The Effective Of Hypericum Perforatum L In The Rat Model Of Acute Paraquat Intoxication

Background and Objective: Acute paraquat (PQ) intoxication can causesevere lung injury, which typically shows alveolar dropsy, pulmonaryhemorrhage, and can develop to pulmonary interstitial fibrosis, leading torespiratory failure and death. There has no specific antidote for the routinetreatment of paraquat intoxication. Lung is the target organ of PQ. Hypericumperforatum L maybe have an important role in the development of lung injuryand pulmonary fibrosis, poisoned behind creates a lot of oxyradical and lead tolipid peroxidation. It is the point of pulmonary fibrosis.In recent years, look for the plant of eliminating oxyradical to used for ananti-fibrosis have already caused a domestic and international attention.Someresearchs prove exeract of Hypericum perforatum L (HP) can preclude oxyradical to be used for anti-fibrosis, the expression of the DDR1 and TGF-β1levels are important factors in pulmonary fibrosis. We measure the expressionof the TGF-β1 and DDR1 in paraquat intoxication, then interfered by HP inorder to observe ability of HP to anti-fibrosis.Measurements: fourty Wister rats were randomized to five groups:Normal controlled group (group 1-N): the control rats were given equivalentvolume of normal saline; acute paraquat intoxication model group (group 2-P):the rats were given paraquat at the dose of 80mg/kg by stomach perfusion. HPtreated groups (group 1,2,3-H): the rats were given paraquat at the dose of80mg/kg by stomach perfusion, after one hour give HP100mg/kg, 200mg/kg,400mg/kg twice a day for seven days. Measurements were determined at 7th,14th days post exposure. Fibrosis level of pulmonary fibrosis in acute paraquat intoxication was detected by HE, Masson tinction.The intensity of expressionof TGF-β1, DDR1 was detected by immunohistochemistry.Main results:①Progressive diffuse airsacculitis, with alveolar dropsy,pulmonary hemorrhage, hyaline membrane and inflammatory cell infiltrationwas found in PQ intoxicated rats. HP treated groups can slow down thedevelopment of the progressive diffuse airsacculitis compared with acuteparaquat intoxication group. HP treated groups can reduce collagen'shyperplasia compare with cute paraquat intoxication group. The levels ofpulmonary fibrosis were significantly lower in HP treated group comparedwith the rats of acute paraquat intoxication model 80mg/kg(p＜0.05). Theintensity of the TGF-β1 expression measured by immunohistochemistry, wassignificantly lower in HP treated groups compare with the rats of acuteparaquat intoxication model (group 2), (p＜0.05). The intensity of the DDR1expression measured by immunohistochemistry, was significantly lower in HPtreated groups compare with the rats of acute paraquat intoxication model(group 2), (p＜0.05). HP400mg/kg can influence the intensity of theTGF-β1 and DDR1 expression significantly compare with other cured groups.Conclusion: These results suggest that the expression of TGF-β1 andDDR1 plays an important role in the pathogenesis of lung injury induced byacute paraquat intoxication. HP could alleviate the lung injury and fibrosisfrom reducing the expression of TGF-β1 and DDR1. HP may have a role indiminishing the level of pulmonary fibrosis induced by acute paraquatintoxication by clearing up oxyradical. HP is a effective medicine to treatpulmonary fibrosis induced by acute paraquat intoxication especiallyHP400mg/kg group.