A Promising MyD88 Inhibitor TJ-M2010-2 Protects Heart from Myocardial Ischemia Reperfusion Injury.

Y. Miao, L. Xie, X. Zhang, Z.-C. Ding, M. Yang, Y. Yang, P. Zhou.

Institute of Qrgan Transplantation, Tongji Hospital, Tongji Medical College, Huazhong University of Science and Technology
Key Labrory of Organ Transplantation, Wuhan, Hubei, China

Meeting: 2017 American Transplant Congress

Abstract number: A160

Keywords: Heart, Immunosuppression, Ischemia, Mice

Session Information

Session Name: Poster Session A: Ischemic Injury and Organ Preservation Session I

Session Type: Poster Session

Date: Saturday, April 29, 2017

Session Time: 5:30pm-7:30pm

Presentation Time: 5:30pm-7:30pm

Location: Hall D1

BACKGROUND: The activation of innate immunity via myeloid differentiation factor 88 (MyD88) contributes to myocardial ischemia reperfusion injury (IRI). This study is to investigate the protective effect of MyD88 inhibitor TJ-M2010-2 on myocardial IRI.

METHODS: We generated a small molecular compound, TJ-M2010-2, which inhibits MyD88 homodimerization and the TLR/MyD88 signal pathway. Mice were equally divided into three groups (n=8 each): the sham group, IRI + carboxymethyl cellulose (CMC) group and the IRI +TJ-M2010-2 group. In the CMC group, mice were treated with CMC, and in the TJ-M2010-2 group, with TJ-M2010-2 dissolved in CMC at 48h, 24h and 6h prior to heart IRI respectively. Myocardial ischemia was induced by ligation of the left anterior descending branch of the coronary artery for 30min, followed by recirculation of the branch artery for 24 hrs. The levels of high-sensitivity troponin I(HSTNI) were determined. The myocardial tissues were harvested for the determination of the area at risk (AAR), the area of infarction (AI), and the percentage of AI/AAR.

RESULTS: Compared with the sham group, the level of HSTNI was increased in IRI+CMC group (HSTNI(U/L): 366.5±33.78 vs 2059±361.8, P<0.05). There were significant difference in HSTNI level and the AI/AAR between IRI+CMC group and IRI+TJ-M2010-2 group ( HSTNI(U/L):2059±361.8 vs 650.5±92.03, P<0.05 ; AI/AAR: 0.5178±0.07490 vs 0.2883±0.02930 ,P <0.05 ).

CONCLUSIONS: MyD88 inhibitor TJ-M2010-2 can attenuate myocardial ischemia reperfusion injury and it might be a promising therapeutic option in heart transplantation and coronary heart diseases.

CITATION INFORMATION: Miao Y, Xie L, Zhang X, Ding Z.-C, Yang M, Yang Y, Zhou P. A Promising MyD88 Inhibitor TJ-M2010-2 Protects Heart from Myocardial Ischemia Reperfusion Injury. Am J Transplant. 2017;17 (suppl 3).

To cite this abstract in AMA style:

Miao Y, Xie L, Zhang X, Ding Z-C, Yang M, Yang Y, Zhou P. A Promising MyD88 Inhibitor TJ-M2010-2 Protects Heart from Myocardial Ischemia Reperfusion Injury. [abstract]. Am J Transplant. 2017; 17 (suppl 3). https://atcmeetingabstracts.com/abstract/a-promising-myd88-inhibitor-tj-m2010-2-protects-heart-from-myocardial-ischemia-reperfusion-injury/. Accessed November 22, 2024.

« Back to 2017 American Transplant Congress