AIM2 gene silencing attenuates diabetic cardiomyopathy in type 2 diabetic rat model

Publication date: Available online 18 February 2019Source: Life SciencesAuthor(s): Xuyang Wang, Jinyu Pan, Hui Liu, Mingjun Zhang, Dian Liu, Lu Lu, Jingjing Tian, Ming Liu, Tao Jin, Fengshuang AnAbstractAimsAbsent in melanoma 2 (AIM2) is a cytosolic DNA sensor which plays an important role in inflammasome formation and is involved in various cellular functions including pyroptosis, fibrosis, and tissue injury. Our study aimed to investigate whether AIM2 plays a role in diabetic cardiomyopathy (DCM) and to explore its potential molecular mechanism.Main methodsSprague-Dawley rats were randomly divided into 4 groups: Control, Diabetes Mellitus (DM), DM + shAIM2, and DM + shNC. The cardiac function of rats was measured. Hematoxylin and eosin staining, Masson's staining, sinus red staining, and immunohistochemistry were performed. H9c2 cardiomyocytes were cultured in DMEM and stimulated with high-glucose treatment (25 mmol/l). The level of reactive oxygen species (ROS) was measured. AIM2-siRNA were used to inhibit the expression of AIM2. TUNEL assay and EthD-III staining were used to measure cell death. The expression levels of AIM2, ASC, caspase-1, IL-1β, and GSDMD-N were measured by western blotting.Key findingsIn the streptozotocin-induced diabetic rat model, AIM2 expression was significantly increased in heart tissue compared with the control. Also, diabetic rats exhibited severe left ventricular dysfunction including metabolic disorder, cardiac fibrosis, and cardio...
Source: Life Sciences - Category: Biology Source Type: research