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Chronic obstructive pulmonary disease is characterized by chronic inflammation of the airway and lungs. Accumulating evidence has suggested that erythromycin (EM) plays a protective role against cigarette smoke-induced oxidative stress and the inflammatory response. However, the underlying mechanisms remain relatively unclear. The present study aimed to investigate the role of EM in inhibiting cigarette smoke-induced inflammation in human macrophages and its potential mechanism. A Cell Counting Kit-8 assay was used to determine the optimum concentration of EM and cigarette smoke extract (CSE) and it was found that 0.1 and 1% CSE and 0.1, 1.0 and 10 μg/ml EM exerted no significant effect on the cell proliferation activity, whereas 2 and 3% CSE exerted a significant inhibitory effect over the cell proliferation activity. We observed that 10 μmol/ml GW9662 (A PPARγ antagonist) and the presence of 1% CSE could promote the expression and activation of NF-κB p65. And this increased the expression of IL-6, IL-8 and reactive oxygen species (ROS). At the same time, 10 μmol/ml GW9662 and 1% CSE was found to inhibit the expression and activation of peroxisome proliferator activated receptors γ (PPARγ); However, 1 μg/ml EM was discovered to reverse these effects. Co-immunoprecipitation subsequently discovered an interaction between PPARγ and NF-κB p65. In conclusion, the present study suggested that EM may reduce the damage of PPARγ by inhibiting oxidative stress and reducing the expression of ROS and finally relieving cigarette smoke-induced inflammation through the PPARγ/NF-κB signaling pathway in macrophages., (Copyright © 2021. Published by Elsevier B.V.)

Prenatal exposure to inflammation produces offspring that are hypertensive in adulthood. The present study was to explore the role of intrarenal renin-angiotensin (Ang) system in the development of hypertension programmed by prenatal exposure to zymosan. Pregnant rats were randomly divided into control group and zymosan group (n = 6). Rats in these two groups were administered intraperitoneally with 0.5 ml vehicle and 2.37 mg/kg zymosan, respectively, on the eighth, tenth, and 12th day during gestation. The results showed the glomerular number and creatinine clearance rate decreased significantly in offspring of zymosan-treated rats. The renal cortex renin mRNA expression, Ang II-positive cells in renal cortex, and Ang II expression in renal medulla increased significantly in offspring of zymosan-treated rats at 7, 16, and 25 weeks of age. The plasma renin activity and Ang II concentration were unchanged. In conclusion, prenatal exposure to zymosan resulted in the activation of intrarenal renin-Ang system in adult offspring rats.