RUI Rong, CHEN Ying, ZHU Bing-bing, CAO Ai-li, WANG Hao, WANG Li. Huangqi Decoction Regulates TLR4/NF-κB Pathway to Improve High Glucose-Induced Podocyte Injury[J]. Journal of Nanjing University of traditional Chinese Medicine, 2022, 38(7): 607-614. DOI: 10.14148/j.issn.1672-0482.2022.0607
Citation: RUI Rong, CHEN Ying, ZHU Bing-bing, CAO Ai-li, WANG Hao, WANG Li. Huangqi Decoction Regulates TLR4/NF-κB Pathway to Improve High Glucose-Induced Podocyte Injury[J]. Journal of Nanjing University of traditional Chinese Medicine, 2022, 38(7): 607-614. DOI: 10.14148/j.issn.1672-0482.2022.0607

Huangqi Decoction Regulates TLR4/NF-κB Pathway to Improve High Glucose-Induced Podocyte Injury

  •   OBJECTIVE  To investigate the effect and mechanism of Huangqi Decoction on high glucose-induced podocyte injury.
      METHODS  Human podocytes were cultured in vitro and treated with 30 mmol·L-1 glucose for 24 h to induce injury. The groups were divided into control group, model group, low-, medium- and high-concentration of Huangqi Decoction groups (10, 30, 100 μg·mL-1). The cell proliferation was detected by CCK-8 method, the mRNA expression of TNF-α and IL-6 was detected by qPCR, the contents of TNF-α and IL-6 in podocyte supernatant were detected by ELISA, and the protein expression of TLR4, p-NF-κB, NF-κB, TNF-α and IL-6 in podocytes was detected by Western blot.
      RESULTS  Compared with the control group, the mRNA expression of TNF-α, IL-6, CCL24, the contents of TNF-α and IL-6 and the protein expression of TLR4, p-NF-κB/NF-κB, TNF-α and IL-6 in podocytes significantly increased (P < 0.05, P < 0.01). Compared with the model group, the mRNA expression and contents of TNF-α, IL-6 and the protein expression of TLR4, p-NF-κB/NF-κB, TNF-α and IL-6 in podocytes of Huangqi Decoction groups significantly decreased (P < 0.05, P < 0.01).
      CONCLUSION  Huangqi Decoction can reduce the inflammatory damage of human podocytes induced by high glucose, enhance cell proliferation and migration, and inhibit cell apoptosis. The mechanism may be related to the inhibition of TLR4/NF-κB signal pathway and down-regulation of the inflammatory factors expression.
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