基于NLRP3炎性小体诱发细胞焦亡思路，探索库尔勒香梨均一多糖PSAP-2、PSAP-1基于NF-κB信号通路调控NLRP3介导细胞焦亡抗炎症分子机制，发现库尔勒香梨均一多糖提高RAW264.7的增殖率，降低IL-18及IL-1β的量，降低GSDMD、NLRP3、Caspase-1、ASC、IL-18及IL-1β mRNA表达水平，抑制GSDMD、NLRP3、Caspase-1、Caspase-4、NF-κB p65蛋白的表达，抑制炎症反应的扩大，减轻炎症反应。由此可以明确证实了库尔勒香梨均一多糖是抗炎活性物质，库尔勒香梨的深层次开发利用提供实验数据支撑和研究策略。
Based on the idea of NLRP3 inflammasome-induced pyroptosis, the molecular mechanism of NLRP3-mediated pyroptosis and anti-inflammatory molecular mechanism of PSAP-2 and PSAP-1 regulating the polysaccharide of Korla fragrant pear based on the NF-κB signaling pathway was exploredA polysaccharide increased the proliferation rate of RAW264.7, reduced the amount of IL-18 and IL-1β, decreased the expression level of GSDMD, NLRP3, Caspase-1, ASC, IL-18 and IL-1β mRNA, inhibited the expression of GSDMD, NLRP3, Caspase-1, Caspase-4 and NF-κB p65 proteins, inhibited the expansion of inflammatory response, and alleviated the inflammatory response. This clearly confirms that the homogeneous polysaccharide of Korla fragrant pear is an anti-inflammatory active substance, and the in-depth development and utilization of Korla fragrant pear provide experimental data support and research strategies.

不同浓度的LPS及ATP刺激RAW264.7细胞发生焦亡，模型的条件为500 ng/mL LPS+5mM ATP同时刺激细胞24 h，此时细胞成不规则形状、细胞膜破裂，NLRP3、GSDMD蛋白表达量及IL-1β、IL-18的mRNA表达量明显升高（P<0.001），PSP、PSN、PSA干预后NLRP3、GSDMD蛋白表达量及IL-1β、IL-18的mRNA表达量明显降低，其中PSA抑制焦亡活性最强，后续PSA进行分离纯化，深入开展抑制焦亡抗炎分子机制研究。
Different concentrations of LPS and ATP stimulated pyroptosis in RAW264.7 cells, and the model conditions were that 500 ng/mL LPS+5mM ATP stimulated the cells for 24 h, at which time the cells formed irregular shapes, the cell membrane ruptured, and the expression levels of NLRP3 and GSDMD proteins and the mRNA expressions of IL-1β and IL-18 were significantly increased (P). <0.001), the expression of NLRP3 and GSDMD proteins and the mRNA expression of IL-1β and IL-18 decreased significantly after PSP, PSN and PSA intervention, among which PSA had the strongest inhibition of pyroptosis.