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. 2021 Dec 23;18:300. doi: 10.1186/s12974-021-02356-z

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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. 3 — Roles of SDV in rhANP-mediated reduction of LPS-induced systemic inflammation and neuroinflammation. a Treatment schedule. Mice were intraperitoneally injected with lipopolysaccharides (LPS, 5 mg/kg). Recombinant human ANP (rhANP; 1.0 mg/kg) or 0.9% saline were intraperitoneally injected to mice at 24 h before and 10 min after LPS injection. Subdiaphragmatic vagotomy (SDV) was performed 14 days prior to LPS injection. Plasma and hippocampus were collected 24 h after LPS injection. b Body weight loss in each group (two-way ANOVA: rhANP: F_1,36 = 7.058, P = 0.0117; SDV: F_1,36 = 12.72, P = 0.0010; interaction: F_1,36 = 4.923, P = 0.0329). The plasma levels of interleukin (IL)-6 (c; two-way ANOVA: rhANP: F_1,36 = 13.07, P = 0.0009; SDV: F_1,36 = 15.60, P = 0.0003; interaction: F_1,36 = 20.51, P < 0.0001), IL-17A (d; two-way ANOVA: rhANP: F_1,36 = 6.111, P = 0.0183; SDV: F_1,36 = 7.794, P = 0.0083; interaction: F_1,36 = 6.027, P = 0.0191), interferon (IFN)-γ (e; two-way ANOVA: rhANP: F_1,36 = 6.460, P = 0.0155; SDV: F_1,36 = 8.447, P = 0.0062; interaction: F_1,36 = 7.836, P = 0.0082), and tumor necrosis factor (TNF)-α (f; two-way ANOVA: rhANP: F_1,36 = 4.828, P = 0.0345; SDV: F_1,36 = 6.217, P = 0.0174; interaction: F_1,36 = 7.883, P = 0.0080). Western blot analysis of ionized calcium-binding adapter molecule 1 (iba-1) (g; two-way ANOVA: rhANP: F_1,36 = 6.208, P = 0.0175; SDV: F_1,36 = 4.772, P = 0.0355; interaction: F_1,36 = 4.996, P = 0.0317), IL-6 (h; two-way ANOVA: rhANP: F_1,36 = 6.286, P = 0.0168; SDV: F_1,36 = 6.894, P = 0.0126; interaction: F_1,36 = 8.569, P = 0.0059), IL-17A (i; two-way ANOVA: rhANP: F_1,36 = 4.268, P = 0.0461; SDV: F_1,36 = 3.363, P = 0.0750; interaction: F_1,36 = 5.503, P = 0.0246), interferon (IFN)-γ (j; two-way ANOVA: rhANP: F_1,36 = 4.706, P = 0.0367; SDV: F_1,36 = 5.685, P = 0.0225; interaction: F_1,36 = 3.530, P = 0.0684), TNF-α (k; two-way ANOVA: rhANP: F_1,36 = 1.598, P = 0.2144; SDV: F_1,36 = 12.72, P = 0.0010; interaction: F_1,36 = 4.345, P = 0.0443), inducible nitric oxide synthase (iNOS) (l; two-way ANOVA: rhANP: F_1,36 = 4.764, P = 0.0357; SDV: F_1,36 = 2.933, P = 0.0954; interaction: F_1,36 = 5.462, P = 0.0251) and their respective β-actin in the hippocampus. Data are shown as mean ± SEM, n = 10/group. ^*P < 0.05, ^**P < 0.01, ^***P < 0.0001; N.S. not significant