Cardioprotection of mAb2G4/ODN/lip on Myocardial Ischemia-Reperfusion Injury via Inhibiting the NF- κ B Signaling Pathway.
Zujin XuZhuoran WeiYali ZhuGuoqing JingLiufang ChenJia ZhanYun WuPublished in: Cardiovascular therapeutics (2023)
Substantial evidence suggests that the interventions of NF- κ B would likely effectively prevent inflammatory response and reduce myocardial damage in the ischemic myocardium. And the NF-кB decoy ODN is a specific inhibitor that suppresses the expression of NF- κ B. Herein, we revealed the effect and possible mechanism of mAb2G4/ODN/lip on myocardial ischemia-reperfusion injury (MI/RI). As shown in the results, post-treatment with mAb2G4/ODN/lip improved the impaired histological morphology in the MI/RI model and elevated cell viability in the H/R model. The mAb2G4/ODN/lip complex inhibited the NLRP3 signaling pathway and decreased the expression of LDH, IL-1 β , TNF- α , IL-6, and MDA. Mechanistically, we demonstrated that post-treatment with mAb2G4/ODN/lip exerted protective effects against I/R injuries by inhibiting the NF-кB-related inflammatory response. In summary, the present study may offer a novel therapeutic strategy for treating MI/RI.
Keyphrases
- signaling pathway
- pi k akt
- ischemia reperfusion injury
- inflammatory response
- lps induced
- epithelial mesenchymal transition
- induced apoptosis
- oxidative stress
- monoclonal antibody
- poor prognosis
- left ventricular
- lipopolysaccharide induced
- cell cycle arrest
- nuclear factor
- rheumatoid arthritis
- cell proliferation
- combination therapy
- long non coding rna
- brain injury