The Role of PI3K/Akt Pathway Regulated by Estradiol in Hypoxia/Reoxygenation Injury of Rat Alveolar Epithelial Type II Cells
YANG Hui1#, LI Shanshan1#, CHEN Leijie2, WANG Zhonghui1, GONG Lingli1, LIAO Shan1, CHEN Lianpu1, YE Kezhong1, ZHAO Min1 *
This study investigated the role and mechanism of estradiol in H/R (hypoxia/reoxygenation) injury of rat AECII (alveolar epithelial type II cells). AECII were used to establish H/R injury model, which were randomly divided into normal control group (NC group), hypoxia/reoxygenation injury group (HR group) and estradiol pretreatment with different concentrations+hypoxia/reoxygenation injury group (E2+HR group). The morphological changes of cells in each group were observed using inverted microscope. Cell viability was detected by cell counting kit-8 assay, and apoptosis rate was detected by flow cytometry. The levels of IL-6 and TNF-α in cell culture supernatant were determined by ELISA. The expression levels of Akt, P-Akt, Gsk3β, P-Gsk3β and Caspase-3 were measured by Western blot assays. The results showed that compared with NC group, the cell viability decreased, apoptosis rates increased significantly in the other groups. The expression of IL-6 and TNF-α increased significantly, the expression of Akt, P-Akt, and P-Gsk3β decreased, and Caspase-3 expression increased. E2+HR group had a higher cell viability, lower expression of IL-6 and TNF-α, and lower apoptosis rate compared with HR group. The expression of Akt, P-Akt and P-Gsk3β increased, while Caspase-3 expression decreased. These results elucidate that PI3K/Akt signaling pathway is involved in H/R injury of rat AECII. Estradiol can reduce AECII injury induced by H/R in rats, and its mechanism is related to activating PI3K/Akt signal pathway, reducing cell apoptosis and promoting cell viability
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