利多卡因通过调节Pink1/Parkin信号通路对缺血再灌注诱导的心肌细胞损伤及自噬的影响

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AbstractObjective：Toobservetheefectoflidocaineoncardiomyocytesinjuryandautophagyinducedbyschemia-reperfusio（/R） throughregulatingthePink1/ParkinsignalingpathwayMethods：ThelogarthmicH9c2celsweredividedintotheNCgroup（normal culture），I/Rgoupowdocaineroup（.5ol/idocaineeforeltreatmet），imdoineoup2.die beforelRtreatment），igh-lidocainegroup（5.Ommo/idocainebeforeI/Rtreatment），andhigh-lidocainePink1/Parkinignaling pathwayactivatogopdocaieo5prolfratiabitfccels，tvesfalodde （MDA），superoidestas（D）ctateroese）iodrialutogndihodralbraet） ineachgroupweredetected.TheexpresionofPink1/Parkinpathwayproteinsandautophagy-relatedproteinsweredetectedbyWester BlotResuts：CompaditeNop，tellpolferatioate，lvelsbbitantiobssodote lighthain3Ⅱ/I（C-I/），ink1，Pakinproteiexpressiosinhe/gropicreasedhilethe，SODlevelsandko isolateprotein1（p62） proteinexpressiondecreased（ P<0.05 ）.ComparedwiththeI/R group，thecell proliferation inhibitionrate，LDH，MDA levels，LC-3Iinkarkinroteiexpessichocerouscasdilevsdote expressionallincreased P<0.05 ），and lidocaineeffectshowedadose-dependent P<0.05 ）.Conclusion：Lidocaine could inhibit mitochondrialautophagyunder/RcondionsandpreventH9c2celsfrombeingdamagedbyoxidativestress.Temechanismmightbe related to the inhibition of the activation of the Pink1/Parkin signaling pathway.

Keywordsischemia-reperfusion;cardiomyocytes;lidocaine;Pink1/Parkinsignalingpathway;autophagy;experimentaltudy

缺血性心脏病（IHD）是临床常见的危重症，具有较高的发病率和死亡率。（剩余7718字）