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. 2015 Jan 21;10(1):e0114963.
doi: 10.1371/journal.pone.0114963. eCollection 2015.

Influence of levosimendan postconditioning on apoptosis of rat lung cells in a model of ischemia-reperfusion injury

Chengxin Zhang  1 , Zhixiang Guo  1 , Haiyuan Liu  2 , Yinglu Shi  3 , Shenglin Ge  1
Affiliations

Influence of levosimendan postconditioning on apoptosis of rat lung cells in a model of ischemia-reperfusion injury

Chengxin Zhang et al. PLoS One. .

Abstract

Objective: To ascertain if levosimendan postconditioning can alleviate lung ischemia-reperfusion injury (LIRI) in rats.

Method: One hundred rats were divided into five groups: Sham (sham), ischemia-reperfusion group (I/R group), ischemic postconditioning (IPO group), levosimendan postconditioning (Levo group) and combination postconditioning group of levosimendan and 5-Hydroxydecanoic acid (Levo+5-HD group). The apoptotic index (AI) of lung tissue cells was determined using the terminal deoxynucleotidyl transferase dUTP nick end labeling (TUNEL) assay. Expression of active cysteine aspartate specific protease-3 ( active caspase-3), Bcl-2 and Bax in lung tissue was determined by immunohistochemical staining. The morphopathology of lung tissue was observed using light and electron microscopy.

Results: AI values and expression of active caspase-3, Bcl-2 and Bax of lung tissue in I/R and Levo+5-HD groups were significantly higher than those in the sham group ( P<0.05). AI values and expression of active caspase-3 and Bax were significantly lower, whereas that of Bcl-2 was higher significantly in the Levo group, compared with I/R and Levo+5-HD groups (P<0.05). Significant differences were not observed in comparisons between I/R and Levo+5-HD groups as well as IPO and Levo groups.

Conclusion: LIRI can be alleviated by levosimendan, which simulates an IPO protective function. A postulated lung-protective mechanism of action could involve opening of mitochondrial adenosine triphosphate-sensitive potassium channels, relieving Ca2+ overload, upregulation of expression of Bcl-2, and downregulation of expression of active caspase-3 and Bax.

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Conflict of interest statement

Competing Interests: The authors have declared that no competing interests exist.

Figures

Figure 1
Figure 1. TUNEL staining of apoptotic lung tissue cells in the five groups (×400 magnification).
A: Sham group; B: I/R group; C: IPO group; D: Levo group; E: Levo+5-HD group. Apoptotic cells are stained brown-yellow.
Figure 2
Figure 2. Western blotting results of active caspase-3, Bax and Bcl-2 in different groups.
Figure 3
Figure 3. H&E staining of lung tissue (×200 magnification).
A: Sham group; B: I/R group; C: IPO group; D: Levo group; E: Levo+5-HD group.
Figure 4
Figure 4. Ultrastructure of type-II alveolar epithelial cells in lung tissue (×20,000 magnification).
A: Sham group; B: I/R group; C: IPO group; D: Levo group; E: Levo+5-HD group.
Figure 5
Figure 5. Results of CSE activity.
See this image and copyright information in PMC

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