PMID- 37486694
OWN - NLM
STAT- MEDLINE
DCOM- 20240229
LR  - 20240229
IS  - 1899-5276 (Print)
IS  - 1899-5276 (Linking)
VI  - 33
IP  - 2
DP  - 2024 Feb
TI  - Oridonin attenuates apoptosis and NLRP3 inflammasome activation in 
      IL-4-stimulated human bronchial epithelial cells in an in vitro pediatric asthma 
      model.
PG  - 163-170
LID - 10.17219/acem/166253 [doi]
AB  - BACKGROUND: Asthma is a chronic illness that causes recurrent inflammation and 
      airway constriction. The primary risk factors for asthma development are exposure 
      to environmental allergens and house dust mites, which can trigger 
      deoxyribonucleic acid (DNA) damage. Oxidative stress can also cause DNA 
      impairments and plays a crucial role in the progression of human immunological 
      disorders. OBJECTIVES: The aim of the study was to evaluate the effects of 
      oridonin (ORD) on proliferation, inflammation and apoptosis in interleukin 4 
      (IL-4)-stimulated human bronchial epithelial (16HBE) cells. MATERIAL AND METHODS: 
      Proliferation was assessed using a 5-Bromo-2-deoxyuridine (BrdU) assay, while 
      acridine orange (AO), ethidium bromide (EB), propidium iodide, and 
      4',6-diamidino-2-phenylindole (DAPI) measured apoptosis. The protein expression 
      levels of apoptosis-associated speck-like protein containing a C-terminal caspase 
      recruitment domain (ASC), cleaved caspase-1, and nucleotide-binding domain and 
      leucine-rich repeat protein 3 (NLRP3) were detected with western blot. RESULTS: 
      The results established that IL-4 stimulation markedly decreased (p < 0.05) the 
      proliferation of 16HBE cells, while the administration of ORD increased their 
      proliferation. Apoptosis and DNA damage were enhanced in the IL-4-stimulated 
      group, whereas ORD exhibited anti-apoptotic activity. Moreover, the treatment 
      with ORD significantly reduced (p < 0.05) the IL-4-induced expression of cleaved 
      caspase-1, ASC and NLRP3 proteins. CONCLUSIONS: The findings suggest that NLRP3 
      is a direct target for ORD-mediated anti-inflammatory actions in injured 16HBE 
      cells. Therefore, ORD may be a novel therapy against NLRP3-related disorders, 
      including pediatric asthma (PA).
FAU - Wang, Weiwei
AU  - Wang W
AD  - Department of Pediatrics, Tianjin Hospital, China.
FAU - Ming, Dan
AU  - Ming D
AD  - Department of Pediatrics, Tianjin Hospital, China.
LA  - eng
PT  - Journal Article
PL  - Poland
TA  - Adv Clin Exp Med
JT  - Advances in clinical and experimental medicine : official organ Wroclaw Medical 
      University
JID - 101138582
RN  - 0 (NLR Family, Pyrin Domain-Containing 3 Protein)
RN  - 0 (Inflammasomes)
RN  - 0APJ98UCLQ (oridonin)
RN  - 207137-56-2 (Interleukin-4)
RN  - EC 3.4.22.36 (Caspase 1)
RN  - 9007-49-2 (DNA)
RN  - 0 (Interleukin-1beta)
RN  - 0 (Diterpenes, Kaurane)
SB  - IM
MH  - Child
MH  - Humans
MH  - *NLR Family, Pyrin Domain-Containing 3 Protein/metabolism
MH  - Inflammasomes/metabolism
MH  - Interleukin-4/pharmacology
MH  - Apoptosis
MH  - Inflammation/metabolism
MH  - Caspase 1/metabolism
MH  - Epithelial Cells/metabolism
MH  - *Asthma/drug therapy
MH  - DNA
MH  - Interleukin-1beta
MH  - *Diterpenes, Kaurane
OTO - NOTNLM
OT  - NLRP3 inflammasome
OT  - apoptosis
OT  - inflammation
OT  - oridonin
OT  - pediatric asthma
EDAT- 2023/07/24 13:07
MHDA- 2024/02/29 06:42
CRDT- 2023/07/24 11:35
PHST- 2022/08/30 00:00 [received]
PHST- 2023/05/16 00:00 [accepted]
PHST- 2024/02/29 06:42 [medline]
PHST- 2023/07/24 13:07 [pubmed]
PHST- 2023/07/24 11:35 [entrez]
AID - 10.17219/acem/166253 [doi]
PST - ppublish
SO  - Adv Clin Exp Med. 2024 Feb;33(2):163-170. doi: 10.17219/acem/166253.