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当归多糖抑制氧化损伤延缓造血干细胞衰老

Keywords: 当归多糖,造血干细胞,细胞衰老,氧化应激

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Abstract:

目的:观察当归多糖(ASP)对小鼠造血干细胞(HSCs)活性氧(ROS)、总抗氧化能力(T-AOC)及p16mRNA表达的影响,探讨ASP延缓HSCs衰老的可能机制。方法:C57BL/6J小鼠随机分为正常组、衰老组,并分别予ASP干预;衰老组采用X线3.0Gy/8F全身均匀照射,建立小鼠HSCs衰老模型;正常、衰老ASP干预组在建模期间均予ASP灌胃;而正常组、衰老组予等体积NS灌胃。免疫磁珠分离HSCs,通过β-半乳糖苷酶(SA-β-Gal)染色、细胞周期分析和混合集落培养观察HSCs生物学特性变化;流式细胞术与免疫荧光检测ROS产量;比色法检测T-AOC;荧光定量PCR检测p16mRNA表达。结果:与正常组比较,3.0Gy/8F的X线能显著增加衰老组HSCsSA-β-Gal染色阳性率和G1期比例;增加ROS产量,上调p16mRNA表达;混合集落形成能力和T-AOC下降。与衰老组比较,ASP能显著降低衰老组HSCs的SA-β-Gal染色阳性率和G1期比例,减少ROS产量,下调p16mRNA;增加混合集落形成能力和T-AOC。结论:3.0Gy/8F的X线能诱导小鼠HSCs衰老;ASP则能通过抑制氧化损伤及下调p16mRNA表达延缓小鼠HSCs衰老。

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