan.
Department of Bioscience Technology, Chung Yuan Christian University, Taoyuan City 32023, Taiwan.
Department of Cosmetic Science, Chang Gung University of Science and Technology, Taoyuan City 33303, Taiwan.
Department of Nutrition, Master Program of Biomedical Nutrition, Hungkuang University, Taichung City 43302, Taiwan.


Previous studies have revealed the anti-inflammatory and neuroprotective properties of Hericium erinaceus extracts, including the fact that the active ingredient erinacine C (EC) can induce the synthesis of nerve growth factor. However, there is limited research on the use and mechanisms of action of EC in treating neuroinflammation. Hence, in this study, the inflammatory responses of human BV2 microglial cells induced by LPS were used to establish a model to assess the anti-neuroinflammatory efficacy of EC and to clarify its possible mechanisms of action. The results showed that EC was able to reduce the levels of nitric oxide (NO), interleukin-6 (IL-6), tumor necrosis factor (TNF)-α, and inducible nitric oxide synthase (iNOS) proteins produced by LPS-induced BV2 cells, in addition to inhibiting the expression of NF-κB and phosphorylation of IκBα (p-IκBα) proteins. Moreover, EC was found to inhibit the Kelch-like ECH-associated protein 1 (Keap1) protein, and to enhance the nuclear transcription factor erythroid 2-related factor (Nrf2) and the expression of the heme oxygenase-1 (HO-1) protein. Taken together, these data suggest that the mechanism of action of EC involves the inhibition of IκB, p-IκBα, and iNOS expressions and the activation of the Nrf2/HO-1 pathway.


Hericium erinaceus mycelium; erinacine C; microglial cells; neuroinflammation; nitric oxide; proinflammatory cytokines

Supplemental Content

Full text links

Icon for Multidisciplinary Digital Publishing Institute (MDPI) Icon for PubMed Central
Loading ...
Support Center