Renoprotective Effect of Oridonin in a Mouse Model of Acute Kidney Injury via Suppression of Macrophage Involved Inflammation

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  • Tan Rui-zhi
    Research Center for Integrated Chinese and Western Medicine, Affiliated Traditional Medicine Hospital, Southwest Medical University
  • Yan Ying
    Research Center for Integrated Chinese and Western Medicine, Affiliated Traditional Medicine Hospital, Southwest Medical University Clinical Laboratory, Affiliated Traditional Medicine Hospital, Southwest Medical University
  • Yu Yan
    Research Center for Integrated Chinese and Western Medicine, Affiliated Traditional Medicine Hospital, Southwest Medical University College of Integrated Chinese and Western Medicine, Southwest Medical University
  • Diao Hui
    Research Center for Integrated Chinese and Western Medicine, Affiliated Traditional Medicine Hospital, Southwest Medical University
  • Zhong Xia
    Research Center for Integrated Chinese and Western Medicine, Affiliated Traditional Medicine Hospital, Southwest Medical University
  • Lin Xiao
    Research Center for Integrated Chinese and Western Medicine, Affiliated Traditional Medicine Hospital, Southwest Medical University
  • Liao Yi-yi
    Research Center for Integrated Chinese and Western Medicine, Affiliated Traditional Medicine Hospital, Southwest Medical University College of Integrated Chinese and Western Medicine, Southwest Medical University
  • Wang Li
    Research Center for Integrated Chinese and Western Medicine, Affiliated Traditional Medicine Hospital, Southwest Medical University

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  • Renoprotective Effect of Oridonin in a Mouse Model of Acute Kidney Injury <i>via</i> Suppression of Macrophage Involved Inflammation

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<p>Ischemia–reperfusion injury (IRI) is the major cause of acute kidney injury (AKI). The previous studies demonstrated that Oridonin can protect kidney against IRI-induced AKI, but the underlying molecular mechanism is unclear. In this study, it showed that Oridonin significantly improved kidney damage, and inhibited the expression of interleukin (IL)-1β, IL-6, tumor necrosis factor (TNF)-α and MCP-1, as well as macrophage marker F4/80 in kidney and the secretion of inflammatory cytokins in serum of AKI mice in vivo. In addition, Oridonin also effectively reduced the expression and secretion of lipopolysaccharide (LPS)-induced inflammatory factors in macrophage cell line RAW264.7 in vitro. Notably, Oridonin strongly downregulated Mincle and AKT/nuclear factor-kappaB (NF-κB) signaling both in vivo and in vitro, and the results of cellular recovery experiments of overexpression of Mincle in macrophage suggested that Oridonin suppressed inflammatory response of macrophage through inhibiting Mincle, which may be the underlying mechanism of Oridonin improving injury in kidney of AKI mice. In summary, the above results indicated that Oridonin can protect kidney from IRI-induced inflammation and injury by inhibiting the expression of Mincle in macrophage.</p>

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