Inhibitory Effect of Baicalin on Collagen-Induced Arthritis in Rats through the Nuclear Factor–<i>κ</i>B Pathway

Wang, Hongzhi; Wang, Hai-He; Huang, Shishun; Cao, Yonggang; Wang, Guangzhi; Wang, Dong; Wang, Zhigang; Liu, Yanhong

doi:10.1124/jpet.114.215145

Cited by 43 publications

(38 citation statements)

References 35 publications

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“…These results suggest that baicalin may attenuate upper airway remodeling. These results are consistent with those of previous studies that reported that baicalin inhibited IL-1β secretion and has therapeutic effects on collagen-induced inflammation in human fibroblast-like synoviocytes and a rat model of collagen-induced arthritis [25]. …”

Section: Discussionsupporting

confidence: 93%

Baicalin Down-Regulates IL-1β-Stimulated Extracellular Matrix Production in Nasal Fibroblasts

et al. 2016

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PurposeBaicalin, a Chinese herbal medicine, has anti-fibrotic and anti-inflammatory effects. The aims of present study were to investigate the effects of baicalin on the myofibroblast differentiation, extracellular matrix production, migration, and collagen contraction of interleukin (IL)-1β-stimulated nasal fibroblasts and to determine the molecular mechanism of baicalin in nasal fibroblasts.MethodsNasal fibroblasts were isolated from the inferior turbinate of patients. Baicalin was used to treat IL-1β-stimulated nasal fibroblasts. To evaluate cytotoxicity, a 3-(4,5-dimethylthiazol-2yl)-2,5-diphenyl-tetrazolium bromide assay was used. The expression levels of α-smooth muscle actin (SMA), fibronectin, phospho-mitogen-activated protein kinase (p-MAPK), p-Akt, p-p50, p-p65, and p-IκBα were measured by western blotting, reverse transcription-polymerase chain reaction (RT—PCR),or immunofluorescence staining. Fibroblast migration was analyzed with scratch assays and transwell migration assays. Total collagen was evaluated with the Sircol collagen assay. Contractile activity was measured with a collagen gel contraction assay.ResultsBaicalin (0–50 μM) had no significant cytotoxic effects in nasal fibroblasts. The expression of α–SMA and fibronectin were significantly down-regulated in baicalin-treated nasal fibroblasts. Migration, collagen production, and contraction of IL-1β-stimulated nasal fibroblasts were significantly inhibited by baicalin treatment. Baicalin also significantly down-regulated p-MAPK, p-Akt, p-p50, p-p65, and p-IκBα in IL-1β-stimulated nasal fibroblasts.ConclusionsWe showed that baicalin down-regulated myofibroblast differentiation, extracellular matrix production, migration, and collagen contraction via the MAPK and Akt/ NF-κB pathways in IL-1β-stimulated nasal fibroblasts.

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Section: Discussionsupporting

confidence: 93%

Baicalin Down-Regulates IL-1β-Stimulated Extracellular Matrix Production in Nasal Fibroblasts

et al. 2016

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“…Dinda et al reported that baicalin inhibited reactive oxygen species (ROS) production in arteriosclerotic vascular disease by suppressing the activation of the NF-κB signaling pathway (17). Wang et al reported that baicalin exerts an inhibitory effect on inflammation-related collagen-induced arthritis via inhibition of the activation of the NF-κB signaling pathway (18). Given its ability to inhibit the activation of NF-κB signaling, it was hypothesized that baicalin may suppress breast cancer growth.…”

Section: Introductionmentioning

confidence: 99%

Baicalin inhibits breast cancer development via inhibiting IĸB kinase activation in vitro and in vivo

et al. 2018

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The aim of the present study was to investigate the effect and therapeutic potential of baicalin in breast cancer. Baicalin is used to treat inflammatory diseases. The effects of baicalin were assessed in breast cancer MCF-7 and MDA-MB-231 cells, and human breast cancer xenograft mice. Cells were treated with 0, 20 or 30 µM baicalin for 48 h, while xenograft mice were treated with intraperitoneal injection of 0, 100 or 200 mg/kg baicalin for 30 days. The results demonstrated that treatment with baicalin dose-dependently suppressed breast cancer cell invasion, migration and proliferation, and also induced G1/S-phase cell cycle arrest in vitro and in vivo. Baicalin alleviated inflammation injury and inhibited the secretion of tumor necrosis factor (TNF)-α and interleukin (IL)-1β, thus suppressing nuclear factor (NF)-ĸB-p65 activation via inhibition of IĸB kinase. Investigation of the mechanism underlying baicalin activity indicated that it inhibited protein expression of NF-ĸB-p65, leading to NF-ĸB-induced increased expression of CCND1, BCL2, BIRC2 and BIRC3, thus inhibiting cell proliferation, invasion and migration and suppressing anti-apoptotic factors in vitro and in vivo. In addition, baicalin did not affect non-tumorigenic normal breast epithelial cells. These results indicate that baicalin may exert therapeutic effects in breast cancer.

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“…Notably, previous studies have shown that baicalin has antidepressant‐like effects and decreases serum corticosterone levels in various depression models (Li et al, ; Yu et al, ; Zhang et al, ; Yu et al, ; Zhang et al, ). Although several recent studies have been conducted to investigate the antidepressant effect of baicalin, few studies have evaluated the mechanism of baicalin reverses inflammation on collagen‐induced arthritis in rats, which is related to the elevation of NF‐κB p65 protein deacetylation by SIRT1 (Wang et al, ). Thus, we hypothesized that baicalin reverses the depression‐like behavior and inflammation in depression via regulation of the SIRT1‐NF‐κB signaling pathway.…”

Section: Introductionmentioning

confidence: 99%

Baicalin reverse depressive‐like behaviors through regulation SIRT1‐NF‐kB signaling pathway in olfactory bulbectomized rats

Zhang

Guan

2019

Phytotherapy Research

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Depression is a common and detrimental illness that affects up to 120 million people worldwide. The present study was designed to evaluate the antidepressant‐like effects and mechanisms of baicalin on olfactory bulbectomized model of depression. Baicalin treatment (20 and 40 mg/kg) significantly reversed the abnormal levels of sucrose consumption, open field test, and forced swimming test. Treatments with baicalin reversed the olfactory bulbectomized‐induced alterations of serum corticosterone levels to a great extent. Our results further demonstrated that baicalin administration negatively regulated the expression of interleukin (IL)‐1β, IL‐6, and tumor necrosis factor (TNF‐α) in the hippocampus and hypothalamus. Furthermore, baicalin regulated Sirtuin 1 (SIRT1) and decreased the levels of p65 acetylation (ac‐p65) in the hippocampus and hypothalamus. Moreover, in lipopolysaccharides‐induced BV‐2 cells, the levels of inflammatory factors (IL‐1β), p65 acetylation at lysine 310, and SIRT1 expression were different in the group treated with both baicalin and nicotinamide compared with the group treated with baicalin, which suggests that baicalin regulates SIRT1 and thereby inhibits p65 acetylation. In summary, administration of baicalin reduces the levels of pro‐inflammatory cytokines, possibly through regulation of SIRT1‐NF‐kB pathway. Our findings suggest a support into the potential of baicalin in therapeutic effect for depression.

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Inhibitory Effect of Baicalin on Collagen-Induced Arthritis in Rats through the Nuclear Factor–κB Pathway

Cited by 43 publications

References 35 publications

Baicalin Down-Regulates IL-1β-Stimulated Extracellular Matrix Production in Nasal Fibroblasts

Baicalin Down-Regulates IL-1β-Stimulated Extracellular Matrix Production in Nasal Fibroblasts

Baicalin inhibits breast cancer development via inhibiting IĸB kinase activation in vitro and in vivo

Baicalin reverse depressive‐like behaviors through regulation SIRT1‐NF‐kB signaling pathway in olfactory bulbectomized rats

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