Objective. To determine the effect and mechanism of the anti-inflammatory agent ghrelin on pulmonary vascular dysfunction (PVD) in lipopolysaccharide- (LPS-) induced acute lung injury (ALI) rat models. Methods. Thirty-two adult male Sprague Dawley rats (n = 16/group) were randomly divided into ghrelin and saline groups, wherein ghrelin (10 nmol/kg) or saline was subcutaneously administered. After 30 min, eight rats from each group were randomly selected, and LPS (5 mg/kg) or saline was administered by intratracheal instillation to induce ALI. Four hours after establishing the ALI rat model, the mean pulmonary arterial pressure (mPAP), mean right ventricular systolic pressure (RVSP), levels of proinflammatory cytokines tumor necrosis factor-α (TNF-α) and interleukin-6 (IL-6) in the bronchoalveolar lavage fluid (BALF), BALF cell count, wet-to-dry (W/D) lung weight ratios, and myeloperoxidase (MPO) activity in lung tissue for all four groups (ghrelin, ghrelin + ALI, saline, and saline + ALI) were measured. Immunohistochemical staining to detect alpha-smooth muscle actin (α-SMA) and proliferating cell nuclear antigen (PCNA) expression was performed to assess the intrapulmonary arterial wall thickness and the proliferation of smooth muscle cells, respectively. Results. The ghrelin-pretreated ALI rats showed lower mPAP, RVSP, PCNA expression, MPO activity, W/D lung weight ratio, TNF-α and IL-6 levels, and BALF cell count than the saline-pretreated ALI rats, but ghrelin had no effect on the intrapulmonary arterial wall thickness of ALI rats. Conclusion. Our results confirmed the association between inflammation and PVD in ALI and suggested that the suppression of inflammation by ghrelin pretreatment could protect LPS-induced ALI rats against PVD.

中文翻译：

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Ghrelin通过抑制炎症作用保护脂多糖诱导的急性肺损伤大鼠免受肺血管功能障碍的影响。

目标。要确定抗炎剂生长素释放肽对脂多糖-（LPS-）诱导的急性肺损伤（ALI）大鼠模型中肺血管功能障碍（PVD）的作用和机制。方法。将32只成年雄性Sprague Dawley大鼠（n  = 16 /组）随机分为生长激素释放肽和生理盐水组，其中皮下注射生长激素释放肽（10 nmol / kg）或生理盐水。30分钟后，从每组中随机选择8只大鼠，并通过气管内滴注LPS（5mg / kg）或盐水以诱导ALI。建立ALI大鼠模型后四小时，平均肺动脉压（mPAP），平均右心室收缩压（RVSP），促炎细胞因子肿瘤坏死因子-α水平（TNF- α）和白细胞介素-6（IL-6）在支气管肺泡灌洗液（BALF），BALF细胞计数，湿-干（W / d）肺的重量比，和髓过氧化物酶（MPO）活性的肺组织在对所有四个组（生长素释放肽，生长素释放肽+ ALI，生理盐水和生理盐水+ ALI）进行了测量。进行免疫组织化学染色以检测α-平滑肌肌动蛋白（α- SMA）和增殖细胞核抗原（PCNA）的表达，以分别评估肺内动脉壁厚度和平滑肌细胞的增殖。结果。ghrelin预处理的ALI大鼠显示出较低的mPAP，RVSP，PCNA表达，MPO活性，W / D肺重量比，TNF- αIL-6水平和BALF细胞计数均高于生理盐水预处理的ALI大鼠，但生长素释放肽对ALI大鼠的肺内动脉壁厚度无影响。结论。我们的结果证实了ALI中炎症与PVD之间的相关性，并表明ghrelin预处理抑制炎症可以保护LPS诱导的ALI大鼠免受PVD的侵害。