促肝细胞生长素对百草枯中毒引起大鼠急性肺损伤的影响

Effect of hepatocyte growth-promoting factor on acute lung injury induced by paraquat poisoning in rats

目的研究促肝细胞生长素(pHGF)对急性百草枯中毒大鼠肺组织凋亡相关蛋白Bcl-2、Bax的表达及血清肿瘤坏死因子α(TNF-α)水平的影响。方法将90只SD大鼠按照随机数字表法随机分为三组:非药物处理组,毒素处理组,治疗组,各组30只。毒素处理组、治疗组均以PQ(25 mg/kg)一次性腹腔注射染毒,治疗组予每天1次pHGF(50μg/kg)腹腔注射,持续至第7天。各组于注射后第1、3、7天时间点处死相同数目大鼠,观察各组病理学变化,并收集血清及肺组织用于相关指标的检测分析。结果与非药物处理组比较,毒素处理组各时间点动脉氧分压(PaO_2)均有不同程度下降,治疗组第1、3天相比毒素处理组PaO_2有所改善(P<0.05),第7天与毒素处理组比较,PaO_2改善不明显(P>0.05);毒素处理组较非药物处理组肺组织Bax、Bcl-2蛋白表达及血清TNF-α水平明显增高(P<0.01),而血清超氧化物歧化酶(SOD)活力明显降低(P<0.01);各时间点治疗组较毒素处理组肺组织中Bax蛋白表达及血清TNF-α水平降低(P<0.05),Bcl-2蛋白表达水平及血清SOD活力升高(P<0.05)。结论pHGF对百草枯中毒大鼠急性肺损伤具有保护作用,其机制可能通过降低炎性反应、减少氧化损伤、抑制细胞凋亡来减轻肺损伤程度。

Objective To observe the effect of hepatocyte growth-promoting factor （pHGF） on the protein expression of Bcl-2 and Bax in lung tissue and serum tumor necrosis factor α （TNF-α） level in acute paraquat poisoning rats. Methods According to random number table, 90 SD rats were randomly divided into three groups： non drug treated group, venoms group, treatment group, with 30 rats in each group. The venoms groups and treatment group were treated with PQ （25 mg/kg） by a single intraperitoneal injection, treatment group was given pHGF （50 μg/kg） by intraperitoneal injection, once a day, for seventh days. A same number of the rats were sacrificed at the 1st day, 3rd day and 7th day, and the pathology change and the related indexes of each group in serum and lung tissue were observed. Results Compared with non drug treated group, PaO2 of the venoms group was decreased inordinately at each time point. Compared to poisoning group, the PaO2 of treatment group was improved at the 1st and 3rd day （P 〈 0.05）, the seventh day had no obvious change （P 〉 0. 05）. Compared with non drug treated group, the protein expression of Bcl-2 and Bax in lung tissue and serum TNF-α level in venoms group were significantly increased （P 〈 0.01）, whereas,the serum SOD activity was decreased obviously （P 〈 0.01）. Compared with poisoning group, Bax protein expression in lung tissue and serum TNF-α level were decreased （P 〈 0.05） and Bcl-2 protein expression and serum SOD activity were increased （P 〈 0.05） in treatment group at each time point. Conclusion pHGF can reduce the damage degree of lung tissue by reducing inflammation, reducing oxidative damage and inhibiting apoptosis.