LPL基因甲基化與腦梗死的關(guān)系
發(fā)布時間：2018-12-15 20:54
【摘要】：目的探討血脂代謝相關(guān)基因甲基化程度與腦梗死及其相關(guān)危險因素的關(guān)系。 方法采用病例-對照研究方法隨機抽取湖南漢族人群腦梗死患者及健康對照者各15名。應(yīng)用亞硫酸氫鹽測序技術(shù)檢測LPL基因啟動子區(qū)甲基化狀態(tài)。 結(jié)果1.病例組和對照組相比,病例組舒張壓、血漿LDL-C水平高于對照組,病例組血漿HDL-C水平低于對照組,差異有統(tǒng)計學(xué)意義(P0.05)。 2.病例組與對照組比較,病例組LPL基因啟動子30個位點整體平均甲基化水平(CpGZ%)顯著高于對照組,差異有統(tǒng)計學(xué)意義(P0.05)。兩組各位點間的平均甲基化水平(CpG%)進行比較,位點CpG9～16,CpG20～21處病例組甲基化水平明顯高于對照組,差異有統(tǒng)計學(xué)意義(P0.05)。 3.腔隙性腦梗死組與動脈粥樣硬化性血栓性腦梗死組LPL基因啟動子平均甲基化水平(CpGZ%)比較無明顯差異(P0.05)。頸動脈粥樣硬化組與無頸動脈粥樣硬化組LPL基因啟動子平均甲基化水平(CpGZ%)比較無明顯差異(P0.05)。 4.所有研究對象血漿HDL-C水平與LPL基因啟動子平均甲基化水平(CpGZ%)存在顯著負(fù)的直線相關(guān)關(guān)系(P=0.001)。CpG9～16位點處直線相關(guān)性顯著,差異有統(tǒng)計學(xué)意義(P0.05)。所有研究對象血漿LDL-C水平與LPL基因啟動子平均甲基化水平(CpGZ%)存在顯著正的直線相關(guān)關(guān)系(P=0.004),CpG10～12、CpG15、CpG20位點處兩者直線相關(guān)性顯著,差異有統(tǒng)計學(xué)意義(P0.05)。 5.年齡與LPL基因啟動子平均甲基化水平(CpGZ%)存在顯著正的直線相關(guān)關(guān)系(P=0.024),CpG9～16位點處直線相關(guān)性顯著,差異有統(tǒng)計學(xué)意義(P0.05)。 6.病例組、對照組和合并組男性與女性LPL基因啟動子平均甲基化水平(CpGZ%)比較無明顯差異(P0.05)。男性病例組與對照組LPL基因啟動子平均甲基化水平(CpGZ%)比較存在顯著差異(P=0.001)。女性病例組與對照組LPL基因啟動子平均甲基化水平(CpGZ%)比較存在顯著差異(P=0.024)。 結(jié)論1.LPL基因啟動子區(qū)高甲基化與腦梗死發(fā)病相關(guān),與血漿低HDL-C水平及血漿高LDL-C水平相關(guān)。 2.LPL基因啟動子區(qū)甲基化可能與梗死灶面積及頸動脈粥樣硬化無關(guān)。 3.LPL基因啟動子區(qū)甲基化水平無性別差異,隨年齡增長有升高趨勢。
[Abstract]:Objective to investigate the relationship between methylation of hyperlipidemia related genes and cerebral infarction and related risk factors. Methods A case-control study was conducted to randomly select 15 patients with cerebral infarction and 15 healthy controls in Hunan Han population. The methylation status of promoter region of LPL gene was detected by bisulfite sequencing. Result 1. Compared with the control group, the diastolic blood pressure and plasma LDL-C level in the case group were higher than those in the control group, and the plasma HDL-C level in the case group was lower than that in the control group (P0.05). 2. Compared with the control group, the global average methylation level (CpGZ%) of 30 sites of LPL gene promoter in the case group was significantly higher than that in the control group (P0.05). The average methylation level (CpG%) of the two groups was significantly higher than that of the control group (P0.05). 3. There was no significant difference in average methylation (CpGZ%) of LPL gene between lacunar infarction group and atherosclerotic thrombotic cerebral infarction group (P0.05). There was no significant difference in average methylation level (CpGZ%) of LPL gene promoter between carotid atherosclerosis group and non-carotid atherosclerosis group (P0.05). 4. There was a significantly negative linear correlation between plasma HDL-C level and the average methylation level (CpGZ%) of LPL gene promoter (P0. 001). The linear correlation at CpG9~16 locus was significant (P0.05). There was a significant positive linear correlation between plasma LDL-C level and average methylation level (CpGZ%) of LPL gene promoter (P0. 004), and a significant linear correlation between plasma LDL-C level and mean methylation level (CpGZ%) at CpG10~12,CpG15,CpG20 locus. The difference was statistically significant (P0.05). 5. There was a significant positive linear correlation between age and average methylation level (CpGZ%) of LPL gene promoter (P0. 024) and a significant linear correlation at CpG9~16 locus (P0.05). 6. There was no significant difference in mean methylation (CpGZ%) level of LPL gene promoter between male and female in case group, control group and combined group (P0.05). The mean methylation level (CpGZ%) of LPL gene promoter was significantly different between male and control group (P0. 001). The mean methylation level (CpGZ%) of LPL gene promoter was significantly different between female and control group (P0. 024). Conclusion hypermethylation in the promoter region of 1.LPL gene is associated with cerebral infarction, low HDL-C level and high LDL-C level. 2.LPL promoter methylation may not be associated with infarct size and carotid atherosclerosis. There was no gender difference in methylation level in promoter region of 3.LPL gene, but it tended to increase with age.
【學(xué)位授予單位】：中南大學(xué)
【學(xué)位級別】：碩士
【學(xué)位授予年份】：2014
【分類號】：R743.3
[Abstract]:Objective to investigate the relationship between methylation of hyperlipidemia related genes and cerebral infarction and related risk factors. Methods A case-control study was conducted to randomly select 15 patients with cerebral infarction and 15 healthy controls in Hunan Han population. The methylation status of promoter region of LPL gene was detected by bisulfite sequencing. Result 1. Compared with the control group, the diastolic blood pressure and plasma LDL-C level in the case group were higher than those in the control group, and the plasma HDL-C level in the case group was lower than that in the control group (P0.05). 2. Compared with the control group, the global average methylation level (CpGZ%) of 30 sites of LPL gene promoter in the case group was significantly higher than that in the control group (P0.05). The average methylation level (CpG%) of the two groups was significantly higher than that of the control group (P0.05). 3. There was no significant difference in average methylation (CpGZ%) of LPL gene between lacunar infarction group and atherosclerotic thrombotic cerebral infarction group (P0.05). There was no significant difference in average methylation level (CpGZ%) of LPL gene promoter between carotid atherosclerosis group and non-carotid atherosclerosis group (P0.05). 4. There was a significantly negative linear correlation between plasma HDL-C level and the average methylation level (CpGZ%) of LPL gene promoter (P0. 001). The linear correlation at CpG9~16 locus was significant (P0.05). There was a significant positive linear correlation between plasma LDL-C level and average methylation level (CpGZ%) of LPL gene promoter (P0. 004), and a significant linear correlation between plasma LDL-C level and mean methylation level (CpGZ%) at CpG10~12,CpG15,CpG20 locus. The difference was statistically significant (P0.05). 5. There was a significant positive linear correlation between age and average methylation level (CpGZ%) of LPL gene promoter (P0. 024) and a significant linear correlation at CpG9~16 locus (P0.05). 6. There was no significant difference in mean methylation (CpGZ%) level of LPL gene promoter between male and female in case group, control group and combined group (P0.05). The mean methylation level (CpGZ%) of LPL gene promoter was significantly different between male and control group (P0. 001). The mean methylation level (CpGZ%) of LPL gene promoter was significantly different between female and control group (P0. 024). Conclusion hypermethylation in the promoter region of 1.LPL gene is associated with cerebral infarction, low HDL-C level and high LDL-C level. 2.LPL promoter methylation may not be associated with infarct size and carotid atherosclerosis. There was no gender difference in methylation level in promoter region of 3.LPL gene, but it tended to increase with age.
【學(xué)位授予單位】：中南大學(xué)
【學(xué)位級別】：碩士
【學(xué)位授予年份】：2014
【分類號】：R743.3
【共引文獻】
相關(guān)期刊論文 前10條
1 沈斌;鮑遠(yuǎn)程;武松;蔣懷周;張娟;方向;王艷昕;;燈盞細(xì)辛與復(fù)方丹參注射液治療腦梗死療效比較的Meta分析[J];安徽中醫(yī)藥大學(xué)學(xué)報;2014年02期
2 徐程;豐蕾;楊帆;李彩霞;Q謎，
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