Ethyl Pyruvate Alleviating Inflammatory Response after Diabetic Cerebral Hemorrhage

• Published in: Current neurovascular research Vol. 19; no. 2; p. 196
• Main Authors: Wang, Yueying, Li, Ke, Liu, Zhiyi, Sun, Yulan, Wang, JiaJun, Liu, Qi, Song, Yuejia, Qi, Jiping
• Format: Journal Article
• Language: English
• Published: United Arab Emirates 01.01.2022
• Subjects: Animals; Cerebral Hemorrhage - complications; Cerebral Hemorrhage - drug therapy; Diabetes Mellitus, Experimental; Inflammasomes - metabolism; Mice; Mice, Inbred C57BL; RNA, Messenger - metabolism; Signal Transduction - physiology; EP; HMGB1; TLR4; inflammasome; ethyl pyruvate; Diabetic cerebral hemorrhage
• ISSN: 1875-5739
• DOI: 10.2174/1567202619666220602153937

This study's purpose is to investigate the neuroprotective role of ethyl pyruvate (EP) in the pathogenesis of diabetic intracerebral hemorrhage. The present study used a mouse model of collagenase-induced intracerebral hemorrhage (ICH) and streptozotocin-induced diabetes. The C57BL/6 mice were randomly divided into 3 groups: sham operation, diabetic cerebral hemorrhage, and diabetic cerebral hemorrhage with EP. The EP (80 mg/kg) and EP (50 mg/kg) were injected intraperitoneally one day and one hour before modeling. The protein expression levels of high mobility group box 1 (HMGB1) and NOD-like receptors 3 (NLRP3) were detected with western blot. The mRNA levels of HMGB1 and toll-like receptor 4 (TLR4) were measured by quantitative real-time polymerase chain reaction (PCR). Immunofluorescence and ELISA were performed to confirm some inflammatory factors. Compared to the normal diabetic intracerebral hemorrhage group, the mRNA and protein expression levels of HMGB1 and TLR4 were downregulated in the EP-affected group with diabetic cerebral hemorrhage, together with the downregulation of the expression of inflammasomes, including NLRP3, apoptosis-associated speck-like protein containing CARD (ASC), and caspase 1. EP can reduce the inflammatory response after diabetic intracerebral hemorrhage and may inhibit the activation of inflammasomes by the HMGB1/TLR4 pathway.