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. 2022 Feb 4;14:26. doi: 10.1186/s13098-021-00780-y

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© The Author(s) 2021

Open AccessThis 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/. The Creative Commons Public Domain Dedication waiver (http://creativecommons.org/publicdomain/zero/1.0/) applies to the data made available in this article, unless otherwise stated in a credit line to the data.

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Fig. 2 — Effect of TLR9 knockdown on the NF-kB-NLRP3 inflammasome pathway in renal tissues of experimental mice (db/db). Experimental mice (db/db) were administered lentiviral-shRNA-NC or lentiviral-shRNA-TLR9 via tail vein injection. A Representative IHC image of TLR9, phosphor NF-kB, and NLRP3 antibodies in the glomeruli of mice (db/m) and mice with DN (db/db). B WB was conducted to determine the protein levels of TLR9, NF-kB, NLRP3, nuclear NF-kB, phosphor NF-kB, PYCARD, IL-1β, and cysteinyl aspartate-specific proteinase-1 in the renal tissues of mice (db/m) and mice with DN (db/db)