CAJ | 학술논문

目的观察四物汤有效成分配伍组方对电离辐射所致人淋巴母细胞AHH-1细胞氧化损伤的辐射防护作用,并初步探讨其作用机制.方法 4.0 Gy60Co γ射线单次照射AHH-1细胞,造成电离辐射损伤.观察不同浓度的四物汤有效成分配伍组方(果糖、阿魏酸、芍药苷、川芎嗪质量比为9 008:53:721:267)对于电离辐射损伤的AHH-1细胞活力、凋亡情况、活性氧(ROS)水平的影响,以及对pGL4-ARE报告基因载体的激活作用.结果四物汤有效成分配伍组方在10 mg/L的浓度下抗辐射效果最为显著,可以减缓受照AHH-1细胞活力下降(t=-8.152,P＜0.05),缓解早期细胞凋亡(t=12.777,P＜0.05),降低ROS水平(t=3.465,P＜0.05),诱导报告基因pGL4-ARE荧光表达倍数提高(t=-19.752,P＜0.05).结论四物汤有效成分配伍组方具有体外抗辐射活性,可能通过激活Nrf2-Keap1-ARE抗氧化通路、降低辐射所致氧化损伤,从而发挥辐射防护作用.
목적 관찰사물탕유효성분배오조방대전리복사소치인림파모세포AHH-1세포양화손상적복사방호작용,병초보탐토기작용궤제.방법 4.0 Gy60Co γ사선단차조사AHH-1세포,조성전리복사손상.관찰불동농도적사물탕유효성분배오조방(과당、아위산、작약감、천궁진질량비위9 008:53:721:267)대우전리복사손상적AHH-1세포활력、조망정황、활성양(ROS)수평적영향,이급대pGL4-ARE보고기인재체적격활작용.결과 사물탕유효성분배오조방재10 mg/L적농도하항복사효과최위현저,가이감완수조AHH-1세포활력하강(t=-8.152,P＜0.05),완해조기세포조망(t=12.777,P＜0.05),강저ROS수평(t=3.465,P＜0.05),유도보고기인pGL4-ARE형광표체배수제고(t=-19.752,P＜0.05).결론 사물탕유효성분배오조방구유체외항복사활성,가능통과격활Nrf2-Keap1-ARE항양화통로、강저복사소치양화손상,종이발휘복사방호작용.
Objective To observe the effects of Siwu Tang formulation, which consists of fructose, ferulic acid, paeoniflorin, and ligustrazine hydrochloride (mass ratio of 9 008 : 53 : 721 : 267) , on the oxidative damage in irradiated AHH-1 cells, and to investigate the underlying protective mechanism.Methods AHH-1 cells were irradiated with a single dose of 4.0 Gy 60Co γ-rays, then cell viability, apoptosis and reactive oxygen species (ROS) level were measured.The activation of Nrf2-Keapl-ARE pathway was observed by transferring pGL4-ARE reporter gene transiently into HEK293 cells before the administration of Siwu Tang.Results At the concentration of 10 mg/L, Siwu Tang components formula had the best efficiency on anti-radiation damage.This drug inhibited the reduction of cell viability (t =-8.152, P ＜ 0.05) , mitigated apoptosis (t =12.777, P ＜ 0.05) , reduced intracellular ROS levels (t =3.465, P ＜0.05), and induced the expression of pGL4-ARE fluorescence reporter gene (t =-19.752, P ＜0.05).Conclusions Siwu Tang formulation has a protective effect against radiation by reducing radiation-induced oxidative damage through the activation of the Nrf2-Keap1-ARE signaling pathway.