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Renal morphological changes were examined using hematoxylin and eosin (H&amp;E) staining, while kidney function and oxidative stress markers were quantitatively assessed. Flow cytometry (FCM) was employed to profile immune cell differentiation and functional status. The mRNA and protein levels of kidney injury\u2013related biomarkers were measured by quantitative real\u2010time PCR (qPCR) and Western blotting, respectively. To unravel the mechanistic basis, key signaling cascades were probed in both renal tissues and isolated immune cells.<\/jats:p>\n                  <\/jats:sec>\n                  <jats:sec>\n                    <jats:title>Results<\/jats:title>\n                    <jats:p>\n                      Administration of TGP attenuated renal histological damage and diminished inflammatory cell infiltration in AKI mice. Notably, TGP recalibrated the function of bone marrow\u2013derived dendritic cells (BMDCs), steering them away from a fully mature phenotype. This was evidenced by a marked reduction in the migratory marker C\u2010C motif chemokine receptor 7 (CCR7) and a reciprocal elevation of the immunoinhibitory checkpoint programmed cell death ligand 1 (PD\u2010L1). Importantly, this phenotypic shift was linked to TGP\u2010induced metabolic reprogramming, as DCs from TGP\u2010treated animals exhibited diminished mitochondrial membrane potential (MMP). The TGP\u2010mediated DC reprogramming translated into a fundamentally rebalanced T\u2010cell compartment: The cytotoxic CD8\n                      <jats:sup>+<\/jats:sup>\n                      effector T cell was actively restrained, while the immunosuppressive regulatory T\u2010cell (T\n                      <jats:sub>reg<\/jats:sub>\n                      ) subset was preferentially expanded. This modulation was further reinforced by elevated programmed cell death protein 1 (PD\u20101) surface expression on T cells. Mechanistic interrogation revealed that TGP concurrently dismantled two interconnected pro\u2010inflammatory signaling nodes essential for DC\u2010T cell communication. By attenuating TLR4\/MyD88 recruitment, TGP curtailed the downstream nuclear translocation of NF\u2010\u03baB, thereby limiting the transcriptional output of DC\u2010derived inflammatory cytokines that drive T\u2010cell polarization. Concomitantly, TGP directly interfered with the JAK2\/STAT3 module, not only diminishing its phosphorylation but also de\u2010repressing the negative feedback regulator SOCS3. This dual blockade synergistically extinguished the inflammatory amplification loop instigated by Cis in the renal microenvironment.\n                    <\/jats:p>\n                  <\/jats:sec>\n                  <jats:sec>\n                    <jats:title>Conclusion<\/jats:title>\n                    <jats:p>Collectively, these findings indicate that TGP exerts a protective effect against Cis\u2010induced AKI by rebalancing immune cell homeostasis and interfering with pro\u2010inflammatory signaling networks, positioning it as a promising candidate for future AKI pharmacotherapy.<\/jats:p>\n                  <\/jats:sec>","DOI":"10.1155\/adpp\/8877828","type":"journal-article","created":{"date-parts":[[2026,10,1]],"date-time":"2026-10-01T05:53:22Z","timestamp":1790834002000},"update-policy":"https:\/\/doi.org\/10.1002\/crossmark_policy","source":"Crossref","is-referenced-by-count":0,"title":["Total Glucosides of Paeony Alleviates Acute Kidney Injury by Inhibiting Dendritic Cells and T\u2010Cell Communication"],"prefix":"10.1155","volume":"2026","author":[{"ORCID":"https:\/\/orcid.org\/0000-0002-4850-2718","authenticated-orcid":false,"given":"Tingting","family":"Liu","sequence":"first","affiliation":[{"name":"Department of Pharmacy The First Affiliated Hospital of Anhui Medical University The Grade 3 Pharmaceutical Chemistry Laboratory of State Administration of Traditional Chinese Medicine  Hefei China  ahmu.edu.cn"},{"name":"School of Pharmaceutical Sciences Anhui Medical University  Hefei China  ahmu.edu.cn"},{"name":"Key Laboratory of Xin\u2019an Medicine Ministry of Education Anhui University of Chinese Medicine  Hefei China  ahtcm.edu.cn"},{"name":"School of Life Sciences State Key Laboratory of Agrobiotechnology The Chinese University of Hong Kong  Hong Kong China  cuhk.edu.hk"}],"role":[{"vocabulary":"crossref","role":"author"}]},{"ORCID":"https:\/\/orcid.org\/0009-0007-6399-6086","authenticated-orcid":false,"given":"Wei","family":"Liang","sequence":"additional","affiliation":[{"name":"Department of Pharmacy Shanghai Hudong Hospital  Shanghai China"}],"role":[{"vocabulary":"crossref","role":"author"}]},{"ORCID":"https:\/\/orcid.org\/0009-0000-5977-8456","authenticated-orcid":false,"given":"Yan","family":"Zhang","sequence":"additional","affiliation":[{"name":"School of Pharmaceutical Sciences Anhui Medical University  Hefei China  ahmu.edu.cn"},{"name":"Department of Pharmacy The Fifth Affiliated Hospital of Anhui Medical University  Hefei China"}],"role":[{"vocabulary":"crossref","role":"author"}]},{"ORCID":"https:\/\/orcid.org\/0009-0000-7919-1476","authenticated-orcid":false,"given":"Xiaoqian","family":"Wu","sequence":"additional","affiliation":[{"name":"Department of Ultrasound The First Affiliated Hospital of Anhui University of Chinese 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