摘要
目的探讨氧化型辅酶Ⅰ(NAD+)对受辐射小鼠免疫功能的影响。方法 60只小鼠随机分为对照组、照射组和NAD+组,每组20只。收集处理24 h后各组小鼠股骨骨髓细胞,进行骨髓有核细胞计数,检测细胞凋亡率、p53和bcl-2蛋白阳性表达以及Caspase-3活性;收集处理后10 d各组小鼠脾脏单核细胞,检测脾淋巴细胞凋亡率、p53和bcl-2蛋白阳性表达以及Caspase-3活性。结果照射组和NAD+组小鼠骨髓有核细胞数显著少于对照组(P<0.05),而NAD+组小鼠骨髓有核细胞数显著高于照射组(P<0.05)。照射组和NAD+组小鼠骨髓有核细胞凋亡率显著高于对照组(P<0.05),而NAD+组小鼠骨髓有核细胞凋亡率显著低于照射组(P<0.05)。照射组和NAD+组小鼠骨髓有核细胞p53蛋白阳性表达率显著高于对照组(P<0.05),而NAD+组小鼠骨髓有核细胞p53蛋白阳性表达率显著低于照射组(P<0.05)。照射组和NAD+组小鼠骨髓有核细胞bcl-2蛋白阳性表达率显著低于对照组(P<0.05),但NAD+组骨髓有核细胞的bcl-2蛋白阳性表达率显著高于照射组(P<0.05)。照射组和NAD+组骨髓有核细胞的Caspase-3活性显著高于对照组(P<0.05),但NAD+组骨髓有核细胞的Caspase-3活性显著低于照射组(P<0.05)。照射组和NAD+组脾淋巴细胞凋亡率和p53蛋白阳性表达率显著高于对照组(P<0.05),NAD+组小鼠脾淋巴细胞凋亡率和p53蛋白阳性表达率显著低于照射组(P<0.05)。照射组和NAD+组小鼠脾淋巴细胞的bcl-2蛋白阳性表达率显著低于对照组(P<0.05),但NAD+组脾淋巴细胞的bcl-2蛋白阳性表达率显著高于照射组(P<0.05)。照射组和NAD+组小鼠脾淋巴细胞Caspase-3活性显著高于对照组(P<0.05),但NAD+组小鼠脾淋巴细胞Caspase-3活性显著低于照射组(P<0.05)。结论 NAD+可通过抑制受辐射损伤小鼠免疫细胞凋亡而发挥免疫防护作用;NAD+发挥抗免疫细胞凋亡作用的分子机制可能是通过下调受辐射损伤细胞p53表达水平、上调bcl-2表达以及抑制Caspase-3活性。
Objective To explore the influence of oxidized form of nicotinamide-adenine dinucleotide （ NAD ＋ ） on the immune function of irradiated mice. Methods Sixty mice were randomly divided into control group, irradiation group and NAD ＋ group,twenty mice in each group. The mice femoral marrow cells were collected at 24 hours after treatment;then, the marrow nucleated cells were counted, the marrow cell apoptosis rate was detected, the positive expression of bcl-2 and p53 was detected, and the activity of Caspase-3 was detected. The mice spleen mononuclear cells were collected at ten days after treat- ment ; then, the apoptosis rate, the positive expression of bcl-2 and p53, and the activity of Caspase-3 of splenic lymphocyte were detected. Results The femoral marrow nucleated cell count in irradiation group and NAD ~ group was less than that in control group （ P 〈 0.05 ）, but the femoral marrow nucleated cell count in NAD ~ group was significantly higher than that in irradiation group（ P 〈 0.05 ）. The marrow nucleated cell apoptosis rate of nucleated cells in irradiation group and NAD ＋ group was signifi- cantly higher than that in control group（ P 〈 0.05）, but the marrow nucleated cell apoptosis rate in NAD ＋ group was signifi- cantly lower than that in irradiation group（ P 〈 0.05 ）. The positive expression rate of p53 protein of nucleated cells in irradia- tion group and NAD ~ group was significantly higher than that in control group（ P 〈 O. 05 ）, but the positive expression rate ofp53 protein in NAD ~ group was significantly lower than that in irradiation group （ P 〈 0.05 ）. The positive expression rate of bcl-2 protein of nucleated cells in irradiation group and NAD ＋ group was significantly lower than that in control group （ P 〈 0. 05 ）, but the positive expression rate of bcl-2 protein in NAD ＋ group was significantly higher than that in irradiation group （ P 〈 0. 05 ）. The activity of Caspase-3 of nucleated cells in irradiation group and NAD ＋ group was significantly higher than that in control group（ P 〈0.05 ）, but the positive expression rate of p53 protein in NAD ~ group was significantly lower than that in irradiation group（P 〈 0.05 ）. The apoptosis rate and the positive expression rate of p53 protein of splenic lymphocyte in irradiation group and NAD ~ group were significantly higher than those in control group（P 〈 0.05） ,but the apoptosis rate and the positive expression rate of p53 protein in NAD ＋group were significantly lower than those in irradiation group（ P 〈 0. 05 ）. The positive expression rate of bcl-2 protein of splenic lymphocyte in irradiation group and NAD ＋ group was significantly lower than that in control group（ P 〈 0.05 ） ,but the positive expression rate of bcl-2 protein in NAD ＋ group was significantly higher than that in irradiation group（ P 〈 0.05 ）. The activity of Caspase-3 of splenic lymphocyte in irradiation group and NAD ＋ group was significantly higher than that in control group（ P 〈 O. 05 ）, but the activity of Caspase-3 in NAD ＋ group was significantly lower than that in irradiation group（P 〈 0.05 ）. Conclusions NAD ＋ can play an immune protective role on mice with radia- tion injury by inhibiting immune cell apoptosis. NAD＋ may show the molecular mechanisms of anti-immune cell apoptosis by decreasing expression of p53 protein, increasing the expression of bcl-2 protein, and inhibiting the Caspase-3 activity of the cells with irradiation damage.
出处
《新乡医学院学报》
CAS
2012年第8期578-581,共4页
Journal of Xinxiang Medical University
基金
广东省中山市科技局资助项目(编号:20102A073)
关键词
辅酶Ⅰ
辐射损伤
免疫功能
nicotinamide-adenine dinucleotide
radiation damage
immune function
