目的了解广州地区伊朗籍献血者CD36表型及基因型。方法对2016年在广州血液中心捐献机采血小板的53例伊朗人献血者标本,应用流式细胞仪分别检测血小板和单核细胞上CD36抗原的表达。对CD36抗原表达异常者提取DNA,采用PCR-SBT测序做CD36的...目的了解广州地区伊朗籍献血者CD36表型及基因型。方法对2016年在广州血液中心捐献机采血小板的53例伊朗人献血者标本,应用流式细胞仪分别检测血小板和单核细胞上CD36抗原的表达。对CD36抗原表达异常者提取DNA,采用PCR-SBT测序做CD36的基因型鉴定并做基因突变分析。结果本组伊朗人群的CD36抗原表达异常率7.55%(4/53),其中2例的CD36抗原在血小板上表达含量低,1例为血小板和单核细胞上均无表达(即CD36Ⅰ型缺失),1例为单核细胞上CD36表达量低,由此得出CD36缺失表达的频率为1.89%(1/53)。PCRSBT法分析:CD36抗原表达异常4例的CD36基因型中,血小板上低表达CD36抗原的2例发生基因突变,分别是exon 10-975T/G和exon11 del CTA,且均为新的基因突变;2例CD36基因型正常。结论本组伊朗献血人群里CD36抗原表达异常者中存在新的基因突变,其对CD36抗原表达的影响尚需进一步认证。展开更多
CD36 is a highly glycosylated integral membrane protein that belongs to the scavenger receptor class B family and regulates the pathological progress of metabolic diseases.CD36 was recently found to be widely expresse...CD36 is a highly glycosylated integral membrane protein that belongs to the scavenger receptor class B family and regulates the pathological progress of metabolic diseases.CD36 was recently found to be widely expressed in various cell types in the nervous system,including endothelial cells,pericytes,astrocytes,and microglia.CD36 mediates a number of regulatory processes,such as endothelial dysfunction,oxidative stress,mitochondrial dysfunction,and inflammatory responses,which are involved in many central nervous system diseases,such as stroke,Alzheimer’s disease,Parkinson’s disease,and spinal cord injury.CD36 antagonists can suppress CD36 expression or prevent CD36 binding to its ligand,thereby achieving inhibition of CD36-mediated pathways or functions.Here,we reviewed the mechanisms of action of CD36 antagonists,such as Salvianolic acid B,tanshinone IIA,curcumin,sulfosuccinimidyl oleate,antioxidants,and small-molecule compounds.Moreover,we predicted the structures of binding sites between CD36 and antagonists.These sites can provide targets for more efficient and safer CD36 antagonists for the treatment of central nervous system diseases.展开更多
文摘目的了解广州地区伊朗籍献血者CD36表型及基因型。方法对2016年在广州血液中心捐献机采血小板的53例伊朗人献血者标本,应用流式细胞仪分别检测血小板和单核细胞上CD36抗原的表达。对CD36抗原表达异常者提取DNA,采用PCR-SBT测序做CD36的基因型鉴定并做基因突变分析。结果本组伊朗人群的CD36抗原表达异常率7.55%(4/53),其中2例的CD36抗原在血小板上表达含量低,1例为血小板和单核细胞上均无表达(即CD36Ⅰ型缺失),1例为单核细胞上CD36表达量低,由此得出CD36缺失表达的频率为1.89%(1/53)。PCRSBT法分析:CD36抗原表达异常4例的CD36基因型中,血小板上低表达CD36抗原的2例发生基因突变,分别是exon 10-975T/G和exon11 del CTA,且均为新的基因突变;2例CD36基因型正常。结论本组伊朗献血人群里CD36抗原表达异常者中存在新的基因突变,其对CD36抗原表达的影响尚需进一步认证。
基金supported by the National Major Project of Research and Development,No.2022YFA1105500(to SZ)the National Natural Science Foundation of China,No.81870975(to SZ)Innovation Program for Graduate Students in Jiangsu Province of China,No.KYCX223335(to MZ)。
文摘CD36 is a highly glycosylated integral membrane protein that belongs to the scavenger receptor class B family and regulates the pathological progress of metabolic diseases.CD36 was recently found to be widely expressed in various cell types in the nervous system,including endothelial cells,pericytes,astrocytes,and microglia.CD36 mediates a number of regulatory processes,such as endothelial dysfunction,oxidative stress,mitochondrial dysfunction,and inflammatory responses,which are involved in many central nervous system diseases,such as stroke,Alzheimer’s disease,Parkinson’s disease,and spinal cord injury.CD36 antagonists can suppress CD36 expression or prevent CD36 binding to its ligand,thereby achieving inhibition of CD36-mediated pathways or functions.Here,we reviewed the mechanisms of action of CD36 antagonists,such as Salvianolic acid B,tanshinone IIA,curcumin,sulfosuccinimidyl oleate,antioxidants,and small-molecule compounds.Moreover,we predicted the structures of binding sites between CD36 and antagonists.These sites can provide targets for more efficient and safer CD36 antagonists for the treatment of central nervous system diseases.
