Author: Wu, Huajie; Li, Yan; Wang, Yanxia; Xu, Dunquan; Li, Congcong; Liu, Manling; Sun, Xin; Li, Zhichao
Title: Tanshinone IIA Attenuates Bleomycin-Induced Pulmonary Fibrosis via Modulating Angiotensin-Converting Enzyme 2/ Angiotensin-(1-7) Axis in Rats Document date: 2014_4_7
ID: td2uk2wc_38
Snippet: ACE-2, a homologue of ACE, was identified in 2000, which finding evoked a new complexity to the RAS [30] . Despite the similar functions as ACE, ACE-2 has different substrates [30, 31] . Previous studies revealed that ACE-2 may negatively regulate the RAS, and counterbalance the functions of ACE [32] . Another study also demonstrates ACE-2 plays a negative regulatory role for severity of lung edema and acute lung failure [13] . Moreover, decrease.....
Document: ACE-2, a homologue of ACE, was identified in 2000, which finding evoked a new complexity to the RAS [30] . Despite the similar functions as ACE, ACE-2 has different substrates [30, 31] . Previous studies revealed that ACE-2 may negatively regulate the RAS, and counterbalance the functions of ACE [32] . Another study also demonstrates ACE-2 plays a negative regulatory role for severity of lung edema and acute lung failure [13] . Moreover, decreased pulmonary ACE-2 activity related with BLM induced lung injury has been reported in both animal and human studies [15, 33] . Our study showed that BLM induced decreased ACE-2 levels in rat lungs, which is consistent with the previous studies. Moreover, TIIA treatment reversed the lowered expression of ACE-2 levels both by immunohistochemical and WB assays. Additionally, the mRNA levels of ACE-2 were also significantly lowered after BLM exposure, which is also in agreement with the study mentioned above.
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