PMID- 37169571
OWN - NLM
STAT- MEDLINE
DCOM- 20230515
LR  - 20230515
IS  - 1578-1267 (Electronic)
IS  - 0301-0546 (Linking)
VI  - 51
IP  - 3
DP  - 2023
TI  - Neferine alleviates ovalbumin-induced asthma via MAPK signaling pathways in mice.
PG  - 135-142
LID - 10.15586/aei.v51i3.840 [doi]
AB  - PURPOSE: To investigate the role of neferine in ovalbumin (OVA)-induced asthma, 
      and to reveal the possible mechanism. METHODS: In OVA-induced asthmatic mice, 
      enzyme-linked-immunosorbent serologic assay was performed to evaluate the level 
      of interleukin (IL)-4, IL-5, IL-13, immunoglobulin E (IgE) in serum and tumor 
      necrosis factor-alpha (TNF-alpha), IL-6, IL-1beta, and monocyte chemoattractant protein-1 
      (MCP-1) in bronchoalveolar lavage fluid (BALF). Eosinophil, neutrophil, and 
      lymphocyte counts in BALF were calculated to assess inflammation. The pulmonary 
      function was measured by airway resistance, peak expiratory flow (PEF) and forced 
      expiratory volume/forced vital capacity (FEV(0.4)/FVC) ratio, and respiratory 
      rate. Hematoxylin and eosin staining and Masson staining were used to evaluate 
      lung injury. Further, Western blot analysis was conducted to detect 
      phosphorylation of extracellular signal-regulated kinase (ERK), c-Jun N-terminal 
      kinase (JNK), and p38 of mitogen-activated protein kinase (MAPK) signaling 
      pathways. RESULTS: Neferine, 20 mg/kg or 40 mg/kg, could significantly decrease 
      the levels of IL-4, IL-5, IL-13, and IgE in OVA-induced serum, and that of TNF-alpha, 
      IL-6, IL-1beta, and MCP-1 in OVA-induced BALF. Moreover, neferine could 
      significantly decline eosinophil, neutrophil, and lymphocyte counts in BALF. 
      Neferine contributed to improve OVA-induced airway resistance, promoted the value 
      of PEF and FEV(0.4)/FVC ratio, and recovered the respiratory rate. It also 
      reduced mucus secretion, distribution of inflammatory and goblet cells around 
      bronchi, and attenuated collagen deposition in lung tissues. Furthermore, 
      neferine reduced the phosphorylation of p38, JNK, and ERK to inhibit MAPK 
      signaling pathways. CONCLUSION: Neferine relieves asthma-induced inflammatory 
      reaction, airway resistance, and lung injury by inhibiting MAPK signaling 
      pathways. This could serve neferine as a novel therapeutic candidate for treating 
      asthma.
FAU - Zhu, Tonggang
AU  - Zhu T
AD  - Department of Respiratory, Affiliated Hospital of Changchun University of 
      Traditional Chinese Medicine, Changchun, Jilin, China.
FAU - Xiao, Xue
AU  - Xiao X
AD  - Department of Cardiology, Affiliated Hospital of Changchun University of 
      Traditional Chinese Medicine, Changchun, Jilin, China.
FAU - Dong, Yufu
AU  - Dong Y
AD  - Department of Respiratory, Affiliated Hospital of Changchun University of 
      Traditional Chinese Medicine, Changchun, Jilin, China.
FAU - Yuan, Chengbo
AU  - Yuan C
AD  - Department of Respiratory, Affiliated Hospital of Changchun University of 
      Traditional Chinese Medicine, Changchun, Jilin, China; ycb8017_dr@163.com.
LA  - eng
PT  - Journal Article
DEP - 20230501
PL  - Singapore
TA  - Allergol Immunopathol (Madr)
JT  - Allergologia et immunopathologia
JID - 0370073
RN  - 9006-59-1 (Ovalbumin)
RN  - 2292-16-2 (neferine)
RN  - 0 (Tumor Necrosis Factor-alpha)
RN  - 0 (Interleukin-13)
RN  - 0 (Interleukin-5)
RN  - 0 (Interleukin-6)
RN  - 37341-29-0 (Immunoglobulin E)
SB  - IM
MH  - Mice
MH  - Animals
MH  - Ovalbumin
MH  - Tumor Necrosis Factor-alpha/metabolism
MH  - Interleukin-13/metabolism
MH  - *Lung Injury
MH  - Interleukin-5/metabolism
MH  - Interleukin-6/metabolism
MH  - *Asthma
MH  - Lung
MH  - MAP Kinase Signaling System
MH  - Inflammation
MH  - Bronchoalveolar Lavage Fluid
MH  - Immunoglobulin E/metabolism
MH  - Mice, Inbred BALB C
MH  - Disease Models, Animal
OTO - NOTNLM
OT  - MAPK pathways
OT  - airway resistance
OT  - asthma
OT  - lung injury
OT  - neferine
COIS- The authors stated that there were no conflicts of interest to disclose.
EDAT- 2023/05/12 01:07
MHDA- 2023/05/15 06:42
CRDT- 2023/05/11 21:23
PHST- 2023/02/09 00:00 [received]
PHST- 2023/03/01 00:00 [accepted]
PHST- 2023/05/15 06:42 [medline]
PHST- 2023/05/12 01:07 [pubmed]
PHST- 2023/05/11 21:23 [entrez]
AID - 10.15586/aei.v51i3.840 [doi]
PST - epublish
SO  - Allergol Immunopathol (Madr). 2023 May 1;51(3):135-142. doi: 
      10.15586/aei.v51i3.840. eCollection 2023.