青霉素通过抑制NLRP3/caspase-1/gsdmd途径来保护胰腺β细胞免受链霉菌素诱导的糖尿病。
摘要来源：
gen comp comp comp comp comp。 2022 Jun 4; 326：114068。 Epub 2022 Jun 4.pmid： 35671834 35671834 Yujin Ma, Liping Li, Liujun Fu, Jie Liu, Hongwei Jiang
Article Affiliation:Jingya Yuan
Abstract:BACKGROUND: Reports in recent years have shown that pancreaticβ-cell pyroptosis represents a critical mechanism involved with the progressive failure of胰腺功能。我们实验室的先前研究表明，丁香可以增加db/db小鼠胰岛中细胞的数量。在这项研究中，我们进一步研究了青霉酸（ART）是否保护胰腺β细胞免受链霉菌的损害CIN（STZ）通过抑制凋亡。
材料和方法： 在体外，暴露于1 mm STZ的MIN6细胞用ART（0.8或1.6μm）处理。通过CCK-8测定法，流式细胞仪和蛋白质印迹评估了ART对STZ处理的细胞的影响，并进一步比较了ART与NLRP3抑制剂，MCC950对使用Western blot的pyroptoptosis途径蛋白的作用。在体内，用单次腹膜内注射STZ给予雄性C57小鼠，并将确认的糖尿病的患者施用ART（饮用水中的0.5或1.0 mg/ml），持续18天。 The effects of ART on STZ-induced diabetes were assessed by the observation of the general situation, glucose tolerance test, hematoxylin-eosin (HE) staining and immunohistochemistry.
RESULTS: In MIN6 cells treated with STZ, we found that ART increased cell viability, decreased the number of晚期凋亡CELLS（包括凋亡细胞），并抑制与凋亡途径相关的蛋白质的表达。 In STZ-induced animal model, the administration of ART reduced blood glucose levels, improved the consumption status within this diabetic mouse model and inhibited the expression of proteins include in the pyroptosis pathway in mice pancreats.
CONCLUSIONS: Inhibition of pyroptosis may be a critical mechanism through which铁酸会对胰腺β细胞发挥保护作用。