The present study investigated whether erythromycin (ERY) reduces cigarette smoke (CS)-induced emphysema in rats and aimed to determine the anti-inflammatory effect of ERY, which may identify potential treatments for chronic obstructive pulmonary disease. Furthermore, the current study focused on the potential effects on the imbalance between matrix metalloprotease (MMP) and anti-MMP activity, the phosphorylation of mitogen-activated protein kinases (MAPKs) and the nuclear factor‑κB (NF‑κB) signaling pathway. Wistar rats were divided into the following three groups (n=12 each): control (ERY vehicle only, without any CS exposure), CS (animals were exposed to CS for 12 weeks) and CS + ERY (animals were exposed to CS for 12 weeks and received 100 mg/kg/day ERY). The recruitment of inflammatory cells into the bronchoalveolar lavage fluid (BALF) and the histopathology of lung tissue from all groups was evaluated to grade the severity of the emphysema. The expression of MMP‑2, MMP‑9 and tissue inhibitor of metalloproteinase‑1 was evaluated by immunohistochemistry and western blotting. The activation of MAPKs, NF‑κB and inhibitor of NF‑κB (IκBα), in lung tissues was examined by western blotting. Treatment with ERY resulted in fewer inflammatory cells and cytokines in the BALF, and fewer emphysema‑associated changes in the lungs compared with control. The stimulus of CS promoted the phosphorylation of extracellular signal‑regulated kinase (ERK)1/2 and p38, but not c‑Jun NH2‑terminal kinase, thereby inducing the activation of the ERK/MAPK signaling pathway in rats. Furthermore, CS exposure increased the expression of NF-κB and decreased the expression of IκBα. The levels of phosphorylated ERK1/2 and p38 were significantly reduced in rats with CS‑induced emphysema when treated with ERY compared with the CS group. The results of the present study therefore indicate that oral administration of ERY may suppress CS‑induced emphysema by regulating inflammatory cytokines and the MMP/anti-MMP imbalance via the MAPK/NF-κB pathway.

译文

:本研究调查了红霉素(ERY)是否能减少香烟烟​​雾(CS)诱导的大鼠肺气肿,并旨在确定ERY的抗炎作用,从而可能确定慢性阻塞性肺疾病的潜在治疗方法。此外,当前的研究集中在对基质金属蛋白酶(MMP)和抗MMP活性,促分裂原活化蛋白激酶(MAPKs)磷酸化和核因子-κB(NF-κB)信号通路之间不平衡的潜在影响。 Wistar大鼠分为以下三组(每组n = 12):对照组(仅ERY媒介物,没有任何CS暴露),CS(动物暴露于CS持续12周)和CS ERY(动物暴露于CS持续12周)周,并接受100 mg / kg /天的ERY)。评价炎症细胞进入支气管肺泡灌洗液(BALF)的募集和所有组肺组织的组织病理学,以对肺气肿的严重程度进行分级。通过免疫组织化学和蛋白质印迹法评估了MMP-2,MMP-9和金属蛋白酶-1组织抑制剂的表达。 Western blot检测肺组织中MAPKs,NF-κB和NF-κB抑制剂(IκBα)的活化。与对照相比,用ERY治疗可减少BALF中的炎症细胞和细胞因子,并减少与肺气肿相关的变化。 CS的刺激促进了细胞外信号调节激酶(ERK)1/2和p38的磷酸化,但不促进c-Jun NH2末端激酶的磷酸化,从而诱导了大鼠ERK / MAPK信号通路的激活。此外,CS暴露增加了NF-κB的表达而降低了IκBα的表达。与CS组相比,用ERY治疗时,CS诱发的肺气肿大鼠的磷酸化ERK1 / 2和p38含量显着降低。因此,本研究的结果表明,口服ERY可以通过调节炎症细胞因子和通过MAPK /NF-κB途径引起的MMP /抗MMP失衡来抑制CS诱发的气肿。

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