Department of Emergency, Suichang People's Hospital, Lishui , PR China.
Department of Nephrology, Suichang People's Hospital, Lishui, PR China.
Histol Histopathol. 2024 Jul;39(7):921-934. doi: 10.14670/HH-18-688. Epub 2023 Dec 12.
NLRP3 inflammasome and Sirt1/autophagy axis are potential targets for advancing acute peritonitis (AP). Honokiol (HNK), a bioactive substance, has the potential to improve AP.
The AP model rats were established by cecal ligation and puncture (CLP). Rats were randomized into the Sham, Sham+HNK, CLP, and CLP+HNK groups. The therapeutic effects of HNK on organ infection, inflammation and immunity were observed in AP rats. The inflammation of RAW 264.7 cells was induced by lipopolysaccharide (LPS) and divided into the Control, HNK, LPS, and LPS+HNK groups. The effects of HNK on immunity and inflammation were observed. Moreover, the inflammatory cell model was further transfected with NLRP3 overexpressing plasmid, and the regulatory effect of HNK on NLRP3 in AP cells was detected.
HNK treatment improved survival, biochemical indexes, and lung and kidney injury and inhibited inflammatory cytokine release and bacterial infection in CLP rats. In CLP rats and RAW 264.7 cells, HNK treatment improved the release of the CD4+ and CD8+ T cells, decreased the associated proteins' levels of the NLRP3 inflammasome, and activated the expression of proteins in the Sirt1/autophagy axis. It improved viability and reduced apoptosis and the degrees of TNF-α, IL-1β, and IL-6 mRNA in RAW 264.7 cells. In addition, HNK treatment antagonized the effect of NLRP3-overexpressed on inflammation and immunity.
HNK improved AP by inhibiting NLRP3 inflammasome and activating the Sirt1 autophagy axis and .
NLRP3 炎性小体和 Sirt1/自噬轴是治疗急性腹膜炎（AP）的潜在靶点。霍诺比林（HNK）是一种具有改善 AP 潜力的生物活性物质。
通过盲肠结扎和穿孔（CLP）建立 AP 模型大鼠。大鼠随机分为 Sham、Sham+HNK、CLP 和 CLP+HNK 组。观察 HNK 对 AP 大鼠器官感染、炎症和免疫的治疗作用。用脂多糖（LPS）诱导 RAW 264.7 细胞炎症，分为对照组、HNK 组、LPS 组和 LPS+HNK 组。观察 HNK 对免疫和炎症的影响。此外，炎性细胞模型进一步转染 NLRP3 过表达质粒，检测 HNK 对 AP 细胞中 NLRP3 的调节作用。
HNK 治疗可提高 CLP 大鼠的存活率、生化指标、肺肾损伤，抑制炎症细胞因子释放和细菌感染。在 CLP 大鼠和 RAW 264.7 细胞中，HNK 治疗可改善 CD4+和 CD8+T 细胞的释放，降低 NLRP3 炎性小体相关蛋白水平，激活 Sirt1/自噬轴蛋白的表达。可提高 RAW 264.7 细胞活力，减少 TNF-α、IL-1β 和 IL-6 mRNA 的凋亡程度。此外，HNK 治疗拮抗了 NLRP3 过表达对炎症和免疫的影响。
HNK 通过抑制 NLRP3 炎性小体和激活 Sirt1 自噬轴来改善 AP。
