INTRODUCTION Previous studies have suggested an association between tobacco smoke exposure and allergic rhinitis. This study aimed to investigate if prenatal or postpartum smoke exposure will increase the risk of allergic rhinitis in offspring. METHODS PubMed, EMBASE, and the Cochrane library were searched from inception to July 2020 for eligible studies investigating the association between smoking exposure and allergic rhinitis. The random-effects model was adopted for the meta-analysis to obtain the summary odds ratio (OR) with a 95% confidence interval (CI). Subgroup analysis based on the age of children was performed. Sensitivity analysis was carried out to check the robustness of the results. Publication bias of included studies was assessed. RESULTS This meta-analysis included nine studies, in which six studies suggested that children exposed to prenatal smoking were more likely to develop allergic rhinitis compared with children who were never exposed (OR=1.12; 95% CI: 1.04–1.21). The subgroup analysis divided children those aged <10 years (OR=1.15; 95% CI: 1.06–1.25) and those aged >10 years (OR=0.99; 95% CI: 0.82–1.20). This meta-analysis revealed a positive relationship between postpartum smoke exposure and the development of allergic rhinitis in offspring (OR=1.19; 95% CI: 1.03–1.39) with marked heterogeneity. The subgroup analysis of age in the postnatal group showed similar results in children aged >10 years (OR=1.17; 95% CI: 1.05–1.30) and children aged <10 years (OR=1.21; 95% CI: 0.91–1.60). CONCLUSIONS This meta-analysis observed an association between parental smoking exposure and allergic rhinitis in offspring. Our findings indicated that both prenatal and postnatal smoke exposure might be risk factors for allergic rhinitis in the offspring.

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JQ1, a BRD4 protein inhibitor, first identified because of its therapeutic role in cancer, has gradually demonstrated a protective effect on the heart in recent years; however, it is unclear whether JQ1 also plays a role in LPS-induced cardiac dysfunction. This paper aims to investigate the effects of the BRD4 inhibitor JQ1 on LPS-induced cardiac dysfunction and its mechanism. In the experiments, we found that BRD4 was significantly upregulated in the hearts of LPS-treated mice.JQ1 treatment improved survival and cardiac function in LPS-treated mice and reduced cardiomyopathologic injury, inflammation, and oxidative injury.JQ1 treatment similarly reduced the release of lactate dehydrogenase and inflammatory factors in H9C2 cells treated with LPS.JQ1 significantly upregulated silent information regulator 1 (SIRT1) expression and suppressed the upregulation of NOD-like receptor protein 3 (NLRP3), cleaved caspase-1, and GSDMD in heart tissues induced by LPS.Meanwhile, we obtained the same results in H9C2 cells treated with LPS. The administration of the SIRT1 inhibitor (EX527) intervention partially blocked the JQ1-mediated downregulation of NLRP3, cleaved caspase-1, GSDMD in LPS-induced H9C2 cells. Therefore, we propose that JQ1 can improve LPS-induced cardiac dysfunction by inhibiting SIRT1-dependent activation of NLRP3 inflammasomes, which may be a promising strategy for treating sepsis cardiomyopathy.