Baicalin is anti-inflammatory in cigarette smoke-induced inflammatory models in vivo and in vitro: A possible role for HDAC2 activity

Li, Lulu; Bao, Hong; Wu, Jinfeng; Duan, Xiaohong; Liu, Baojun; Sun, Jing; Gong, Wei; Lv, Yubao; Zhang, Hongying; Luo, Qingli; Wu, Xiao; Dong, Jingcheng

doi:10.1016/j.intimp.2012.03.001

Cited by 70 publications

(41 citation statements)

References 40 publications

Supporting

Mentioning

Contrasting

Unclassified

Order By: Relevance

“…The antitumor functions of these flavones are primarily due to their abilities to induce cell cycle arrest, regulate apoptosis-related proteins expression, eliminate adhesion and migration capacities and inhibit metastasis (22,23). Previous studies from our laboratory have shown that baicalin attenuated cigarette smoke-induced pulmonary chronic inflammation, declined inflammatory cells as well as tumor necrosis factor (TNF)-α, interleukin (IL)-6, IL-8 and MMP-9 production, decreased nuclear transcription factor-kappaB (NF-κB) p65 expression in the lung, and inhibited the activation of NF-κB (24,25). Pulmonary chronic inflammation and lung cancer are closely correlated.…”

Section: Flavonoid Components In Scutellaria Baicalensis Inhibit Nicomentioning

confidence: 99%

Flavonoid components in Scutellaria baicalensis inhibit nicotine-induced proliferation, metastasis and lung cancer-associated inflammation in vitro

Gong

Liu

et al. 2014

International Journal of Oncology

Self Cite

View full text Add to dashboard Cite

Abstract. The objective of the present study was to investigate the therapeutic efficacy of flavonoid components in Scutellaria baicalensis on proliferation, metastasis and lung cancer-associated inflammation during nicotine induction in the A549 and H1299 lung cancer cell lines. After experimental period, augmentation of proliferation was observed, accompanied by marked decrease in apoptotic cells in nicotine-induced lung cancer cells; additionally, nicotine-exposed cells exhibited increased invasive and migratory abilities based on invasion and wound-healing assay. Flavones in Scutellaria, baicalin, baicalein and wogonin significantly counteracted the above deleterious changes. Moreover, assessment of tumor apoptotic and metastatic factors on mRNA levels by quantitative PCR and protein levels by western blotting revealed that these phytochemical treatments effectively negated nicotine-induced upregulated expression of bcl-2, bcl-2/bax ratio, caspase-3, matrix metalloproteinase (MMP)-2 and MMP-9 as well as downregulated expression of bax. Further analysis of inflammatory markers such as tumor necrosis factor (TNF)-α and interleukin (IL)-6 in cell culture supernatant and mRNA and protein expression of nuclear transcription factor-kappaB (NF-κB) and I kappa B-alpha (IκB-α) was carried out to substantiate the anti-inflammatory effect of flavones in Scutellaria in nicotine-exposed lung cancer cells. The therapeutic effects observed in the present study are attributed to the potent potential against proliferation, metastasis and inflammatory microenvironment by flavonoid components in Scutellaria in nicotine-induced lung cancer cells.

show abstract

Section: Flavonoid Components In Scutellaria Baicalensis Inhibit Nicomentioning

confidence: 99%

Flavonoid components in Scutellaria baicalensis inhibit nicotine-induced proliferation, metastasis and lung cancer-associated inflammation in vitro

Gong

Liu

et al. 2014

International Journal of Oncology

Self Cite

View full text Add to dashboard Cite

show abstract

“…Baicalin, 7-glucuronic acid, 5,6-dihydroxy-flavone, is an extracted flavonoid compound from Scutellaria baicalensis Georgi and has potent anti-inflammatory activity [11][12][13]. Baicalin has been used for the treatment of ulcerative colitis [14], endotoxemia [15], periodontitis [16] and various inflammatory diseases [17,18]. Other studies have shown that baicalin promotes human periodontal ligament cell (HPLC) proliferation, reduces the ratio of receptor activator of nuclear factor-kappaB ligand (RANKL) to osteoprotegerin (OPG) expression [19], cyclooxygenase-2 (COX-2) and inducible nitric oxide synthase (iNOS) activity [16], interleukin-6 (IL-6) and IL-8 expression [20], and protects against tissue damage in animal models of periodontitis [16].…”

Section: Contents Lists Available At Sciencedirectmentioning

confidence: 99%

Baicalin inhibits toll-like receptor 2/4 expression and downstream signaling in rat experimental periodontitis

Sun

Dong

et al. 2016

International Immunopharmacology

View full text Add to dashboard Cite

“…Erythromycin, a macrolide, restored the effect of cigarette smokeinduced decline in HDAC1, HDAC2, and HDAC3 levels associated with inhibition of NF-B activation (68). Baicalin, a flavonoid compound isolated from the root of Scutellaria baicalenis Georgi, can influence cigarette smoke-induced inflammation and overcome steroid resistance via inhibiting HDAC2 phosphorylation in mouse lungs (67). Similarly, longacting ␤ 2 -agonists and corticosteroids restore the reduction of HDAC activity and inhibit H 2 O 2 -induced proinflammatory mediator release from human alveolar macrophages (99).…”

Section: Hdac2 In Inflammation and Steroid Resistancementioning

confidence: 99%

Role of histone deacetylase 2 in epigenetics and cellular senescence: implications in lung inflammaging and COPD

Yao

Rahman

2012

American Journal of Physiology-Lung Cellular and Molecular Phys

View full text Add to dashboard Cite

Histone deacetylase 2 (HDAC2) is a class I histone deacetylase that regulates various cellular processes, such as cell cycle, senescence, proliferation, differentiation, development, apoptosis, and glucocorticoid function in inhibiting inflammatory response. HDAC2 has been shown to protect against DNA damage response and cellular senescence/premature aging via an epigenetic mechanism in response to oxidative stress. These phenomena are observed in patients with chronic obstructive pulmonary disease (COPD). HDAC2 is posttranslationally modified by oxidative/carbonyl stress imposed by cigarette smoke and oxidants, leading to its reduction via an ubiquitination-proteasome dependent degradation in lungs of patients with COPD. In this perspective, we have discussed the role of HDAC2 posttranslational modifications and its role in regulation of inflammation, histone/DNA epigenetic modifications, DNA damage response, and cellular senescence, particularly in inflammaging, and during the development of COPD. We have also discussed the potential directions for future translational research avenues in modulating lung inflammaging and cellular senescence based on epigenetic chromatin modifications in diseases associated with increased oxidative stress.

show abstract

Baicalin is anti-inflammatory in cigarette smoke-induced inflammatory models in vivo and in vitro: A possible role for HDAC2 activity

Cited by 70 publications

References 40 publications

Flavonoid components in Scutellaria baicalensis inhibit nicotine-induced proliferation, metastasis and lung cancer-associated inflammation in vitro

Flavonoid components in Scutellaria baicalensis inhibit nicotine-induced proliferation, metastasis and lung cancer-associated inflammation in vitro

Baicalin inhibits toll-like receptor 2/4 expression and downstream signaling in rat experimental periodontitis

Role of histone deacetylase 2 in epigenetics and cellular senescence: implications in lung inflammaging and COPD

Contact Info

Product

Resources

About