Trimethylamine N-Oxide (TMAO) has been shown to be an independent risk factor for cardiovascular disease. Our aim is to study the effects of TMAO on type 2 diabetes mellitus-coronary heart disease and to explore its mechanism.
A total of 50 healthy controls , 50 T2DM patients and 50 T2DM combined with CHD patients were enrolled. Serum samples were collected to detect glucose, myocardial enzyme spectrum and TMAO level. The 16S rRNA gene sequencing analyzed the diversity of intestinal flora. Taking the ZDF rat as the experimental object, the model of T2DM combined with CHD was established in rats. Blood samples were taken to detect glucose, myocardial enzyme spectrum and TMAO level. The inflammatory protein and mRNA expression of TLR4, NLRP3, Caspase-1 and IL-1β were detected by Western blot and RT-qPCR. In vitro culture of H9c2(2-1) for experiments. The CCK-8 method was used to detect the survival rate of cells after glucose and TMAO treatment. After the cells were treated with selected glucose and TMAO, the cells were treated with selected glucose, TMAO and BAY11-7082, Western blot detected the presence of pyroptosis and the pathway of TLR4/NF-κB/NLRP3. RT-qPCR was used to determine the mRNA level of inflammatory factor.
Changes in the composition of intestinal flora in patients with type 2 diabetes can lead to elevated serum TMAO levels. Animal and cell experiments have confirmed that elevated TMAO level may lead to inflammatory myocardial injury in rats and is related to the mechanism of TLR4/NF-κB/NLRP3.