IMR Press / JIN / Volume 22 / Issue 2 / DOI: 10.31083/j.jin2202048
Open Access Original Research
Neuroprotection of Emodin by Inhibition of Microglial NLRP3 Inflammasome-Mediated Pyroptosis
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1 Department of Neurology, Nantong Hospital to Nanjing University of Chinese Medicine, Nantong Hospital of Traditional Chinese Medicine, 226001 Nantong, Jiangsu, China
2 Department of Neurology, Affiliated Hospital of Nanjing University of Chinese Medicine, 210004 Nanjing, Jiangsu, China
3 Department of Physiology, School of Medicine, Nantong University, 226001 Nantong, Jiangsu, China
4 Department of Acupuncture and Massage, Affiliated Hospital of Nantong University, 226001 Nantong, Jiangsu, China
*Correspondence: (Xi-Wu Yan); (Cheng Chang)
These authors contributed equally.
J. Integr. Neurosci. 2023, 22(2), 48;
Submitted: 4 January 2023 | Revised: 28 January 2023 | Accepted: 2 February 2023 | Published: 6 March 2023
Copyright: © 2023 The Author(s). Published by IMR Press.
This is an open access article under the CC BY 4.0 license.

Background: Neuroinflammation triggered by chronic cerebral ischemia-induced microglial pyroptosis is a significant contributor to vascular cognitive impairment. It has been shown that emodin possesses anti-inflammatory and neuroprotective properties, however, it’s potential molecular and signaling transduction pathway remains to be illuminated. This study researched the neuroprotective mechanisms of emodin focussing on emodin effects on lipopolysaccharide/adenosine triphosphate (LPS/ATP)-caused pyroptosis in BV2 cells and HT-22 hippocampal neurons. Methods: To explore the neuroprotective effect of emodin, Emodin was applied to BV2 cells, HT-22 hippocampal neurons, and BV2/HT-22 co-cultures stimulated with LPS/ATP to evaluate the cell morphology, levels of inflammatory factors, NLRP3 inflammatory inflammasome activity and focal pyroptosis-related protein expression, as same as neuronal apoptosis. Results: Emodin alleviated LPS/ATP-induced pyroptosis of BV2 cells by preventing the activity of the NLRP3 inflammasome and the cleavage of pyroptosis executive protein Gasdermin D (GSDMD). Furthermore, levels of interleukin (IL)-18, IL-1β and tumor necrosis factor (TNF)-α were reduced, the apoptosis of HT-22 hippocampal neurons was attenuated, and cell viability was restored. Conclusions: Emodin can antagonize microglial neurotoxicity by inhibiting microglial pyroptosis, thereby exerting anti-inflammatory and neuroprotective effects.

NLRP3 inflammasome
82201586/National Natural Science Foundation of China
MB2021028/Nantong Municipal Health and Family Planning Commission Science Foundation
MS22022048/Scientific Research Fund for Nantong social livelihood science and technology plan
TZYK202102/Scientific Research Fund for Nantong TCM Medical Alliance
KYCX22_1893/Research and Practice Innovation Program of Nanjing University of Chinese Medicine
Fig. 1.
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