川芎嗪对严重烧伤早期心肌损害的保护及初步机制

Protective effects of liqustrazine on myocardial damage in severely burned rats

目的:观察川芎嗪对大鼠严重烧伤后心肌损害的影响。方法:用健康W istar大鼠,随机分为对照组、烧伤组(造成30%TBSAⅢ度烫伤)和治疗组(烧伤后腹腔注射川芎嗪,剂量20 mg/kg)。于伤后1、3、6、12、24和48 h检测血浆TNFα、AngⅡ和cTnT含量与心肌中TNFα、AngⅡ含量,电镜观察心肌形态结构变化。结果:烧伤组于伤后3 h血浆cTnT呈显著升高达1.87±0.04(P<0.01),伤后6 h血浆TNFα(38.96±5.71)和心肌组织TNFα含量(1.98±0.08)显著高于对照组(P<0.01),12 h达峰值,伤后1 h血浆AngⅡ即显著升高达175.66±18.91(P<0.01),各指标在伤后48 h仍无恢复;川芎嗪治疗组血浆cTnT、TNFα和AngⅡ水平较烧伤组均有显著性降低(P<0.01)。组织学观察显示:烧伤早期心肌结构有明显的损害,如肌丝断溶、线粒体肿胀、嵴突减少等,川芎嗪治疗组心肌损害明显较轻。结论:川芎嗪能抑制大鼠严重烧伤后TNFα和AngⅡ的生成,对严重烧伤后心肌损害有较好的保护作用。

AIM： To investigate the effect of liqustrazine on myocardial damage following severe burns. METHODS： A total of 130 healthy adult Wistar rats were randomly divided into 3 groups ：The control group （n = 10,without burns） ,the burn group （n =60,subjected to a 30% TBSA Ⅱ degree scald injury）. And the treatment group （n = 60） ,treated by intraperitoneal injection of liqustrazine （20 mg/kg） immediately after scald injury. Levels of tumor necrosis factor alpha （TNFα） ,cardiac troponin T （cTnT） and angiotensin Ⅱ （Ang Ⅱ ） in plasma and contents of TNF α,Ang Ⅱ in myocardium were assayed at 1 ,3,6,12,24 and 48 postburn hours （PBHs）. The morphological change in rat myocardium was observed by electron microscope （EM）. RESULTS： Plasma cTnT level （ 1.87 ± 0.04） was markedly high at 3 PBH （ P 〈 0.01 ）, peaked （6.32 ± 0.41 ） at 12 PBHs, and it was still higher at 48 PBHs than that of the control （0.16± 0.03） ;TNFα level in plasma （38.96 ±5.71 ） and myocardium （1.98±0.08） were also markedly high at 6 PBHs （P 〈0.01 ） ,peaked at 12 PBHs and it was somewhat decreased at 48 PBHs,and it was still higher than that of the control group. Plasma Ang Ⅱ level （175.66±18.91 ） was markedly high at 1 PBH （ P 〈 0.01 ）, peaked at 6 PBHs, Ang li content of the myocardium was also higher than that of the control group significantly, All the indices were still no recovery at 48 PBHs. Treatment group with liqustrazine, however,levels of cTnT ,TNFα and AngⅡ in the plasma and myocardium were significantly decreased compared with that of the burn group. It was revealed by histological examination that there were different degrees of myocardial damage during early postburn stage, such as focal dissolution and fragmentation of myofilament, mitochondria edema,but all the above changes in the treatment group with liqustrazine were evidently ameliorated to near normal. CONCLUSION： Liqustrazine can protect myocardium from injury during early postburn stage, for it can inhibit the production of inflammatory factors and Ang Ⅱ.