Intestinal ischemia/reperfusion (I/R) is a clinical emergency, which often causes lung injury with high morbidity and mortality. Although dexmedetomidine has been identified to have a protective effect on lung injury caused by intestinal I/R, its specific mechanism is still elucidated. In recent years, the cannabinoid (CB₂) receptor pathway has been found to be involved in I/R injury of some organs. In the current study, we investigated whether the CB₂ receptor pathway contributes to the protective effect of dexmedetomidine on the intestinal I/R-induced lung injury in rats. Dexmedetomidine treatment upregulated the expression of CB₂ receptor and suppressed the I/R-induced increases in lung injury scores, inflammatory cell infiltration, lung wet/dry ratio, MPO activity, MDA level, inflammatory cytokines, and caspase-3 expression while augmenting SOD activity and Bcl-2 expression, indicating attenuation of lung injury. Dexmedetomidine treatment also increased the expression of Akt. The protective effects of dexmedetomidine treatment were reversed by the CB₂ receptor antagonist AM630 or the PI3K inhibitor wortmannin. And the CB₂ receptor antagonist AM630 also downregulated the expression of Akt. Thus, our findings suggest that treatment with dexmedetomidine provides a protective role against lung injury caused by intestinal I/R in rats, possibly due to the upregulation of the CB₂ receptor, followed by the activation of the PI3K/Akt pathway.

中文翻译：

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右美托咪定通过上调大麻素受体2消除磷脂酰肌醇3-激酶/ Akt途径，从而减轻肠缺血/再灌注引起的肺损伤。

肠缺血/再灌注（I / R）是一种临床急症，通常会导致肺损伤，并具有较高的发病率和死亡率。尽管已确认右美托咪定对肠道I / R引起的肺损伤具有保护作用，但仍未阐明其具体机制。近年来，已发现大麻素（CB ₂）受体途径与某些器官的I / R损伤有关。在当前的研究中，我们调查了CB ₂受体途径是否有助于右美托咪定对大鼠肠I / R诱导的肺损伤的保护作用。右美托咪定治疗上调了CB ₂的表达受体并抑制I / R诱导的肺损伤评分，炎性细胞浸润，肺湿/干比，MPO活性，MDA水平，炎性细胞因子和caspase-3表达增加，同时增加SOD活性和Bcl-2表达，表明减轻肺损伤。右美托咪定治疗也增加了Akt的表达。CB ₂受体拮抗剂AM630或PI3K抑制剂渥曼青霉素逆转了右美托咪定的保护作用。CB ₂受体拮抗剂AM630也下调了Akt的表达。因此，我们的研究结果表明，右美托咪定治疗可预防大鼠肠I / R引起的肺损伤，这可能是由于CB ₂上调引起的 受体，然后激活PI3K / Akt途径。