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Aim:Angiotensin Ⅱ is believed to play an important role in tissue repair andremodeling in lungs by the angiotensin type I(AT1)receptor via a number ofpotential mechanisms.However,the role of the AT1 receptor in early lung injuryhas not been characterized.Methods:Bleomycin-induced pulmonary fibrosis(PF)in rats was utilized to value the treatment with valsartan,an AT1 receptorantagonist,by measurement of body weight,wet weight of the left lung,hydroxy-proline content,mRNA expression of collagen Ⅰ/Ⅲ,and the degree of fibrosis inlung tissues on d 21.Tissue injury in the early phase was assessed on d 1,3 and7 by apoptosis,malondialdehyde content,myeloperoxidase activity,inflamma-tory cell count and protein content.Angiotensin converting enzyme(ACE)activ-ity and the AT1 receptor in lung tissues were analyzed by biochemistry methodand Western blotting,respectively.Results:Valsartan ameliorated PF induced bybleomycin in the rats on d 21.After bleomycin was injected intratracheally,in-creases in the lung AT1 receptor and ACE activity were observed by d 1,3 and 7.Lung injury deteriorated in the early phase.Valsartan reduced the increase of theAT1 receptor,ACE activity and lung injury induced by bleomycin in the earlyphase.Conclusion:These observations suggest that angiotensin Ⅱ may play apotent role in early lung injury via the AT1 receptor.AT1 receptor antagonistsshould be assessed as potential new therapies for fibrotic lung disease.
Aim: Angiotensin II is believed to play an important role in tissue repair and remodeling in lungs by the angiotensin type I (AT1) receptor via a number of potential mechanisms. Although the role of the AT1 receptor in early lung injury has not been characterized. Methods: Bleomycin-induced pulmonary fibrosis (PF) in rats was utilized to value the treatment with valsartan, an AT1 receptor antagonist, by measurement of body weight, wet weight of the left lung, hydroxy-proline content, mRNA expression of collagen I / III, and the degree of fibrosis inlung tissues on d 21. Tissue injury in the early phase was assessed on d 1,3 and 7 by apoptosis, malondialdehyde content, myeloperoxidase activity, inflamma-tory cell count and protein content. Angiotensin converting enzyme (ACE) activ- ity and the AT1 receptor in lung tissues were analyzed by biochemistry method and Western blotting, respectively. Results: Valsartan ameliorated PF induced bybleomycin in the rats on d 21. After bleomycin was injected intratracheally, in-cre ases in the lung AT1 receptor and ACE activity were observed by d 1,3 and 7. Lung injury deteriorated in the early phase. Valsartan reduced the increase of the AT1 receptor, ACE activity and lung injury induced by bleomycin in the earlyphase. Confclusion: These Observations suggest that angiotensin II may play apotent role in early lung injury via the AT1 receptor. AT1 receptor antagonistsshould be assessed as potential new therapies for fibrotic lung disease.