目的:探讨贯叶连翘提取物对百草枯诱导的大鼠肺纤维化模型的干预作用及机制。方法:20只Sprague-dawly大鼠随机等分为4组:百草枯组,贯叶连翘提取物组,百草枯+贯叶连翘提取物组和对照组。百草枯液按80mg/kg一次性灌胃，贯叶连翘提取物按400mg/kg灌胃，连用3d,对照组仅用生理盐水。于21d处死后取肺脏行HE染色鉴定,并用碱水解法测羟脯氨酸含量,同时以八木国夫荧光法测定肺组织脂质过氧化产物,盐酸羟胺法测定组织总超氧化物歧化酶的酶活力。结果:百草枯染毒动物可致肺纤维化,羟脯氨酸和丙二醛含量明显增高。百草枯+贯叶连翘提取物组与百草枯组比较,第21天时肺纤维化减轻,羟脯氨酸和丙二醛含量减少(Plt;0.05),与对照组相比总超氧化物歧化酶无明显变化(Pgt;0.05)。结论:贯叶连翘提取物对百草枯诱导的大鼠肺纤维化模型有抑制作用,其机制可能与抑制脂质过氧化有关。
目的:观察百草枯中毒大鼠血浆和肺组织匀浆中的内皮素-1的动态变化,探讨大鼠PQ中毒肺损伤的可能机制。方法:将雄性Wistar大鼠随机分成百草枯中毒组和生理盐水对照组,分别给予16mg/kg百草枯或等体积生理盐水腹腔内注射,并在给药后6、12、24和72 h处死大鼠,观察其一般表现、肺的病理变化。测定肺系数、肺组织匀浆和血浆中内皮素-1的含量。结果: 百草枯中毒后大鼠出现呼吸困难,活动能力下降,肺系数增加,并随时间变化,光镜下表现为肺出血、水肿等不同程度的肺损伤改变。血浆和组织匀浆中内皮素-1在中毒后与对照组大鼠比较明显升高,并随时间变化(Plt;0.01)。结论:在百草枯中毒肺损伤中,内皮素-1可能发挥了重要作用。
【摘要】 目的 探讨口服百草枯中毒患者口腔护理的方法及早期护理的临床意义。 方法 2009年1月-2010年3月，采用半随机方法将62例白草枯中毒患者按中毒时间的长短分A组（中毒时间lt;3 d，n=32）、B组（中毒时间gt;3 d，n=3），比较两组患者口腔溃疡的治愈率、并发症发生状况，分析早期口腔护理的必要性。 结果 A组患者百草枯所致的口腔黏膜损害明显减轻，并发症发生率降低，为改善预后提供了条件，显示了早期加强口腔护理的成效。 结论 重视百草枯早期口腔护理，能够减轻口腔糜烂溃疡痛苦，减少并发症，提高患者生活质量。【Abstract】 Objective To investigate the clinical significance of early oral care for paraquat-poisoned patients. Methods A quasi-randomized controlled trial was used. A total of 62 paraquat-poisoned patients (from January 2009 to March 2010) were divided into experimental group and control group in order to compare the healing rate of oral ulcer, complications and the necessity of early oral care between the two groups. Results The oral mucosa lesions in experimental group obviously alleviated and the complications decreased. The effective early oral care provided the very favorable conditions for better prognosis. Conclusion The early oral care for paraquat-poisoned patients could relieve the pain of oral ulcer, reduce the complications and improve patient′s life quality.
目的 探讨急性百草枯(PQ)中毒鼠肺组织病理损伤和肺组织血红素氧合酶-1（HO-1）的表达及三七总皂甙（PNS）的保护作用。 方法 150只SD雄性鼠分为正常对照组（C组）30只、PQ中毒组（PQ组）60只及PNS组60只。PQ组和PNS组一次性灌胃PQ 25 mg/kg染毒，C组给予等体积生理盐水灌胃。其中PNS组于染毒前15 min以PNS 50 mg/kg阴茎静脉注射保护，以后1次/d给药直至处死前；PQ组、C组分别在同时间点给予等体积生理盐水。观察各组大鼠在中毒后6、12 h，1、3、5、7 d肺组织病理改变，采用蛋白质印迹法分析肺组织HO-1蛋白表达和反转录-聚合酶链反应方法测定鼠肺组织HO-1 mRNA的表达。 结果 C组HO-1蛋白和HO-1 mRNA绝大多数标本有弱表达，个别标本不表达；与C组相比PQ组及PNS组HO-1蛋白和HO-1 mRNA表达增强，差异有统计学意义（P＜0.05）；PQ组HO-1蛋白和HO-1 mRNA的表达在1 d达高峰之后下降，第3天基本恢复到C组水平；PNS组与PQ组相似，但在6 h、12 h、1 d及3 d高于PQ组，差异有统计学意义（P＜0.05），至第5天和第7天二者相比差异无统计学意义（P＜0.05）。PQ组肺组织病理损伤评分在6、12 h，1、3 、5、7 d各亚组均高于PNS相应组，差异有统计学意义（P＜0.05），C组肺组织病理大致正常，与PQ组及PNS组相比，差异有统计学意义（P＜0.001）。 结论 HO-1参与PQ中毒所致急性肺损伤，PNS对PQ中毒所致急性肺损伤有保护作用。
ObjectiveTo establish paraquat (PQ)-induced acute respiratory distress syndrome (ARDS) mice model via gavage, in order to simulate oral adminitration in clinical situations.MethodsSeventy-eight 6-8-week-old, specific pathogen free female C57 mice were chosen in this study. The mice were randomly divided into the control group (n=6) and the PQ model group(n=36); the mice in the latter group were randomly divided into 6 poisoning model subgroups further, with 6 mice in each, to find out the suitable concentration of PQ to establish stable ARDS model. The mice in the control group were given phosphatebuffer saline (PBS) by gavage, 200 μL per mouse; while the mice in the 6 poisoning model subgroups were given PQ with varies doses of 3, 10, 30, 100, 150, 300 mg/kg respectively by gavage. The clinical manifestations were observed for 7 days, and the ratio of lung wet/dry (W/D) was measured. After the suitable concentration of PQ for stable ARDS mice model was found, the other 36 mice were randomly divided into the controlgroup and the poisoning model group, both were divided into 4 subgroups, according to different observation point in time (1 day and 2, 3, 4 days after PQ gavage). The mice in the 4 control subgroups (n=3) were given PBS by gavage, 200 μL per mouse; while the mice in the 4 poisoning model subgroups (n=6) were given PQ with the suitable concentration for ARDS mice model by gavage. Pathological manifestations by Haematoxylin-Eosin staining and lung injury score were observed and analyzed.ResultsThe mice began to die at the PQ dosage of 150 mg/kg; while the death rate was stable at 300 mg/kg. On the 2nd and 4th day after PQ gavage, lung W/D was 5.335, 6.113, and 5.525, and 6.403, respectively in the mice in 150 and 300 mg/kg subgroup, which differed much from those in the control group (P<0.001). Congestion, edema, hemorrhage, alveolar structure damage, inflammation cells infiltration of lung tissue were observed, and lung injury score increased.ConclusionPQ-induced ARDS mice model by gavage is established successfully.
ObjectiveTo investigate the changes of inflammatory cytokines in bronchoalveolar lavage fluid (BALF) in rats exposed to paraquat (PQ). MethodsAdult healthy SD rats were randomly divided into a control group (n=8) and three experimental groups (PQ in low dosage of 15 mg/kg,medium dosage of 30 mg/kg,and high dosage of 60 mg/kg,n=24 in each group). The rats in three experimental groups were intragastrically administered with PQ,and the rats in the control group were treated with saline by gavage. Two rats in the control group and six rats in three experimental groups were sacrificed on 1st,7th,14th,and 21st day after exposure respectively. BALF was collected for measurement of interleukin-1(IL-1),IL-6,macrophage inflammatory protein-2(MIP-2),monocyte chemoattractant protein-1(MCP-1),and biopterin by ELISA. ResultsThe levels of cytokines in all experimental groups were higher than those in the control group at any time point. In the exposure day 1 to day 14, IL-1 and biopterin levels in BALF increased significantly with the increase in PQ dose. On 14th and 21st day,IL-6 level in BALF increased significantly with the increase in PQ dosage. The levels of IL-1,IL-6,and biopterin in the experimental groups reached the peak on 14th day. On 14th day,the MIP-2 level in BALF of high-dosage group was significantly higher than that of low-dosage and medium-dosage groups (all P<0.05). The level of MCP-1 in the low-dosage group was lower than that in the medium-dosage and high-dosage groups at any time point (P<0.05). ConclusionIL-1,IL-6,MIP-2,MCP-1,and biopterin may play important roles in the development and progression of PQ-induce lung inflammation.