3,3′-Diindolylmethane protects cardiomyocytes from LPS-induced inflammatory response and apoptosis

• DOI: 10.1186/s40360-018-0262-x
• Publication Date: 2018-11-09T08:33:49Z
• Authors: Qiang Luo; Ankang Yang; Quan Cao; Hongjing Guan
• Keywords: Lipopolysaccharides; LPS; Indoles; Anti-Inflammatory Agents; Apoptosis; RM1-950; Antioxidants; Cell Line; 03 medical and health sciences; RA1190-1270; Animals; Myocytes, Cardiac; DIM; bcl-2-Associated X Protein; 0303 health sciences; Interleukin-6; Tumor Necrosis Factor-alpha; NF-kappa B; ROS; Rats; 3. Good health; Proto-Oncogene Proteins c-bcl-2; Septic cardiomyopathy; Toxicology. Poisons; H9C2; Therapeutics. Pharmacology; NFκB; Research Article

3,3′-Diindolylmethane (DIM) has been extensively studied as a potential therapeutic drug with free radical scavenging, antioxidant and anti-angiogenic effects. However, whether DIM similar effects on cardiomyocytes remains unknown. Here we evaluated DIM's influence inflammation apoptosis of H9C2 induced by LPS to explore the possible mechanism cells were incubated (10, 20 30 μM) or without for 24 h. The cytotoxicity was detected CCK-8. levels tumour necrosis factor (TNF)-α interleukin (IL)-6 then measured using RT-qPCR ELISA. Cell rate reactive oxygen species (ROS) content after treatment flow cytometry. Expressions NFκB, P-NFκB, IκBa, P-IκBa, Bax Bcl-2 western blot. NFκB nuclear translocation determined immunocytochemical analysis. stimulation promoted TNF-α IL-6 mRNA expression. After various concentrations μM), expression clearly impaired, especially in + DIM30(μM) group. ELISA used measure cellular supernatant, result verified be consistent RT-qPCR. Additionally, significantly blocked LPS-induced oxidative stress inhibited according results Moreover, compared alone, phosphorylation (p-NFκB) increased may have protective effect against inflammatory response apoptosis. new insight into septic cardiomyopathy.