Curcumin attenuates lung ischemia-reperfusion injury in mice through inhibiting JNK pathway and excessive endoplasmic reticulum stress

AIM: To investigate the role of curcumin (Cur) in attenuating lung ischemia-reperfusion (I/R) injury by inhibiting c-Jun N-terminal kinase(JNK) pathway and excessive endoplasmic reticulum stress (ERS) in mice. METHODS: Mouse model of lung I/R injury in situ was established in the left lung in vivo. Sixty mice were randomly divided into 6 groups (n=10 in each group), including sham group, I/R group, dimethyl sulfoxide solvent control group (I/R+DMSO group) and curcumin groups (I/R+ low, medium or high dose of Cur group). Left lung tissue was isolated after the experiment. The ratio of wet lung weight to dry lung weight (W/D), and total lung water content (TLW) were measured. The histological structure and ultrastructure of the left lung were observed under light and electron microscopes, and scored by alveolar damage index of quantitative assessment (IQA). The mRNA expression and protein levels of JNK and GRP78 were measured by RT-PCR and Western blotting. Apoptotic cells in the lung tissue were determined by TUNEL method. RESULTS: Compared with sham group, all indexes above in I/R group and DMSO group were significantly increased. No significant difference of all indexes between I/R group and DMSO group was observed. Compared with DMSO group, the indexes above in low, medium and high doses of Cur groups were decreased, especially in high dose of Cur group, but the expression level of GRP78 had no statistical difference. CONCLUSION: I/R induces excessive ERS in the lung tissue and results in lung injury. Cur has a protective effect on lung against I/R injury, which may be related to inhibition of apoptosis mediated by JNK pathway in ERS.