Dexmedetomidine Leads to the Mitigation of Myocardial Ischemia/Reperfusion-Induced Acute Lung Injury in Diabetic Rats Via Modulation of Hypoxia-Inducible Factor-1α

被引:6
|
作者
Chen, Siyu [1 ]
Wu, Jianjiang [1 ]
Yang, Long [1 ]
Tailaiti, Taiwangu [1 ]
Zou, Tiantian [1 ]
Huan, Yidan [1 ]
Wang, Jiang [1 ]
机构
[1] Xinjiang Med Univ, Affiliated Hosp 1, 137 Liyushan South Rd, Urumqi 830000, Xinjiang Uygur, Peoples R China
基金
中国国家自然科学基金;
关键词
Dexmedetomidine; Acute Lung Injury; Myocardial Ischemia Reperfusion; Hypoxia-Inducible Factor 1; Diabetes; up-Regulation; ISCHEMIA-REPERFUSION INJURY; OXIDATIVE STRESS; RESPONSES; PROTECTS;
D O I
10.21470/1678-9741-2020-0591
中图分类号
R5 [内科学];
学科分类号
1002 ; 100201 ;
摘要
Introduction: The objective of this study is to investigate the protective mechanism of dexmedetomidine (Dex) in myocardial ischemia/reper fusion (MIR)-induced acute lung injury (ALI) of diabetic rats by inhibiting hypoxia-inducible factor-1 alpha (HIF-1 alpha). Methods: Initially, healthy male Sprague Dawley rats were treated with streptozocin to induce diabetes. Then, three weeks after the induction, Dex or lentiviral vector (LV)-HIF-1 alpha was injected into the rats 30 minutes prior to the MIR modeling. After four weeks, lung tissues were harvested for pathological changes observation and the wet/dry weight (W/D) ratio determination. Afterwards, oxidative stress indicators and pro inflammatory factors were measured. In addition, HIF-1 alpha expression was assessed by immunohistochemistry and western blot analysis. Results: Dex could suppress inflammatory cell infiltration, improve lung tissue structure, reduce pathological score and the W/D ratio, and block oxidative stress and inflammatory response in MIR-induced ALI of diabetic rats. Besides, Dex could also inhibit HIF-1 alpha expression. Moreover, Dex + LV-HIF-1 alpha reversed the protective role of Dex on diabetic MIR-induced ALI. Conclusion: Our study has made it clear that Dex inhibited the upregulation of HIF-1 alpha in diabetic MIR-induced ALI, and thus protect lung functions by quenching the accumulation of oxygen radical and reducing lung inflammatory response.
引用
收藏
页码:370 / 379
页数:10
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