Mechanism of Xiao Qinglongtang Intervening Ferroptosis in Allergic Rhinitis Rats via Regulating SIRT1/SLC7A11 Signaling Pathway
10.13422/j.cnki.syfjx.20250836
- VernacularTitle:小青龙汤调节SIRT1/SLC7A11信号通路干预变应性鼻炎大鼠铁死亡的机制
- Author:
Yuanyuan JI
1
;
Hong ZHU
1
;
Jingjuan AN
1
;
Heng XIN
2
Author Information
1. The Second Affiliated Hospital of Nanjing University of Chinese Medicine，Nanjing 210017，China
2. Nanjing First Hospital，Nanjing 210006，China
- Publication Type:Journal Article
- Keywords:
Xiao Qinglongtang;
sirtuin 1 （SIRT1）/solute carrier family 7 member 11 （SLC7A11） signaling pathway;
allergic rhinitis;
ferroptosis;
lipid peroxidation
- From:
Chinese Journal of Experimental Traditional Medical Formulae
2026;32(1):113-119
- CountryChina
- Language:Chinese
-
Abstract:
ObjectiveTo observe the effect of Xiao Qinglongtang on ferroptosis in allergic rhinitis rats and explore its specific mechanism of action. MethodsSixty SD rats were randomly divided into a blank group， a model group， a loratadine group （0.9 mg·kg-1）， and low-， medium-， and high-dose Xiao Qinglongtang groups （2.14， 4.28， and 8.56 g·kg-1）， 10 rats per group. After 2 weeks of drug treatment， behavioral scores were observed in 6 groups of rats. Hematoxylin-eosin （HE） staining was used to observe changes in nasal mucosal tissue morphology， and Prussian blue staining was used to observe iron deposition. Enzyme-linked immunosorbent assay （ELISA） was used to detect reactive oxygen species （ROS）， Fe2+ ions， malondialdehyde （MDA）， superoxide dismutase （SOD）， and glutathione peroxidase （GSH） in each group. Immunofluorescence assay was used to detect ROS content and sirtuin 1 （SIRT1） expression in nasal mucosal tissue. Western blot was used to detect the expression of SIRT1， solute carrier family 7 member 11 （SLC7A11）， p53 acyl-CoA synthetase long-chain family member 4 （ACSL4）， and glutathione peroxidase 4 （GPX4） proteins in nasal mucosal tissue. ResultsCompared with the blank group， the model group exhibited obviously increased behavioral scores， severe nasal mucosal damage， obvious increase in iron deposition， significant decreases in GSH and SOD levels， obvious increases in MDA， Fe2+， and ROS fluorescence area proportions （P<0.05）， decreased protein expression levels of GPX4， SLC7A11， and SIRT1， and obvious increases in p53 and ACSL4 expression （P<0.05）. Compared with the model group， Xiao Qinglongtang groups of all doses showed reduced rat behavioral scores， obviously improved nasal mucosal damage， obviously reduced iron deposition （P<0.05）， obviously increased GSH and SOD levels， obviously reduced MDA， Fe2+， ROS fluorescence area proportions （P<0.05）， increased GPX4， SLC7A11， and SIRT1 protein expression levels， and obviously reduced p53 and ACSL4 （P<0.05）. ConclusionXiao Qinglongtang may achieve the goal of treating allergic rhinitis by regulating the SIRT1/SLC7A11 signaling pathway and inhibiting lipid peroxidation and ferroptosis.
