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| The effect of erythropoietin on the lung ischemia/reperfusion injury in rats |
| JIN Xiaosheng, LI Guoping,ZHENG Jisheng, XU Xianrong. |
| Pulmonary and Critical Care Medicine, Tongde Hospital of Zhejiang Province,Hangzhou 310000, China |
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| Cite this article: |
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JIN Xiaosheng. The effect of erythropoietin on the lung ischemia/reperfusion injury in rats[J]. JOURNAL OF WEZHOU MEDICAL UNIVERSITY, 2024, 54(5): 378-383..
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Abstract Objective: To explore the role and mechanism of erythropoietin (EPO) on lung ischemia/reperfusion injury (LIRI). Methods: Adult male Sprague-Dawley rats were randomly divided into 5 groups (n=8): Control group, EPO single administration group (3 000 U/kg), LIRI Model group, LIRI model+EPO pretreatment group (3 000 U/kg) (EPO pretreatment group), LIRI model+EPO treatment group (3 000 U/kg) (EPO treatment group). The mRNA expression of Bcl-2, Bax and caspase-3 was measured by RT-qPCR. The pneumocyte apoptosis was achieved by TUNEL method. The level of FGF23 in lung tissues was determined by immunohistochemistry. The protein levels of FGF23, FGFR4 and p-ERK1/2 was detected by Western blot.The morphology of lung tissue was observed under the ordinary light microscope. Results: Compared with the control group, the expression of Bax and caspase-3 of LIRI model group had a significant increase (P<0.01),while the Bcl-2, FGF23, FGFR4 and p-ERK1/2 expression levels significantly decreased (P<0.01), and the lung tissue injury and cell apoptosis were aggravated. Compared with LIRI model group, the expression of Bax and caspase-3 of EPO pretreatment group and EPO treatment group was significantly decreased (P<0.01), while the Bcl-2, FGF23, FGFR4 and p-ERK1/2 expression levels significantly increased (P<0.01), and the lung tissue injury and cell apoptosis were reduced. Conclusion: Erythropoietin can effectively improve the lung ischemia/reperfusion injury, which may be related to the activation of the FGF23/FGFR4/p-ERK1/2 signaling pathway,up-regulating the expression of apoptosis inhibitor Bcl-2 while down-regulating the expression of pro-apoptotic genes Bax and caspase-3.
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Received: 30 January 2024
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