ACSL4對(duì)MPP+處理后N2a細(xì)胞線粒體數(shù)量的影響

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[關(guān)鍵詞]輔酶A連接酶類(lèi);1-甲基-4-苯基吡啶;線粒體;電壓依賴(lài)性陰離子通道1;帕金森病[中圖分類(lèi)號(hào)]R338.2 [文獻(xiàn)標(biāo)志碼]A [文章編號(hào)] 2096-5532(2025)03-0327-04doi:10.11712/jms.2096-5532.2025.61.081 [開(kāi)放科學(xué)(資源服務(wù))標(biāo)識(shí)碼(OSID)][網(wǎng)絡(luò)出版]https://link.cnki.net/urlid/37.1517.R.20250716.1027.004; 2025-07-1615:08:55
Efectof acy-CoAsynthetaselong-chainfamilymember4onmitochondrialnumberinN2acelsafter1-methyl-4-phenylpyridinim treatmentLIU Siqi,LIU Mengru,JIANG Hong(State KeyDisciplines:Physiology (Incubation),Departmentof Physiolo gy,Qingdao University,Qingdao ,China)
[Abstract]ObjectiveToinvestigate theefectofacyl-CoA synthetaselong-chain family member4(ACSL4)onmitochondrial number in N2a cells after1-methyl-4-phenylpyridinium ( .MPP+ )treatment. MethodsWestern blotting was used to measure the protein expression level of ACSL4 in N2a cells after MPP+ treatment. N2a cels were transfected with Flag-Vector or FlagACSL4 plasmids,and Westernbloting wasused toobservethe efect of ACSL4overexpressonontheexpressonlevelsofvoltage dependentanionchanel1(VDAC1)and mitochondrial import receptor subunit TOM20 homolog(TOMM2o)in N2acels after (20號(hào) MPP+ treatment. ResultsCompared with the control group,the MPP+ treatment group had a significant increase in the protein expression level of ACSL4 in N2a cells Ω′t=3.965,P<0.05) . Compared with the control group,the MPP+ treatment group had significant increases in the expresson levels of VDAC1 and TOMM20 ( F=28.59,15.15,P<0.01) ,while compared with the MPP+ treatment group,ACSL4 overexpression had no further impact on the expresson levels of VDAC1 and TOMM20 in N2a (204號(hào) cells (P>0.05 ).ConclusionACSL4 overexpression has no impact on mitochondrial number in N2a cells after MPP+ treatment,sugestingthattheroleof ACSL4inthepathogenesisofParkinson’sdiseasedoes not involveitsimpactonmitochondrial number.
[Key words] coenzyme A ligases;1-methyl-4-phenylpyridinium; mitochondria;voltage-dependent anion channel 1; Parkinson disease
帕金森?。≒D)是一種常見(jiàn)的神經(jīng)退行性疾病,主要病理特征為中腦黑質(zhì)多巴胺能神經(jīng)元選擇性缺失,殘存的神經(jīng)元內(nèi)出現(xiàn)以 α- 突觸核蛋白( ?a- Syn)異常聚集為主的路易小體[2]。(剩余8849字)