活性炭加灶心土对急性百草枯中毒大鼠肺损伤治疗作用的机制研究

A mechanism study on activated carbon with addition of furnace soil for treatment of rats with pulmonary injury caused by acute paraquat intoxication

目的 研究活性炭加灶心土对急性百草枯（PQ）中毒大鼠肺损伤的治疗作用及相关机制.方法 选用健康成年SD大鼠140只,按随机数字表法分为正常对照组、中毒模型组、活性炭组和活性炭加灶心土组,每组35只.采用一次性腹腔注射PQ 300 mg/kg制备PQ中毒肺损伤模型;正常对照组腹腔注射等量生理盐水.制模后活性炭组每日给予活性炭20 g/kg灌胃;活性炭加灶心土组每日给予活性炭20 g/kg加灶心土20 g/kg灌胃;正常对照组和中毒模型组每日给予等量生理盐水灌胃.观察4组大鼠一般状况、肺组织湿/干质量（W/D）比值、血清丙二醛（MDA）、超氧化物歧化酶（SOD）活性、肺组织αl-抗胰蛋白酶（α1-AT）含量及肺组织病理学变化.结果 正常对照组、活性炭组和活性炭加灶心土组大鼠各时间点精神状态、活动度均表现良好,呼吸平稳.与中毒模型组比较,活性炭组、活性炭加灶心土组大鼠一般状况、肺组织病理学变化及肺W/D比值、MDA、SOD、α1-AT均明显改善,且活性炭加灶心土组改善程度均显著优于单用活性炭组[MDA（μmol/L）：染毒后2h为5.87±0.25比7.82±0.21,染毒后4h为6.24±0.28比9.89±0.24,染毒后8h为6.85±0.30比10.32±0.22,染毒后12h为7.47±0.34比9.68±0.25,染毒后24 h为6.79±0.37比9.71±0.29,染毒后48 h为5.98±0.34比8.84±0.31,染毒后72 h为5.62±0.33比7.58±0.32;SOD活性（kU/L）：染毒后2h为322.8±14.2比294.3±14.9,染毒后4h为328.5±16.4比286.6±18.8,染毒后8h为312.8±16.3比275.7±17.4,染毒后12h为317.4±17.6比262.5±18.6,染毒后24 h为315.2±18.4比278.4±17.7,染毒后48 h为314.7±17.4比296.2±19.1,染毒后72 h为319.5±16.5比294.8±18.5;肺W/D比值：3.87±1.00比4.75±1.24;α 1-AT（A值）：染毒后4h为0.50±0.04比0.40±0.03,染毒后8h为0.32±0.05比0.24±0.03,染毒后12h为0.29±0.06比0.17±0.05,染毒后24h为0.35±0.05比0.15±0.02,染毒后48 h为0.38±0.03比0.16±0.01,染毒后72 h为0.36±0.05比0.18±0.05,均P＜0.05].结论 活性炭对PQ中毒引起的急性肺损伤（ALI）有一定的治疗作用;活性炭加灶心土可减轻PQ中毒引起的肺组织损伤,对PQ中毒引起的ALI有较好的治疗作用,其机制为清除氧自由基,提高机体抗氧化损伤,抑制脂质过氧化,并可促进α 1-AT表达.

Objective To study the therapeutic effect of activated carbon with addition of furnace soil for treatment of rats with pulmonary injury caused by acute paraquat （PQ） poisoning and its mechanisms. Methods One hundred and forty healthy adult Sprague-Dawley （SD） rats were randomly divided into normal control group, poisoning model group, activated carbon group and activated carbon with furnace soil group, each group n = 35 rats. The lung injury model induced PQ poisoning was ~pvoduced by intraperitoneal injection of one-time PQ 300 mg/kg; equal volume of saline solution was given to the normal control group by intraperitoneal injection. After modeling, the activa^d carbon 20 g/kg was given to activated carbon group by garage daily; activated carbon 20 g/kg plus furnace soil 20 g/kg were applied to activated carbon with furnace soil group by gavage daily; normal control group and poisoning model group were given the same amount of saline by gavage daily. The general condition of rats, lung wet/dry weight （W/D） ratio, the content of malondialdehyde （MDA） and activity of superoxide dismutase （SOD） in serum, the expression of α 1-antitrypsin （ α 1-AT） in lung tissue, histological and pathological changes of lung tissue were observed in the four groups. Results The rats in normal control group, activated carbon group and activated carbon plus furnace soil group showed good mental state, mobility behavior quite well and breath smooth at each time point. Compared with poisoning model group, the rats＇ general condition, lung tissue pathological changes, lung W/D ratio, MDA, SOD, α1-AT were significantly improved in activated carbon and activated carbon plus focal subsoil groups, and the degree of improvement in latter group was markedly superior to that of activated carbon alone group [MDA （μmol/L）： after poisoning for 2 hours was 5.87±0.25 vs. 7.82±0.21, after poisoning for 4 hours was 6.24±0.28 vs. 9.89±0.24, after poisoning for 8 hours was 6.85±0.30 vs. 10.32±0.22, after poisoning for 12 hours was 7.47±0.34 vs. 9.68±0.25, after poisoning for 24 hours was 6.79±0.37 vs. 9.71±0.29, after poisoning for 48 hours was 5.98 ±0.34 vs. 8.84±0.31, after poisoning for 72 hours was 5.62±0.33 vs. 7.58 ± 0.32; SOD activity （kU/L）： after poisoning for 2 hours was 322.8±14.2 vs. 294.3±14.9, after poisoning for 4 hours was 328.5± 16.4 vs. 286.6±18.8, after poisoning for 8 hours was 312.8 ±16.3 vs. 275.7 ±17.4, ＇after poisoning for 12 hours was 317.4±17.6 vs. 262.5 ± 18.6, after poisoning for 24 hou~ was 315.2±18.4 vs. 278.4 ± 17.7, after poisoning for 48 hours was 314.7±17.4 vs. 296.2±19.1, after poisoning for 72 hours was 319.5 ± 16.5 vs. 294.8±18.5; lung W/D ratio： 3.87 ± 1.00 vs. 4.75 ±1.24; α 1-AT （A value）： after poisoning for 4 hours was 0.50 ±0.04 vs. 0.40 ±0.03, after poisoning for 8 hours was 0.32±0.05 vs. 0.24 ±0.03, after poisoning for 12 hours was 0.29± 0.06 vs. 0.17±0.05, after poisoning for 24 hours was 0.35± 0.05 vs. 0.15 ± 0.02, after poisoning for 48 hours was 0.38± 0.03 vs. 0.16±0.01, after poisoning for 72 hours was 0.36 ±0.05 vs. 0.18±0.05, all P 〈 0.05]. Conclusions Activated carbon has a certain therapeutic effect for therapeutic of acute lung injury. （ALI） caused by PQ poisoning; activated carbon with addition of filrnaee subsoil can also alleviate the ALI induced by PQ poisoning and its therapeutic effect is relatively good; the mechanisms are related to the removal of oxygen free radical, elevation of the organism＇s resistance to oxidation damage, inhibition of lipid peroxidation and promotion of α 1-AT expression.