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

Xu, Min; Xie, Xiaoyan; Fan, Qi-Xin; Mu, Deguang; Zhang, Yong; Cao, Fa-Le; Wang, Yanxia; Zhao, Peng; Zhang, Bo; Jin, Fang; Li, Zhichao

doi:10.1111/j.1440-1681.2011.05498.x

Cited by 27 publications

(28 citation statements)

References 38 publications

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“…We here first demonstrated that Tan ⅡA could reduce BLMeinduced CD-68-positive macrophage infiltration in rat lung tissue. Our study along with several previous studies [17,32] reveals an anti-inflammatory role of Tan ⅡA in lung diseases. However, whether Tan ⅡA had antifibrotic potential in lung fibrosis remains poorly understood.…”

Section: Discussionsupporting

confidence: 52%

“…Antitumor activities, cardioprotective, and neuroprotective effects of Tan ⅡA have been reported in many earlier studies [13e15]. Notably, Tan ⅡA has also been proven to effectively mitigate seawater exposure-induced lung injuries such as lung edema and vascular leakage in rodents [16,17], suggesting that Tan ⅡA has a protective activity in pulmonary diseases. Fu et al [18] have found that Tan ⅡA blocks EMT in MCF-7 and HCC1973 breast cancer cell lines Q5 .…”

Section: Introductionmentioning

confidence: 89%

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Tanshinone IIA ameliorates bleomycin-induced pulmonary fibrosis and inhibits transforming growth factor-beta-β–dependent epithelial to mesenchymal transition

Tang¹,

He²,

Hong³

et al. 2015

Journal of Surgical Research

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Section: Discussionsupporting

confidence: 52%

Section: Introductionmentioning

confidence: 89%

Tanshinone IIA ameliorates bleomycin-induced pulmonary fibrosis and inhibits transforming growth factor-beta-β–dependent epithelial to mesenchymal transition

Tang¹,

He²,

Hong³

et al. 2015

Journal of Surgical Research

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“…We also showed that pretreatment with TIIA greatly decreased the production of pro-inflammatory cytokines in both LPS-treated mice and cultured macrophages, which most likely correlated with the inhibition of HIF-1α expression by TIIA [9] . Moreover, we further indicated that pretreatment with TIIA could significantly attenuate the severity of ALI in seawater-challenged rats through the depression of macrophage migration inhibitory factor [12] , aquaporins (AQP) 1 and AQP5 expression [11] and apoptosis [13] and up-regulation of Na + ,K + -ATPase activity [10] .…”

Section: Discussionmentioning

confidence: 97%

“…Apoptotic cells were found in the damaged alveolar epithelium of patients with ARDS [37] , and in murine models of pulmonary fibrosis and LPS [34,35,38] and seawater exposure-induced ALI [13] . Although TIIA could prevent and treat lung injury induced by LPS, little is known about the effect of TIIA on apoptosis in mice with ALI.…”

Section: Discussionmentioning

confidence: 99%

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Tanshinone IIA therapeutically reduces LPS-induced acute lung injury by inhibiting inflammation and apoptosis in mice

Cao

Zhang

et al. 2014

Acta Pharmacol Sin

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Geraniol (GOH), a special type of acyclic monoterpene alcohol, has been widely used to treat many diseases associated with inflammation and apoptosis. Acute lung injury (ALI) is a common clinical disease in humans characterized by pulmonary inflammation and apoptosis. In the present study, we investigated the protective effects of GOH in a mouse model of ALI induced by the intranasal administration of lipopolysaccharide (LPS) and elucidated the underlying molecular mechanisms in RAW 264.7 cells. In vivo, GOH treatment markedly ameliorated pathological injury and pulmonary cell apoptosis and reduced the wet/dry (W/D) weight ratio of lungs, myeloperoxidase (MPO) activity and the production of pro-inflammatory cytokines (IL-1β, IL-6, and TNF-α). In vitro, the levels of pro-inflammatory cytokines, iNOS and COX-2 were significantly increased in LPS-stimulated RAW 264.7 cells, an effect that was decreased by GOH treatment. Moreover, GOH treatment dramatically reduced the expression of Toll-like receptor 4 (TLR4) and then prevented the nuclear factor-κB (NF-κB) activation. GOH treatment also promoted anti-apoptotic Bcl-2 expression and inhibited pro-apoptotic Bax and Caspase-3 expression. Furthermore, knockdown of TLR4 expression exerted a similar effect and inhibited the phosphorylation of p65, as well as the Bax and Caspase-3 expression. Taken together, these results suggest that GOH treatment alleviates LPS-induced ALI via inhibiting pulmonary inflammation and apoptosis, a finding that might be associated with the inhibition of TLR4-mediated NF-κB and Bcl-2/Bax signalling pathways.

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Hydrogen Gas Inhalation Attenuates Seawater Instillation-Induced Acute Lung Injury via the Nrf2 Pathway in Rabbits

Diao

Zhang

et al. 2016

Inflammation

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Seawater instillation-induced acute lung injury involves oxidative stress and apoptosis. Although hydrogen gas inhalation is reportedly protective in multiple types of lung injury, the effect of hydrogen gas inhalation on seawater instillation-induced acute lung injury remains unknown. This study investigated the effect of hydrogen gas on seawater instillation-induced acute lung injury and explored the mechanisms involved. Rabbits were randomly assigned to control, hydrogen (2 % hydrogen gas inhalation), seawater (3 mL/kg seawater instillation), and seawater + hydrogen (3 mL/kg seawater instillation + 2 % hydrogen gas inhalation) groups. Arterial partial oxygen pressure and lung wet/dry weight ratio were detected. Protein content in bronchoalveolar lavage fluid (BALF) and serum as well as tumor necrosis factor (TNF)-α, interleukin (IL)-1β, and IL-6 levels were determined. Hematoxylin-eosin staining was used to monitor changes in lung specimens, and malondialdehyde (MDA) content and myeloperoxidase (MPO) activity were assayed. In addition, NF-E2-related factor (Nrf) 2 and heme oxygenase (HO)-1 mRNA and protein expression were measured, and apoptosis was assessed by measuring caspase-3 expression and using terminal deoxy-nucleotidyl transferase dUTP nick end-labeling (TUNEL) staining. Hydrogen gas inhalation markedly improved lung endothelial permeability and decreased both MDA content and MPO activity in lung tissue; these changes were associated with decreases in TNF-α, IL-1β, and IL-6 in BALF. Hydrogen gas also alleviated histopathological changes and cell apoptosis. Moreover, Nrf2 and HO-1 expressions were significantly activated and caspase-3 expression was inhibited. These results demonstrate that hydrogen gas inhalation attenuates seawater instillation-induced acute lung injury in rabbits and that the protective effects observed may be related to the activation of the Nrf2 pathway.

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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

Cited by 27 publications

References 38 publications

Tanshinone IIA ameliorates bleomycin-induced pulmonary fibrosis and inhibits transforming growth factor-beta-β–dependent epithelial to mesenchymal transition

Tanshinone IIA ameliorates bleomycin-induced pulmonary fibrosis and inhibits transforming growth factor-beta-β–dependent epithelial to mesenchymal transition

Tanshinone IIA therapeutically reduces LPS-induced acute lung injury by inhibiting inflammation and apoptosis in mice

Hydrogen Gas Inhalation Attenuates Seawater Instillation-Induced Acute Lung Injury via the Nrf2 Pathway in Rabbits

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