LOX-1 In CME Effect And Mechanism Of Myocardial Damage Caused

Objective To Explore the role of lectin-like oxidized low-densitylipoprotein receptor (LOX-1) after coronary microembolization (CME) inswine. Methods establishing coronary microembolization (CME) modelof Bama miniature pig through intervention method.50Bama miniaturepigs were randomly divided into the CME group and the sham group(Sham group), n=25. CME group were injected105count polyestermicrospheres into the middle left anterior descending artery (LAD)selectively, Sham group were injected the same volume of saline into themiddle of LAD. cardiac function were detected after3h,6h,12h,24h,48h. each time point selected five pigs in both group. after sacrificeing,detecting myocardial tissue HBFP staining and the expression of LOX-1,TNF-α mRNA and protein in cardiac tissue. Results1compared with theSham group, the LVEF, FS, CO of CME Group was significantly lower at corresponding time points (P <0.05), and after12h reached the lowestlevel; compared with Sham group, LVEDd were significantly higher atthe corresponding time points (P <0.05), and after12h reached the highestlevel;2compared with Sham group, LOX-1mRNA, TNF-α mRNAexpression of CME group were significantly increased at each time point(P <0.05), and the greatest expression was at CME12h;3compared withSham group, the LOX-1protein and TNF-α protein levels of CME groupwere significantly increased at each time point (P <0.05), and highestexpression levels at the CME12h;4the LOX-1mRNA relative expressionlevel of CME group was significantly positively related to the TNF-αmRNA relative expression level of CME group. the LOX-1mRNArelative expression level of CME group and LVEF was significantlynegatively correlated. Conclusions LOX-1expression increasedsignificantly after CME, and the expression reached a peak at12h, whichmay exacerbated inflammatory response, resulting cardiac dysfunction,which may be one of the important mechanisms of myocardial injuryafter CME. Objective To explore the expression of lectin-like oxidizedlow-density lipoprotein receptor (LOX-1) after coronarymicroembolization (CME) and the mechanism of myocardial injury inswine. Methods establishing coronary microembolization (CME) modelof Bama miniature pig through intervention method.50Bama miniaturepigs were randomly divided into sham group (Sham group)、CME group、LOX-1siRNA group、p38MAPK inhibitor group、non-specific siRNAgroup、non-specific inhibitor group, n=5. CME group were injected105count polyester microspheres into the middle left anterior descendingartery (LAD) selectively, Sham group were the same volume of salineinto the middle of LAD, The remaining groups injected drugs to LADafter CME. cardiac function were detected after12h. after sacrificeing, detected myocardial tissue HE and HBFP staining, Serum cTnI levels, theexpression of LOX-1, TNF-αmRNA and LOX-1、p38MAPK、p-p38MAPK、p65NF-κB、TNF-αprotein in cardiac tissue. Results1Compared with Sham group, the cardiac function of other groups weresignificantly decreased (P <0.05); Compared with LOX-1siRNA groupand p38MAPK inhibitor group, the cardiac function of CME group,non-specific siRNA/inhibitor group improved significantly (P <0.05);2compared with Sham group, the cTnI level and infarct size of othergroups were significantly increased (P <0.05); compared withLOX-1siRNA group and p38MAPK inhibitor group, cTnI level andinfarct size of CME group, non-specific siRNA/inhibitor groupsignificantly increased (P <0.05);3compared with Sham group, theexpression of LOX-1mRNA、TNF-αmRNA of other groups weresignificantly increased (P <0.05); compared with LOX-1siRNA group andp38MAPK inhibitor group, the expression of LOX-1mRNA、TNF-αmRNA of CME group, non-specific siRNA/inhibitor group significantlyincreased (P <0.05);4compared with Sham group, the expression ofLOX-1、p38MAPK、p-p38MAPK、p65NF-κB、TNF-αprotien of othergroups were significantly increased (P <0.05); compared withLOX-1siRNA group, the expression of LOX-1、 p38MAPK、p-p38MAPK、p65NF-κB、TNF-αprotien of CME group, non-specificsiRNA/inhibitor group significantly increased (P <0.05); compared with p38MAPK inhibitor group, the expression of p38MAPK、p-p38MAPK、p65NF-κB、TNF-αprotien of CME group, non-specific siRNA/inhibitor group significantly increased (P <0.05). Conclusions Themechanism of increased LOX-1induced myocardial injury after CMEwas mainly through LOX-1/p38MAPK/NF-κB/TNF-α pathway, whichcan be used as a new target for prevention and treatment of CME.