[Hesperidin调节JAGGED1/NOTCH1途径以促进巨噬细胞极化并减轻细支气管炎小鼠的肺损伤]。
摘要来源：
ehongguo yi yi xue yi xue ke xue yuan yuan yuan xue bao。 2022年10月; 44（5）：777-784。 pmid： 36325774“> 36325774 Bo Huang
文章隶属关系：Xingyan Zhao
摘要：目的是探索氧化胺在治疗肺部伴有伴合胞病毒（RSV）诱导支气管炎小鼠肺损伤中的作用和机制。方法建立了RSV诱导的细支气管炎的小鼠模型，并将60个BALB/C小鼠分为对照组，模型组，一个低剂量的Hesperidin（18 mg/kg）组，一个高剂量羟基植物（36 mg/kg）组和高剂量果仁蛋白（36 mg/kg）的方法（36 mg/kg）+JAG/KG 1（36 mg/kg）+JAG/kG 1（1 mg/kg）（1 mG1）（1 mG 1 MG 1 MG1（1 mG）（1 mG1）在每个组中。 corresponding doses of drugs were administrated for intervention,and the control group and model group were administrated with the same amount of saline.The bronchoalveolar lavage fluid (BALF) samples were collected and alveolar macrophages were isolated.ELISA was employed to detect the levels of interleukin (IL)-4,IL-6,tumor necrosis factor-α (TNF-α),and IL-10在BALF和流式细胞术中，分别进行了检测巨噬细胞的M1/M2极化。QRT-PCR和Western印迹分别进行了检测诱导型一氧化氮合酶（INOS），精氨酸酶1（arg-1），Jagged1，Jagged1，Jagged1和Notch1的mRNA和蛋白质水平。 ResultsCompared with the control group,the modeling of RSV-induced bronchiolitis elevated the IL-4,IL-6,and TNF-α levels,increased the proportion of M1-type macrophages and the lung inflammation and mucus secretion scores,and up-regulated the mRNA and protein levels of iNOS,Jagged1,and Notch1 in BALF (all<0.001).Meanwhile,the建模降低IL-10水平，降低sed the proportion of M2-type macrophages,and down-regulated the mRNA and protein levels of Arg-1 (all<0.001).Compared with the model group,low- and high-dose hesperidin lowered the IL-4,IL-6,TNF-α levels,decreased the proportion of M1-type macrophages and the lung inflammation and mucus secretion scores,and down-regulated the mRNA and protein levels of iNOS,Jagged1,and Notch1 in BALF (all<0.05).Moreover,hesperidin elevated the IL-10 level,increased the proportion of M2-type macrophages,and up-regulated the mRNA and protein levels of Arg-1 (all<0.001).Using recombinant Jagged1 protein to activate Notch1 signaling pathway can significantly attenuate the promotion of high-dose Hesperidin对M2巨噬细胞极化和肺部炎症损伤的改善（全<0.01）。结论Hesperidin可以通过抑制JAGGED1/NOTCH1信号通路并促进巨噬细胞的M2型极化，从而通过RSV诱导的细支气管炎来减轻小鼠的肺部炎症损伤。