Baicalin attenuates inflammation in mice with OVA-induced asthma by inhibiting NF-κB and suppressing CCR7/CCL19/CCL21.
Baicalin, extracted and purified from the Chinese medicinal plant, Scutellaria baicalensis Georgi (Huang qin in Chinese), exhibits potent anti-inflammatory activity against asthma. However, it remains unknown whether baicalin inhibits the activity of CC chemokine receptor 7 (CCR7) and its ligands, which are crucial for the initiation of airway inflammation. In the present study, we investigated the effects of baicalin on CCR7 and its ligands, CCL19 and CCL21, as well as on the nuclear factor-κB (NF-κB) pathway in a mouse model of asthma. A mouse model of acute asthma was established by exposing the mice to ovalbumin (OVA) (by intraperitoneal injection and inhalational challenge). Within 24 h of the final OVA challenge, lung function was detected by direct airway resistance analysis. Lung tissues were examined for pathological changes. Inflammatory cell counts in bronchoalveolar lavage fluid (BALF) were assessed. ELISA was utilized to evaluate the OVA-IgE, CCL19 and CCL21 levels in BALF. The interleukin (IL)-6 and tumor necrosis factor (TNF)-α levels in serum were also detected by ELISA. The protein expression levels of CCR7, as well as that of phosphorylated IκBα (p-IκBα) and phosphorylated p65 (p-p65) were determined by western blot analysis and RT-qPCR was used to determine the CCR7 mRNA levels. Our data demonstrated that the oral administration of baicalin significantly improved pulmonary function and attenuated inflammatory cell infiltration into the lungs. Baicalin also decreased the levels of OVA-IgE, IL-6, TNF-α and CCR7, as well as those of its ligand, CCL19; the levels of NF-κB were also markedly suppressed by baicalin. The CCR7 mRNA level was substantially decreased. Our results thus suggest that baicalin exerts an inhibitory effect on airway inflammation, and this effect may be associated with the inhibition of CCR7 and CCL19/CCL21, which may provide new mechanistic insight into the anti‑inflammatory effects of baicalin.
Department of Integrative Medicine, Huashan Hospital, Fudan University, Shanghai 200040, P.R. China.
Jiaqi
J
Liu
Department of Integrative Medicine, Huashan Hospital, Fudan University, Shanghai 200040, P.R. China.
Ying
Y
Wei
Department of Integrative Medicine, Huashan Hospital, Fudan University, Shanghai 200040, P.R. China.
Qingli
Q
Luo
Department of Integrative Medicine, Huashan Hospital, Fudan University, Shanghai 200040, P.R. China.
Fei
F
Xu
Department of Integrative Medicine, Huashan Hospital, Fudan University, Shanghai 200040, P.R. China.
Zhengxiao
Z
Zhao
Department of Integrative Medicine, Huashan Hospital, Fudan University, Shanghai 200040, P.R. China.
Hongying
H
Zhang
Department of Integrative Medicine, Huashan Hospital, Fudan University, Shanghai 200040, P.R. China.
Linwei
L
Lu
Department of Integrative Medicine, Huashan Hospital, Fudan University, Shanghai 200040, P.R. China.
Jing
J
Sun
Department of Integrative Medicine, Huashan Hospital, Fudan University, Shanghai 200040, P.R. China.
Feng
F
Liu
Department of Integrative Medicine, Huashan Hospital, Fudan University, Shanghai 200040, P.R. China.
Xin
X
Du
Department of Integrative Medicine, Huashan Hospital, Fudan University, Shanghai 200040, P.R. China.
Mihui
M
Li
Department of Integrative Medicine, Huashan Hospital, Fudan University, Shanghai 200040, P.R. China.
Kai
K
Wei
Department of Integrative Medicine, Huashan Hospital, Fudan University, Shanghai 200040, P.R. China.
Jingcheng
J
Dong
D000818:Animals; D000894:Anti-Inflammatory Agents, Non-Steroidal / Q000737:chemistry / Q000494:pharmacology; D001249:Asthma / Q000139:chemically induced / Q000378:metabolism / Q000517:prevention & control*; D015153:Blotting, Western; D001992:Bronchoalveolar Lavage Fluid / Q000737:chemistry / Q000166:cytology; D054415:Chemokine CCL19 / Q000378:metabolism*; D054421:Chemokine CCL21 / Q000378:metabolism*; D004195:Disease Models, Animal; D005260:Female; D005419:Flavonoids / Q000737:chemistry / Q000494:pharmacology*; D006801:Humans; D007249:Inflammation / Q000235:genetics / Q000378:metabolism / Q000517:prevention & control*; D015850:Interleukin-6 / Q000097:blood / Q000378:metabolism; D008168:Lung / Q000187:drug effects / Q000378:metabolism / Q000473:pathology; D008807:Mice, Inbred BALB C; D015394:Molecular Structure; D016328:NF-kappa B / Q000378:metabolism*; D010047:Ovalbumin; D054400:Receptors, CCR7 / Q000235:genetics / Q000378:metabolism*; D020133:Reverse Transcriptase Polymerase Chain Reaction; D015398:Signal Transduction / Q000187:drug effects; D014409:Tumor Necrosis Factor-alpha / Q000097:blood / Q000378:metabolism
D000894:Anti-Inflammatory Agents, Non-Steroidal; C515461:Ccl19 protein, mouse; C515371:Ccr7 protein, mouse; D054415:Chemokine CCL19; D054421:Chemokine CCL21; D005419:Flavonoids; D015850:Interleukin-6; D016328:NF-kappa B; D054400:Receptors, CCR7; D014409:Tumor Necrosis Factor-alpha; C038044:baicalin; D010047:Ovalbumin