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. 2021 Oct 13;21:495. doi: 10.1186/s12872-021-02307-9

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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. 1 — Generation of rats with diabetic nephropathy (DN).The rats were fed a high fat diet containing 0.75% adenine for 8 weeks and performed a single STZ (35 mg/kg) injection intraperitoneally. Rats were divided into four groups: control rats fed with normal diet and saline injection (C), high fat and adenine-fed and STZ-injected rats (DN), DN rats with sodium hydrosulfide (NaHS) treatment (DN + NaHS), and control rats with NaHS treatment (C + NaHS), A–E, Body weight (A), the concentration of glucose (B), H₂S (C), creatinine (D), and urea nitrogen (E) in plasma were determined. n = 6 ~ 7 rats. Values represent the means ± SEM.*p < 0.05 compared to control rats. #p < 0.05 compared to DN rats