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. 2023 Jul 18;29:98. doi: 10.1186/s10020-023-00698-3

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© The Author(s) 2023

Open Access This article is licensed under a Creative Commons Attribution 4.0 International License, which permits use, sharing, adaptation, distribution and reproduction in any medium or format, as long as you give appropriate credit to the original author(s) and the source, provide a link to the Creative Commons licence, and indicate if changes were made. The images or other third party material in this article are included in the article's Creative Commons licence, unless indicated otherwise in a credit line to the material. If material is not included in the article's Creative Commons licence and your intended use is not permitted by statutory regulation or exceeds the permitted use, you will need to obtain permission directly from the copyright holder. To view a copy of this licence, visit http://creativecommons.org/licenses/by/4.0/.

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Fig. 6 — CQYG attenuates neuroinflammation in high glucose injured Schwann cells. A ELISA detection of IL-6, IL-1β, and TNF-α levels in RSC96 cells treated with high glucose, CQYG and TMAO. B Intracellular ROS levels (Ratios of 2-OH-E + /DHE) in RSC96 cells treated with high glucose, CQYG and TMAO. C JC-1 monomer levels (Ratios of red/green) in RSC96 cells treated with high glucose, CQYG and TMAO. D Apoptosis detection by flow cytometry in RSC96 cells treated with high glucose, CQYG and TMAO. E Apoptosis rate of RSC96 cells. *P < 0.05 vs control group; ^#P < 0.05 vs high glucose group