Objective To investigate the mechanismof lung injury caused by paraquat poisoning by observing the changes of fibrogenic cytokines in acute paraquat poisoned rats and the effects of pyrrolidine dithiocarbamate ( PDTC) . Methods Sprague-Dawley rats were randomly divided into three groups, ie. acontrol group ( n =6) , a PDTC group ( n =36) , a paraquat group ( n = 36) , and a paraquat + PDTC group( n =36) . The rats in the PDTC group, the paraquat group, and the paraquat + PDTC group were subdivided into 6 subgroups sacrificed respectively on 1st, 3rd,7th,14th, 28th and 56th day after the treatment. The levels of transforming growth factor-β1( TGF-β1 ) , platelet-derived growth factor ( PDGF) , insulin-like growthfactor-1 ( IGF-1) in serum were measured. Meanwhile the expression of connective tissue growth factor ( CTGF) and hydroxyproline in lung tissues were detected. The relationship of above cytokines with hydroxyproline was analyzed. Results The destructive phase in early ( 1 ～7 d) was characterized by hemorrhage, alveolar edema, and inflammatory cell infiltration. The proliferous phase in later stage ( 14 ～56 d) was characterized by diffused alveolar collapse with fibroblast proliferation and patchy distribution of collagen fibers. Compared with the control group, the level of TGF-β1 on all time points, the level of PDGF from7th to 56th day, the level of IGF-1 from3rd to 56th day in the paraquat group all significantly increased ( P lt;0. 01) . Immunohistochemistry results showed CTGF positive cells mainly located in aleolar epithelialcells, endothelial cells,macrophages in early stage, and fibroblasts were main positive cells on the 28th and the 56th day. The expression of CTGF in the paraquat group increased gradually compared with the control group on different time points ( P lt; 0. 05 or P lt; 0. 01) . Meanwhile, the levels of above cytokines were positively correlated with the level of hydroxyproline. Noteworthy, PDTC treatment led to significant decreases of above cytokines compared with the paraquat group in corresponding time points ( P lt;0. 05 or P lt;0. 01) .Conclusions Over expressions of IGF-1, TGF-β1 , PDGF, IGF-1 and CTGF may play important roles in lung fibrosis of paraquat poisoned rats. PDTC, as a b NF-κB inhibitor, may inhibits NF-κB activity and further significantly decreases expressions of cytokines, leading to significantly attenuated pulmonary inflammation and fibrosis. However, the mechanisms of PDTC intervention still remain to be explored.
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。
【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.
【摘要】 目的 观察百草枯中毒大鼠肾组织中血红素氧合酶1(HO1)的表达,探讨其病理生理机制。 方法 SD大鼠126只随机分为空白对照组、中毒组和褪黑素组,各42只。中毒组、褪黑素组予以百草枯(25 mg/kg)腹腔注射染毒,对照组予以等量生理盐水腹腔注射,15 min后褪黑素组予以褪黑素(10 mg/kg)腹腔注射,对照组、中毒组予以等量生理盐水腹腔注射。于1、3、6、12 h,1、2、3、5 d时各组随机取6只处死。苏木精〖CD3/5〗伊红（HE）染色观察各组肾组织病理学变化,采用免疫组识化学和RTPCR观察肾组织HO1蛋白和mRNA表达。 结果 ①与对照组相比,中毒组染毒后3 h即可见充血、水肿及空泡变性等病理变化,1 d达顶峰,病理损伤评分3.30±0.31(Plt;0.05),其后缓解趋势不明显；而褪黑素组病理变化明显减轻且缓解趋势明显,1 d时病理损伤评分2.70±0.26,与中毒组相比差异有统计学意义(Plt;0.05)。②与对照组相比,中毒组染毒3 h在皮质部肾小管上皮细胞的细胞膜及细胞浆HO1呈阳性表达,免疫组识化学评分(IHS)3.33±1.75,HO1 mRNA表达增强,与对照组相比差异有统计学意义(Plt;0.05),1 d达顶峰,HIS为7.00±2.00,之后减弱,5 d仍有阳性表达,但与对照组相比差异无统计学意义(Pgt;0.05)；褪黑素组HO1表达较中毒组明显增强,IHS评分6 h~3 d差异具有统计学意义(Plt;0.05),5 d不再有统计学意义(Pgt;005)。 结论 HO1在百草枯中毒大鼠肾组织中呈高表达,褪黑素能明显改善百草枯中毒肾脏病理损伤,增强HO1表达可能是其作用途径之一,而氧化损伤可能是百草枯中毒肾损伤病理生理机制之一。【Abstract】 Objective To investigate the expression of heme oxygenase1 (HO1) in paraquartinduced renal injury in rats and the protective effects of melatonin, and explore possible mechanism of paraquartinduced renal injury. Methods One hundred and twentysix adult healthy SpragneDawley rats were randomly divided into three groups and 42 in each group: control group (A), paraquart group (B), and melatonin group (C). The rats in group B and group C were treated with paraquart (25 mg/kg) intraperitoneally, the rats in group A were treated with the same dose of normal saline. In 15 minutes, the rats in group C were given melatonin intraperitoneally at a dose of 10 mg/(kg·d) and the rats in group A and B were treated intraperitoneally with the same dose of normal saline. Six rats in each group were randomly sacrificed at one, three, 12 hours and one, tou, three, five days respectively. Renal histopathological changes were observed under light microscope by HE staining. The protein and mRNA expressions of HO1 were evaluated by immunohistochemical staining and RTPCR respectively. Results ①In group B, there were obvious lesions in the renal tubule of cortical part, including edema, congestion and vacuolar degeneration. These pathologic changes gradually reached the peak on the first day and did not relieved till the end of this study, the pathologic injury score was 3.30±0.31, and there was a statistical significance between group B and group A (Plt;0.05). The aforementioned pathological lesion was more palliative in group C, the pathologic injury score was 2.70±0.26 at the first day; Compared with group B, there was a statistical significance. ②In group A, there was no or weak expression of HO1 and HO1 mRNA. At the third hour, the expression of HO1 in group B was observed in the membrane and cytoplasm of renal tubular epithelial cell of cortical part. Immunohistochemistry score (IHS) was 3.33±1.75 and the expression of HO1 mRNA increased, there was a statistical significance between group B and group A (Plt;0.05). It reached the peak on the first day, IHS was 7.00±2.00, but there was no statistical difference between group B and group A on the fifth day (Pgt;0.05); Compared with group B, the expression in group C was enhanced obviously, IHS were higher obviously on the six hour till to the third day (Plt;0.05), but there were no statistical differences on the fifth day (Pgt;0.05). Conclusion The expression of HO1 in the paraquartdamaged kidney increases and melatonin surely has an protective effect by increasing the expression of HO1, which suggests that oxidative injury might be the main mechanism of paraquartinduced renal injury.
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。
ObjectiveTo analyze the clinical and pathologic features of paraquat poisoning, discuss the damage mechanism of pulmonary fibrosis caused by paraquat poisoning. MethodsWe retrospectively analyzed the paraquat poisoning-related cases collected in recent years from January 2010 to December 2013, and compared the clinical features and pathologic changes between acute and chronic paraquat poisoning cases. ResultsThe main clinical and pathologic manifestation of paraquat poisoning was multiple organ damage, especially with lung as its target organ. In acute poisoning deaths, the lung injury was characterized by the pulmonary edema and formation of lung transparent membrane; In chronic poisoning deaths, the injury was characterized by the formation of lung transparent membrane and pulmonary fibrosis. ConclusionIn order to make an earlier diagnosis in clinical cases, we should strengthen the cognition of clinical manifestations and damage mechanism of paraquat poisoning. To obtain an accurate conclusion in forensic medicine appraisal, we should draw a comprehensive analysis of the forensic case, the clinical data, the toxicological analysis and the autopsical results.