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作 者:王玉彩[1,2] 菅向东[1] 张忠臣[1] 宁琼[1,3] 赵波[1,4]
机构地区:[1]山东大学齐鲁医院中毒与职业病科,济南250012 [2]山东省齐河县人民医院内科 [3]山东省济南医院职业病科 [4]山东省聊城市人民医院急诊科
出 处:《中华劳动卫生职业病杂志》2012年第3期220-222,共3页Chinese Journal of Industrial Hygiene and Occupational Diseases
摘 要:目的观察康复新液对百草枯染毒大鼠上消化道损伤的治疗作用,并探讨可能的作用机制。方法成年雄性Wistar大鼠120只,随机分为对照组、模型组和治疗组,每组40只。模型组与治疗组经口灌入质量浓度为20%的百草枯50mg/kg。2h后开始,治疗组经口灌人康复新液1.5ml,每日3次。对照组同时给予等量生理盐水。每组每次取8只大鼠,分别于3、6,9、12、15d时下腔静脉采血处死,取食管及胃组织,HE染色观察组织黏膜的损伤情况,同时测定血清中超氧化物歧化酶(SOD)活力和丙二醛(MDA)含量。结果在3、6,9、12、15d时,HE染色结果显示,治疗组大鼠的黏膜损伤情况较模型组明显减轻;与对照组相比,模型组血清中SOD活力明显降低,MDA含量则明显升高,差异均有统计学意义(P〈0.05);与模型组相比,治疗组血清中SOD活力明显升高,MDA含量明显降低,差异均有统计学意义(P〈0.05)。结论康复新液对百草枯染毒大鼠上消化道损伤具有治疗作用,其机制可能与提高体内抗氧化酶SOD活力,清除自由基,抑制脂质过氧化有关。Objective To investigate the therapeutical effects of KANGFUXINYE on the upper gastrointestinal injury induced by paraquat in rats, and to explore the proper mechanism. Methods A total of 120 adult Wistar male rats were randomly divided into three groups, control group (CG), model group (MG) and treatment group (TG), 40 rats each group. The MG and TG were given 20% paraquat 50 mg/kg by oral administration, after 2 h the TG was given KANGFUXINYE solution 1.5 ml by oral administration, 3 times a day. The CG was given normal saline. On the 3rd, 6th, 9th, 12th and 15th days after exposure, 8 rats of each groupwere killed respectively, and the tissues from esophagus and stomach were collected and examined by HE staining for observing the mucosa injury. The superoxide dismutase (SOD) and malondialdehyde (MDA) of serum were detected. Results On the 3rd, 6th, 9th, 12th and 15th days after exposure, the results of pathological examination showed that the mucosa injury in TG was significantly relieved as compared with MG, the activity of serum SOD reduced obviously and the MDA levels increased significantly in MG, as compared with CG (P〈0.05). The activity of serum SOD increased obviously and the MDA levels decreased significantly in TG, as compared with MG (P〈0.05). Conclusion The results of present indicate that KANGFUXINYE has the therapeutical effects on the upper gastrointestinal injury caused by paraquat in rats. The mechanism of therapeutical effects may be due to the increasing SOD activity, eliminating free radicles and inhibiting the lipid peroxidation.
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