内皮细胞EA.hy926氧化损伤及药物保护的脂质组学研究
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摘要
氧化胁迫环境诱发内皮功能失调,并导致一系列心脑血管疾病的发生,内皮细胞氧化损伤过程中磷脂代谢的变化规律研究,对解释该过程机制具有重要意义。本文以外源性过氧化氢损伤的人脐静脉内皮细胞系EA.hy926为模型,运用高通量的脂质组学研究策略,结合信号转导,研究这一过程中川芎嗪(TMP)和丁烯苯酞(BP)的作用机制。
在本研究中,基于LC/ESI/MSn的脂质组学手段,建立了EA.hy926细胞的磷脂图谱,获得了8类(PG、PE、PC、PI、PS、PA、LPC和LPE)共200多种磷脂分子的准确定性定量信息。结合多元统计分析,发现氧化损伤进程中,具有长链、多不饱和烃链的磷脂及醚基磷脂被氧化降解最多,同时伴有PLA2酶的激活和溶血性磷脂LPC、LPE的产生。细胞磷脂随时间延长大量降解及溶血性磷脂生成,造成细胞膜性质改变是细胞损伤的根本原因。
研究表明,加入TMP预处理,可显著增加氧化损伤细胞PC含量,具有抗氧化和抑制PLA2酶,减少溶血磷脂产生的作用,且对增加具长链、多不饱和的磷脂和醚基磷脂有偏好;BP预处理除此之外,还可一定程度增加PI含量,表明其对PI-PLC酶的抑制作用。TMP和BP的抗磷脂氧化特性和改变相关磷脂酶活性的功能,使其具有卓越的细胞保护特性。
由于PLA2酶在以上研究中显示出其重要的研究价值,因此加入其相关信号转导MAPK途径和COX、LOX途径的抑制剂PD98059和ETYA。通过多元统计分析发现ETYA和TMP预处理细胞在磷脂代谢模式上有一定相似之处,而ETYA对醚基磷脂有更强的偏好,但对其他易氧化磷脂无明显选择性,意味着其抗氧化作用弱于TMP;PD98059和BP预处理细胞预处理细胞具有类似代谢模式,均可抑制PI-PLC酶活力,但PD98059促进长链PS合成,可导致细胞凋亡性死亡,对细胞无保护作用。
进一步通过加入分子荧光探针证实了氧化胁迫过程中PLA2酶的作用和溶血性磷脂的产生,通过蛋白免疫印迹实验证明急性氧化损伤过程中cPLA2活性增强是通过磷酸化途径,且与ERK磷酸化之间的互为调控,并据此初步构建了ERK途径和脂质信号途径之间的转导模型。
The study of phospholipids metabolism changes in oxidative stress induced endothelial cells (ECs) is important to elicit the link between endothelium dysfunction and cerebral/cardio vascular diseases. In this research, we set exogenous H2O2 induced human unbilic vein endothelial cell line EA.hy926 as the model, and applied lipidomics with signal transduction strategy together to explore the underlying mechanisms of tetramethylpyrazine (TMP) and butylidenephthalide (BP) protection of endothelial cells against oxidative stress.
In this research, we establish the phospholipids profile of EA.hy926 cell using high-throughput LC/ESI/MSn techniques. Eight main classes (PG, PE, PC, PI, PS, PA, LPC and LPE) including more than 200 species of phospholipids was detected and analyzed qualitatively and quantitatively. By multi-statistic analysis, we found the phospholipids with long carbon chain, polyunsaturated fatty acids (PUFAs) or ether link in sn-1 position (ether phospholipids) take priorities in oxidative degradation; meanwhile, phospholipase A2 was activated to generated a great amount of lysophospholipids including LPC and LPE. These above two main findings were responsible to the injury of ECs.
Our results showed that with TMP pretreatment, content of PCs, especially the PCs with long carbon chain, PUFAs or ether PCs in injured cells was largely increased and, contents of LPC and LPE were decreased. These results indicated the antioxidation activity and inhibition of PLA2 effect of TMP. Beside of these properties, BP also had inhibitory effect over PI-PLC and consequentially increased PI contents. TMP and BP showed extraordinary abilities in protection of ECs for its antioxidation of phospholipids and alteration of phospholipase activation properties.
Since PLA2 was one of the key factors in our results, we add PD98059 and ETYA, inhibitors of MAPK pathway and of COX, LOX pathway which were supposed to be the upstream and downstream signal of PLA2, to the injury model. With multi-statistic analysis, we find similarity in phospholipids metabolism pattern between ETYA and TMP pretreated ECs. However, ETYA showed stronger preference over ether PC than PCs with long carbon chain or polyunsaturated fatty acids, which indicated that the antioxidation activity of ETYA was not as good as TMP. Similarity in phospholipids metabolism pattern between BP and PD98059 pretreated ECs was also found on the basis of inhibitory effect on PI-PLC activation; however, the long carbon chain PSs were synthesized with PD98059 pretreatment to induce apoptotic death in ECs.
Fluorescent substrate was utilized to prove the activation of PLA2 and generation of LPC; western blot method was employed to show the phosphorylation of cPLA2 in acute oxidative injury of ECs in which existed cross-talk between phosphorylated cPLA2 and ERK1/2. Based on these above findings, a phospholipids and phospholipase based signal transduction model was established to summarize our basic findings in this research.
在本研究中,基于LC/ESI/MSn的脂质组学手段,建立了EA.hy926细胞的磷脂图谱,获得了8类(PG、PE、PC、PI、PS、PA、LPC和LPE)共200多种磷脂分子的准确定性定量信息。结合多元统计分析,发现氧化损伤进程中,具有长链、多不饱和烃链的磷脂及醚基磷脂被氧化降解最多,同时伴有PLA2酶的激活和溶血性磷脂LPC、LPE的产生。细胞磷脂随时间延长大量降解及溶血性磷脂生成,造成细胞膜性质改变是细胞损伤的根本原因。
研究表明,加入TMP预处理,可显著增加氧化损伤细胞PC含量,具有抗氧化和抑制PLA2酶,减少溶血磷脂产生的作用,且对增加具长链、多不饱和的磷脂和醚基磷脂有偏好;BP预处理除此之外,还可一定程度增加PI含量,表明其对PI-PLC酶的抑制作用。TMP和BP的抗磷脂氧化特性和改变相关磷脂酶活性的功能,使其具有卓越的细胞保护特性。
由于PLA2酶在以上研究中显示出其重要的研究价值,因此加入其相关信号转导MAPK途径和COX、LOX途径的抑制剂PD98059和ETYA。通过多元统计分析发现ETYA和TMP预处理细胞在磷脂代谢模式上有一定相似之处,而ETYA对醚基磷脂有更强的偏好,但对其他易氧化磷脂无明显选择性,意味着其抗氧化作用弱于TMP;PD98059和BP预处理细胞预处理细胞具有类似代谢模式,均可抑制PI-PLC酶活力,但PD98059促进长链PS合成,可导致细胞凋亡性死亡,对细胞无保护作用。
进一步通过加入分子荧光探针证实了氧化胁迫过程中PLA2酶的作用和溶血性磷脂的产生,通过蛋白免疫印迹实验证明急性氧化损伤过程中cPLA2活性增强是通过磷酸化途径,且与ERK磷酸化之间的互为调控,并据此初步构建了ERK途径和脂质信号途径之间的转导模型。
The study of phospholipids metabolism changes in oxidative stress induced endothelial cells (ECs) is important to elicit the link between endothelium dysfunction and cerebral/cardio vascular diseases. In this research, we set exogenous H2O2 induced human unbilic vein endothelial cell line EA.hy926 as the model, and applied lipidomics with signal transduction strategy together to explore the underlying mechanisms of tetramethylpyrazine (TMP) and butylidenephthalide (BP) protection of endothelial cells against oxidative stress.
In this research, we establish the phospholipids profile of EA.hy926 cell using high-throughput LC/ESI/MSn techniques. Eight main classes (PG, PE, PC, PI, PS, PA, LPC and LPE) including more than 200 species of phospholipids was detected and analyzed qualitatively and quantitatively. By multi-statistic analysis, we found the phospholipids with long carbon chain, polyunsaturated fatty acids (PUFAs) or ether link in sn-1 position (ether phospholipids) take priorities in oxidative degradation; meanwhile, phospholipase A2 was activated to generated a great amount of lysophospholipids including LPC and LPE. These above two main findings were responsible to the injury of ECs.
Our results showed that with TMP pretreatment, content of PCs, especially the PCs with long carbon chain, PUFAs or ether PCs in injured cells was largely increased and, contents of LPC and LPE were decreased. These results indicated the antioxidation activity and inhibition of PLA2 effect of TMP. Beside of these properties, BP also had inhibitory effect over PI-PLC and consequentially increased PI contents. TMP and BP showed extraordinary abilities in protection of ECs for its antioxidation of phospholipids and alteration of phospholipase activation properties.
Since PLA2 was one of the key factors in our results, we add PD98059 and ETYA, inhibitors of MAPK pathway and of COX, LOX pathway which were supposed to be the upstream and downstream signal of PLA2, to the injury model. With multi-statistic analysis, we find similarity in phospholipids metabolism pattern between ETYA and TMP pretreated ECs. However, ETYA showed stronger preference over ether PC than PCs with long carbon chain or polyunsaturated fatty acids, which indicated that the antioxidation activity of ETYA was not as good as TMP. Similarity in phospholipids metabolism pattern between BP and PD98059 pretreated ECs was also found on the basis of inhibitory effect on PI-PLC activation; however, the long carbon chain PSs were synthesized with PD98059 pretreatment to induce apoptotic death in ECs.
Fluorescent substrate was utilized to prove the activation of PLA2 and generation of LPC; western blot method was employed to show the phosphorylation of cPLA2 in acute oxidative injury of ECs in which existed cross-talk between phosphorylated cPLA2 and ERK1/2. Based on these above findings, a phospholipids and phospholipase based signal transduction model was established to summarize our basic findings in this research.
引文
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