TY - JOUR
T1 - Magnoliae flos Downregulated Lipopolysaccharide-Induced Inflammatory Responses via NF- κ B/ERK-JNK MAPK/STAT3 Pathways
AU - Gil, Tae Young
AU - Jin, Bo Ram
AU - Cha, Yun Yeop
AU - An, Hyo Jin
N1 - Publisher Copyright:
© 2022 Tae-Young Gil et al.
PY - 2022
Y1 - 2022
N2 - Background. Magnoliae flos is the dried flower bud of Magnolia biondii and related plants. It has been used as a medicinal herb for the treatment of rhinitis, sinusitis, and sinus headaches. Nevertheless, the effects of Magnoliae flos in microbial infection or sepsis remain unclear. In this study, we investigated the anti-inflammatory effects of Magnoliae flos water extract (MF) in lipopolysaccharide- (LPS-) induced septic mice and LPS-stimulated RAW264.7 macrophages. Results. We found that MF reduced the mortality of LPS-challenged mice. Enzyme immunoassays and reverse transcription polymerase chain reaction analysis revealed that MF administration attenuated mRNA expression and protein production of proinflammatory mediators, including cyclooxygenase 2, inducible nitric oxide synthase, tumor necrosis factor-α, and interleukin-6. In parallel to these results in mice, pretreatment with MF suppressed the LPS-induced production of proinflammatory mediators in RAW264.7 macrophages. In addition, we found that MF exerted its suppressive effects by inhibiting the activation of the mitogen-activated protein kinase, nuclear factor-κB, and signal transducer and activator of transcription pathways at the protein level. Conclusion. MF could be a potential therapeutic agent for regulating excessive inflammatory responses in sepsis.
AB - Background. Magnoliae flos is the dried flower bud of Magnolia biondii and related plants. It has been used as a medicinal herb for the treatment of rhinitis, sinusitis, and sinus headaches. Nevertheless, the effects of Magnoliae flos in microbial infection or sepsis remain unclear. In this study, we investigated the anti-inflammatory effects of Magnoliae flos water extract (MF) in lipopolysaccharide- (LPS-) induced septic mice and LPS-stimulated RAW264.7 macrophages. Results. We found that MF reduced the mortality of LPS-challenged mice. Enzyme immunoassays and reverse transcription polymerase chain reaction analysis revealed that MF administration attenuated mRNA expression and protein production of proinflammatory mediators, including cyclooxygenase 2, inducible nitric oxide synthase, tumor necrosis factor-α, and interleukin-6. In parallel to these results in mice, pretreatment with MF suppressed the LPS-induced production of proinflammatory mediators in RAW264.7 macrophages. In addition, we found that MF exerted its suppressive effects by inhibiting the activation of the mitogen-activated protein kinase, nuclear factor-κB, and signal transducer and activator of transcription pathways at the protein level. Conclusion. MF could be a potential therapeutic agent for regulating excessive inflammatory responses in sepsis.
UR - http://www.scopus.com/inward/record.url?scp=85133569530&partnerID=8YFLogxK
U2 - 10.1155/2022/6281892
DO - 10.1155/2022/6281892
M3 - Article
C2 - 35795403
AN - SCOPUS:85133569530
SN - 0962-9351
VL - 2022
JO - Mediators of Inflammation
JF - Mediators of Inflammation
M1 - 6281892
ER -