川芎嗪对失神经骨骼肌萎缩大鼠FoXO3a、MAFbx以及MuRF1表达的影响

目的研究川芎嗪对失神经骨骼肌萎缩中FoXO3a、MAFbx及MuRF1表达的影响。方法 8周龄雌性SD大鼠54只,体重(200±10)g。随机分为3组,即正常对照组(A组,n=6)、失神经对照组(B组,n=24)、干预组(C组,n=24)。B、C组实验动物制备右下肢失神经腓肠肌动物模型,C组于模型制备后每日腹腔注射川芎嗪注射液80 mg/(kg.d),B组每日腹腔注射等剂量生理盐水;A组实验动物不作任何处理。取A组实验动物以及造模后2、7、14、28 d B、C组实验动物各6只,处死取其双侧腓肠肌称湿重,计算腓肠肌肌湿重比;另取右侧肌组织采用RT-PCR及Western blot检测各时间点FoXO3a、MAFbx、MuRF1 mRNA和蛋白表达水平。结果与A组比较,随着大鼠失神经时间延长,B、C组腓肠肌肌湿重比逐渐下降,差异均有统计学意义(P<0.05);造模后7、14、28 d,C组腓肠肌肌湿重比高于B组,且差异有统计学意义(P<0.05)。B、C组造模后7、14、28 d,FoXO3a、MAFbx、MuRF1 mRNA和蛋白表达水平均较A组高,C组各时间点均较B组降低,差异均有统计学意义(P<0.05)。结论川芎嗪可能通过降低FoXO3a、MAFbx以及MuRF1 mRNA和蛋白表达水平进而延缓失神经骨骼肌萎缩。

Effect of Ligustrazine on expressions of FoXO3a, MAFbx, and MuRF1 in denervated skeletal

Objective To investigate the effect of Ligustrazine on the expressions of FoXO3a,MAFbx,and MuRF1 in denervated skeletal muscle atrophy rats. Methods Fifty-four 8-week-old female Sprague Dawley rats were randomly divided into 3 groups: normal control group(group A,n=6),denervated control group(group B,n=24),and Ligustrazine intervention group(group C,n=24).After the denervated gastrocnemius models were established in the rats of groups B and C,saline and Ligustrazine 80 mg/(kg·d)] were given every day by intraperitoneal injection,respectively.However,no treatment was done in group A.At 2,7,14,and 28 days after denervation,the wet weight of gastrocnemius was measured to calculate the ratio of wet weight.The mRNA and protein expression levels of FoXO3a,MAFbx,and MuRF1 were detected by RT-PCR and Western blot. Results The ratio of gastrocnemius wet weight decreased with time after denervation in groups B and C,showing significant differences when compared with that of group A(P < 0.05),and group C were significantly higher than that of group B at 7,14,and 28 days(P < 0.05).The mRNA and protein expressions of FoXO3a,MAFbx,and MuRF1 in groups B and C were significantly higher than those in group C at 7,14,and 28 days(P < 0.05),and group C was significantly lower than group B(P < 0.05).Conclusion Ligustrazine may postpone denervated skeletal muscle atrophy by reducing mRNA and protein expressions of FoXO3a,MAFbx,and MuRF1.