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DOI 10.1016/j.mvr.2020.104009

Медицинская библиотека · Microvascular research · 2020

Expression and regulation of tumor necrosis factor-α-induced protein-8-like 2 is associated with acute lung injury induced by myocardial ischemia reperfusion in diabetic rats.

Kong Qian, Yuan Min, Ming Tingqian, Fang Qing, Wu Xiaojing, Song Xuemin

СтатьяПоддержка исследования: вне правительства СШАПеревод пока не подготовлен

Аннотация

AIMS: The purpose of the present study was to investigate the possible role of TIPE2 on acute lung injury (ALI) induced by myocardial ischemia/reperfusion (MIR) in diabetic rats.

METHODS

Sprague-Dawley (SD) rats were randomly separated into four groups: control+sham (C + sham); control+MIR (C + MIR); diabetes+sham (D + sham); diabetes+MIR (D + MIR). Diabetes was induced using streptozotocin. Eight weeks after diabetes induction, MIR was conducted. At 2 h after MIR, myocardial injury indices were assessed; arterial blood, bronchoalveolar lavage fluid (BALF) and lung tissues were collected for corresponding detection.

RESULTS

Rats subjected to MIR showed serious ALI (estimated via pathological changes, lung injury score and Wet/Dry weight ratio), lung inflammation and pulmonary cell apoptosis compared with sham groups, especially in D + MIR group. Evaluation of protein expression in lung tissues showed that p-JNK and nuclear NF-κB p65 protein levels were higher in D + MIR group as compared with C + MIR group. Besides, either hyperglycemia or MIR can significantly upregulate TIPE2 protein levels.

CONCLUSIONS

In conclusion, diabetic lungs are more susceptible to MIR. TIPE2 may involve in this pathological process, possibly through regulation of inflammation, oxidative stress and apoptosis.

Для цитирования: Kong Qian, Yuan Min, Ming Tingqian, Fang Qing, Wu Xiaojing, Song Xuemin. Expression and regulation of tumor necrosis factor-α-induced protein-8-like 2 is associated with acute lung injury induced by myocardial ischemia reperfusion in diabetic rats.. Microvascular research. 2020. DOI: 10.1016/j.mvr.2020.104009.

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