Patients with asthma experience circadian variations in their symptoms. However it remains unclear how specific aspects of this common airway disease relate to clock genes, which are critical to the generation of circadian rhythms in mammals. Here, we used a viral model of acute and chronic airway disease to examine how circadian clock disruption affects asthmatic lung phenotypes. Deletion of the core clock gene bmal1 or environmental disruption of circadian function by jet-lag exacerbated acute viral bronchiolitis caused by Sendai virus (SeV) and influenza A virus (IAV) in mice. Post-natal deletion of bmal1 was sufficient to trigger increased SeV susceptibility and correlated with impaired control of viral replication. Importantly, bmal1−/− mice developed much more extensive asthma-like airway changes post-infection, including mucus production and increased airway resistance. In human airway samples from two asthma cohorts, we observed altered expression patterns of multiple clock genes. Our results suggest a role for bmal1 in the development of asthmatic airway disease via the regulation of lung antiviral responses to common viral triggers of asthma.
Berberine can down-regulate the expression levels of UCP2 mRNA and UCP2 proteins of hepatic tissue in NAFLD rats. It can promote the recovery of hepatocyte steatosis and improve lipid metabolism disorder in NAFLD rats. Berberine shows a potential therapeutic effect on NAFLD.
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