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Tanshinone IIA suppresses lung injury and apoptosis, and modulates protein kinase B and extracellular signal‐regulated protein kinase pathways in rats challenged with seawater exposure
Author(s) -
Li JiaHuan,
Xu Min,
Xie XiaoYan,
Fan QiXin,
Mu DeGuang,
Zhang Yong,
Cao FaLe,
Wang YanXia,
Zhao PengTao,
Zhang Bo,
Jin FaGuang,
Li ZhiChao
Publication year - 2011
Publication title -
clinical and experimental pharmacology and physiology
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 0.752
H-Index - 103
eISSN - 1440-1681
pISSN - 0305-1870
DOI - 10.1111/j.1440-1681.2011.05498.x
Subject(s) - tunel assay , apoptosis , protein kinase b , kinase , lung , bronchoalveolar lavage , seawater , medicine , pharmacology , chemistry , andrology , biology , biochemistry , ecology
Summary 1. Tanshinone IIA (TIIA) is one of the main active components of the Chinese herb, Danshen. In the present study, we investigated the role of apoptosis in seawater exposure‐induced acute lung injury (ALI), and explored the effects of TIIA on lung injury, apoptosis, and protein kinase B (Akt) and etracellular signal‐regulated protein kinase (ERK) pathways in seawater‐challenged rats. The rats were randomly divided into four groups: (i) naive group, no drug was given; (ii) TIIA control group, TIIA (50 mg/kg) was given intraperitoneally; (iii) seawater (SW) group, seawater (4 mL/kg) was given; and (iv) TIIA/SW group, TIIA (50 mg/kg) was injected intraperitoneally 10 min after seawater instillation. 2. The results showed that TIIA treatment significantly improved seawater exposure‐induced lung histopathological changes, alleviated the decrease in PaO 2 , and reduced lung oedema, vascular leakage and cell infiltration. As shown by terminal deoxynucleotidyl transferase‐mediated nick end labelling (TUNEL) assay, seawater exposure induced apoptosis in lung tissue cells. Furthermore, seawater exposure also changed apoptosis‐related factors Bcl‐2 and caspase‐3, and caused a reduction in the activation of Akt and ERK1/2 pathways. Furthermore, TIIA treatment decreased the number of apoptotic cells, reversed changes in Bcl‐2 and caspase‐3, and upregulated the activation of Akt and ERK1/2 in seawater‐challenged rats. 3. In conclusion, the data suggest that apoptosis might play an important role in seawater exposure‐induced lung injury and that TIIA could significantly attenuate the severity of ALI and apoptosis in seawater‐challenged rats, which is possibly through modulation of Akt and ERK1/2 pathways.