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Kim, Seong-Ryeol,Song, Jae-Hyoung,Ahn, Jae-Hee,Lee, Geun-Shik,Ahn, Huijeong,Yoon, Sung-il,Kang, Seung Goo,Kim, Pyeung-Hyeun,Jeon, Sang-Min,Choi, Eun-Ji,Shin, Sooyoung,Cha, Younggil,Cho, Sungchan,Kim, Elsevier 2018 Antiviral research Vol.151 No.-
<P>Human rhinovirus (HRV) infection causes more than 80% of all common colds and is associated with severe complications in patients with asthma and chronic obstructive pulmonary disease. To identify antiviral drug against HRV infection, we screened 800 FDA-approved drugs and found budesonide as one of the possible drug candidates. Budesonide is a corticosteroid, which is commonly used to prevent exacerbation of asthma and symptoms of common cold. Budesonide specifically protects host cells from cytotoxicity following HRV infection, which depend on the expression of glucocorticoid receptor. Intranasal administration of budesonide lowered the pulmonary HRV load and the levels of IL-1 beta cytokine leading to decreased lung inflammation. Budesonide regulates IL-1 beta production following HRV infection independent of inflammasome activation. Instead, budesonide induces mitochondrial reactive oxygen species followed by activation of autophagy. Further, the inhibition of autophagy following chloroquine or bafilomycin Al treatment reduced the anti-viral effect of budesonide against HRV, suggesting that the antiviral activity of budesonide was mediated via autophagy. The results suggest that budesonide represents a promising antiviral and anti-inflammatory drug candidate for the treatment of human rhinovirus infection.</P>
Obovatol inhibits NLRP3, AIM2, and non-canonical inflammasome activation
Kim, Jeongeun,Ahn, Huijeong,Han, Byung-Cheol,Shin, Hyunjung,Kim, Jin-Chul,Jung, Eui-Man,Kim, Juyeol,Yang, Heejung,Lee, Jeonghyun,Kang, Seung Goo,Lee, Seung-Ho,Lee, Geun-Shik Elsevier 2019 Phytomedicine Vol.63 No.-
<P><B>Abstract</B></P> <P><B>Background</B></P> <P>Obovatol, a biphenolic chemical originating from <I>Magnolia obovata</I>, has been utilized as a traditional medicine for the treatment of inflammatory diseases. Inflammasome induces maturation of inflammatory cytokines in response to intracellular danger signals, and its dysregulation induces inflammatory diseases.</P> <P><B>Purpose</B></P> <P>The effect of obovatol on inflammasome activation has not been reported, although its anti-inflammatory properties have been studied.</P> <P><B>Study design/methods</B></P> <P>Obovatol was treated to macrophages with inflammasome triggers, and secretions of interleukin (IL)-1β, IL-18, and caspase-1 were measured as readouts of inflammasome activation. In addition, Asc pyroptosome formation, caspase-1 activity, and mitochondrial reactive oxygen species (ROS) production were analyzed in mechanical studies. Anti-inflammasome properties of obovatol were confirmed in an animal model.</P> <P><B>Results</B></P> <P>Obovatol inhibited NLRP3, AIM2, and non-canonical inflammasomes through inhibition of Asc pyroptosome formation and mitochondrial ROS generation. In addition, obovatol disrupted the priming step of inflammasome activation and inhibited transcription of inflammatory cytokines. In mice, obovatol attenuated serum IL-1β elevation in response to monosodium urate crystals.</P> <P><B>Conclusion</B></P> <P>Obovatol is suggested as an inhibitor of NLRP3, AIM2, and non-canonical inflammasomes.</P> <P><B>Graphical abstract</B></P> <P>[DISPLAY OMISSION]</P>
Huijeong Ahn,Byung-Cheol Han,Jeongeun Kim,Seung Goo Kang,Pyeung-Hyeun Kim,Kyoung Hwa Jang,Seung Ho So,Seung-Ho Lee,Geun-Shik Lee 고려인삼학회 2019 Journal of Ginseng Research Vol.43 No.2
Background: Ginsenosides of Korean Red Ginseng extracts (RGE) and its saponin components suppress secretion of inflammasome-mediating cytokines, whereas the nonsaponin fraction (NS) of RGE oppositely stimulates cytokine secretion. Although direct exposure of NS to macrophages in mice induces cytokine production, oral administration of NS has not been studied in inflammasome-related disease in animal models. Methods: Mice were fed RGE or NS for 7 days and then developed peritonitis. Peritoneal cytokines were measured, and peritoneal exudate cells (PECs) were collected to assay expression levels of a set of tolllike receptors (TLRs) and cytokines in response to NS ingestion. In addition, the role of intestinal bacteria in NS-fed mice was assessed. The effect of preexposure to NS in bone marrowederived macrophages (BMDMs) on cytokine production was further confirmed. Results: NS ingestion attenuated secretion of peritoneal cytokines resulting from peritonitis. In addition, the isolated PECs from NS-fed mice presented lower TLR transcription levels than PECs from control diet efed mice. BMDMs treated with NS showed downregulation of TLR4 mRNA and protein expression, which was mediated by the TLR4-MyD88-NFkB signal pathway. BMDMs pretreated with NS produced less cytokines in response to TLR4 ligands. Conclusion: NS administration directly inhibits TLR4 expression in inflammatory cells such as macrophages, thereby reducing secretion of cytokines during peritonitis.