摘要
目的研究ω-3多不饱和脂肪酸对严重烧伤大鼠心脏功能保护作用的机理。方法清洁级成年SD大鼠72只,随机分成3组:正常对照组(A组,共8只),20%中长链脂肪酸对照组(B组,共32只),10%ω-3多不饱和脂肪酸治疗组(C组,共32只)。采用大鼠30%TBSAⅢ度烫伤模型,A组大鼠经尾静脉注射生理盐水2 mL·kg-1·d-1,B组每天定时经尾静脉注射20%中长链脂肪乳,1 mL·kg-1·d-1,C组在相同时间点经尾静脉注射与B组等氮等热量的10%ω-3多不饱和脂肪酸(尤文),2 mL·kg-1·d-1。分别检测伤前(A组)以及伤后1 d、4 d、7 d、10 d四个时相点大鼠血清中TNF-α、肌钙蛋白I(cTnI)的水平,免疫组织化学染色法观察心肌组织中NF-κBp65的表达水平。结果 B、C两组大鼠血清TNF-α水平在伤后各时相点均显著高于A组(P<0.05);C组血清TNF-α水平低于B组,在伤后4 d、7 d、10 d与B组相比较差异有统计学意义(P<0.05)。免疫组化结果显示:与A组相比,B、C两组心肌组织NF-κBp65表达增强;与B组相比,C组心肌组织NF-κBp65表达减弱(P<0.05)。B、C两组血清中cTnI水平在伤后各时相均显著高于A组(P<0.05);在伤后1 d、4 d、7 d、10 d,C组cTnI水平明显低于B组(P<0.05)。结论 NF-κBp参与了烧伤后由炎症所致的心肌细胞损伤过程;ω-3 PUFAs可能通过抑制NF-κB信号通路的激活,减少各种炎症介质的产生,进而对严重烧伤后大鼠心肌起到保护作用。
Objective To investigate the protective function on myocardial of ω-3 polyunsaturated fatty acids（PUFAs） in seriously burned rats. Methods A number of 72 SD rats with 30% total body surface area（TBSA） full thickness burn were randomly divided into 3 groups ： normal control group （ A group, n = 8 ）, experimental group （ B group, n =32） and treatment group （ C group, n = 32 ）. Rats in A group were injected with NS 2 mL · kg-1·d-1 by tail vein, rats in B group were injected with 20% middle - long - chain fatty emulsion 1 mL · kg-1·d-1 and C group with 10%ω-3 PUFAs 2 mL · kg-1·d-1 by tail vein at the same time everyday. Levels of serum TNF -α of before injury group （A group） and after injury groups （B group, C group） were measured respectively,levels of cardiac troponin T （cTnI） were measured by ELISA and expression levels of NF - κBp65 in cardiac muscular tissue were detected by immunohistochemical staining. Each subgroup included 8 rats. Results The levels of TNF -α in the blood serum of B group and C group were significantly higher than A group （P 〈0.05）. TNF -α levels of the C group were lower than those of B group at postburn 4 d, 7 d , 10 d（P 〈0.05）. The expression levels of NF - κBp 65 in cardiac muscular tissue of B group and C group were higher than those of A group detected by immunohistochemical staining. Compared with B group, expression levels in C group declined （ P 〈 0.05 ）. The cTnI levels of B group and C group wewe significantly higher than A group at every phase point （P 〈 0.05 ） ; Compared with B group ,the cTnI levels of C group were obviously lower at postburn 4 d, 7 d 10 d （ P 〈 0. 05 ）. Conclusion NF - κB is involved in the procedure of postburn cardiomyocytes damage caused by inflammatory, ω-3 PUFAs may protect cardiomyocyte by blocking the activating of signal path of NF - κB consequently reducing productions of the various inflammation mediators.
出处
《安徽医学》
2012年第5期515-519,共5页
Anhui Medical Journal
基金
安徽省自然基金资助项目(090413267X)
