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目的探讨依达拉奉(edaravone,ED)对急性百草枯(paraquat,PQ)中毒致肺损伤的作用及可能机制。方法 108只SPF级SD大鼠随机分为空白对照组、PQ组和治疗组。PQ和治疗组灌胃(40mg/kg)染毒建立中毒模型,对照组等量生理盐水灌胃。染毒后30 min治疗组腹腔注射ED(4mg/kg),1次/d。检测染毒后12、24、48、72h血清超氧化物歧化酶(SOD)、丙二醛(MDA)含量及第14天、第28天血清转化生长因子β1(TGF-β1)和Ⅲ型前胶原肽(PⅢP)水平,同时观察肺组织病理改变。结果与对照组比较,PQ和治疗组血清SOD活力明显下降,MDA含量、TGF-β1和PⅢP水平均明显升高,尤以PQ组为甚,差异有统计学意义(P<0.05)。随染毒时间延长,PQ和治疗组肺组织相继发生肺泡炎和肺纤维化,但治疗组病理改变较轻。结论 ED可抑制脂质过氧化反应,调控细胞因子表达和释放,对PQ引起的肺损伤具有一定保护作用。
Objective To investigate the effect of edaravone (ED) on lung injury induced by acute paraquat (PQ) poisoning and its possible mechanism. Methods 108 SPF SD rats were randomly divided into blank control group, PQ group and treatment group. PQ and treatment group by intragastric administration (40mg / kg) to establish poisoning model, the control group, the same amount of saline gavage. 30 min after exposure to the treatment group, intraperitoneal injection of ED (4mg / kg), 1 time / d. Serum levels of superoxide dismutase (SOD) and malondialdehyde (MDA) at 12, 24, 48 and 72 h after exposure were measured. Serum levels of transforming growth factor β1 (TGF-β1) and type Ⅲ Collagen peptide (PⅢP) levels, while observing the pathological changes of lung tissue. Results Compared with the control group, the activity of SOD in serum of PQ group and treatment group decreased significantly, and the levels of MDA, TGF-β1 and PⅢP were significantly increased, especially in PQ group, the difference was statistically significant (P <0.05). With the prolongation of exposure time, alveolitis and pulmonary fibrosis occurred in the lungs of PQ and treatment groups, but the pathological changes of the treatment group were lighter. Conclusion ED can inhibit lipid peroxidation, regulate the expression and release of cytokines, and have certain protective effect on PQ-induced lung injury.