Huangqin Decoction Attenuates DSS-Induced Mucosal Damage and Promotes Epithelial Repair via Inhibiting TNF-α-Induced NF-κB Activation
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Original Article|Updated:2022-02-22
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Huangqin Decoction Attenuates DSS-Induced Mucosal Damage and Promotes Epithelial Repair via Inhibiting TNF-α-Induced NF-κB Activation
Huangqin Decoction Attenuates DSS-Induced Mucosal Damage and Promotes Epithelial Repair via Inhibiting TNF-α-Induced NF-κB Activation
Chinese Journal of Integrative Medicine2022年28卷第2期 页码:124-129
Affiliations:
1.Gastroenterology Department, Affiliated Hospital of Integrated Traditional Chinese and Western Medicine, Nanjing University of Chinese Medicine, Nanjing (210028), China
2.Gastroenterology Department, Jiangsu Province Hospital on Integration of Chinese and Western Medicine, Nanjing (210028), China
3.Jiangsu Province Academy of Traditional Chinese Medicine,Nanjing (210028), China
Author bio:
Prof. TIAN Yao-zhou, E-mail:tianyaozhou1960@163.com
Funds:
the Scientific Research Project of Jiangsu Provincial Administration of Traditional Chinese Medicine(JD2019SZXYB05);Natural Science Foundation of Nanjing University of Chinese Medicine(XZR2020030);National Administration of Traditional Chinese Medicine: 2019 Project of Building Evidence-Based Practice Capacity for Traditional Chinese Medicine(2019XZZX-XH007)
To investigate the protective effect of Chinese herbal formula Huangqin Decoction (HQD) on ulcerative colitis mouse model induced by dextran sulphate sodium (DSS) and human intestinal epithelial cell injury induced by tumour necrosis factor-α (TNF-α).
Methods:
2
In vivo
30 male C57BL/6 mice were divided into 5 groups using a random number table (
n
=6 per group)
including control
DSS
5-aminosalicylic acid (5-ASA)
HQD low- (HQD-L) and high-dose (HQD-H) groups. The colitis mouse model was established by 3% (w/v) DSS water for 5 days. Meanwhile
mice in the HQD-L
HQD-H and 5-ASA groups were administrated with 100
200 mg/kg HQD or 100 mg/kg 5-ASA
respectively
once daily by gavage. After 9 days of administration
the body weight
disease activity index (DAI) score and colon length of mice were measured
the pathological changes of colons were analyzed by hematoxylin-eosin staining (HE) staining
and the levels of serum interleukin (IL)-6
IL-1β and TNF-α were measured by enzyme linked immunosorbent assay.
In vitro
the human colon epithelial normal cells (FHC cells) were exposed to HQD (0.6 mg/mL) for 12 h and then treated with TNF-α (10 ng/mL) for 24 h. The tight junction (TJ) protein expression levels of Claudin-4 and Occludin
and the protein phosphorylation levels of p65 and inhibitor of nuclear factor kappaB (NF-κB)-α (IκBα) were measured by Western blot.
Results:
2
In vivo
compared with the DSS group
HQD-H treatment attenuated the weight loss and reduced DAI score of mice on the 8th day (
P
<
0.05). Moreover
HQD-H treatment ameliorated the colon shortening in the DSS-induced colitis mice (
P
<
0.05). HE staining showed HQD attenuated the pathological changes of colitis mice
and the histological scores of HQD-H and 5-ASA groups were significantly decreased compared with the DSS group (
P
<
0.05). Meanwhile
HQD-H and 5-ASA significantly decreased the serum IL-1β
IL-6 and TNF-α levels of mice (
P
<
0.05).
In vitro
experiments showed that HQD up-regulated Occludin and Claudin-4 protein expressions and inhibited p-p65 and p-IκBα levels in FHC cells compared with the TNF-α group (
P
<
0.05).
Conclusion:
2
HQD significantly relieved the symptoms in DSS-induced colitis mice by inhibiting pro-inflammatory cytokines expression and maintained the homeostasis of TJ protein in FHC cells by suppressing TNF-α-induced NF-κB activation.
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