Wedelolactone protects human bronchial epithelial cell injury against cigarette smoke extract-induced oxidant stress and inflammation responses through Nrf2 pathway

Ding, Shumin; Hou, Xuefeng; Yuan, Jiarui; Tan, Xuecai; Chen, Juan; Yang, Nan; Luo, Yi; Jiang, Ziyu; Jin, Ping; Dong, Zibo; Feng, Liang; Jia, Xiao‐Bin

doi:10.1016/j.intimp.2015.09.015

Cited by 37 publications

(55 citation statements)

References 35 publications

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“…To determine the role of Nrf2 in zedoarondiol-mediated protective effect on ox-LDL-induced HUVECs injury, cells were divided into the five groups: (1) control group; (2) Zed group; (3) ox-LDL group; (4) oxLDL+Zed group: HUVECs were pretreated with zedoarondiol (20 μg/mL) for 2 h and then treated with ox-LDL (150 μg/mL) for 24 h; (5) ox-LDL+Zed+ATRA group: HUVECs were pretreated with zedoarondiol (20 μg/mL) and ATRA (5 µmol/L) [18] for 2 h and then treated with ox-LDL (150 μg/mL) for 24 h. The treatment of the first three groups was same to the above.…”

Section: Cell Culture and Treatmentmentioning

confidence: 99%

Zedoarondiol Attenuates Endothelial Cells Injury Induced by Oxidized Low-Density Lipoprotein via Nrf2 Activation

Mao

Tao

Wang

et al. 2018

Cell Physiol Biochem

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Background/Aims: Zedoarondiol, a sesquiterpene lactone compound, showed an anti-proliferative activity on vascular smooth muscle cells in our previous study. However, whether it has a beneficial effect on endothelial cells injury induced by oxidized low-density lipoprotein (ox-LDL) remains unclear. This study was designed to investigate the protective effect of zedoarondiol on ox-LDL-induced injury of endothelial cells and explored its underlying mechanism. Methods: The protective effect of zedoarondiol on ox-LDL-induced human umbilical vein endothelial cells (HUVECs) injury were evaluated by Cell Counting Kit-8 (CCK-8) assay and released lactic dehydrogenase (LDH) activity assay. Oxidative stress was determined by malonedialdehyde (MDA) content and superoxide dismutase (SOD) activity. The level of reactive oxygen species (ROS) was measured by dichlorodihydrofluorescin diacetate (DCFH-DA) staining. The culture supernatant was collected for enzyme linked immune-sorbent assays (ELISA) of interleukine-1β (IL-1β), tumor necrosis factor-α (TNF-α), and monocyte chemoattractant protein-1 (MCP-1). Immunofluorescence staining was used to observe NF-E2-related factor 2 (Nrf2) translocation. Western blotting was performed to determine the expression of IL-1β, TNF-α, MCP-1, Kelch-like ECH associated protein 1 (Keap1), heme oxygenase-1 (HO-1), NAD(P)H: quinone oxidoreductase-1 (NQO1), and Nrf2. Results: Zedoarondiol attenuated HUVECs injury, up-regulated SOD activity, suppressed formation of MDA and ROS, and secretion and protein expression of IL-1β, TNF-α, and MCP-1 in injured HUVECs induced by ox-LDL. Zedoarondiol induced nuclear Nrf2 translocation from cytoplasm into nucleus and up-regulated expression of HO-1, NQO1, and Nrf2 in nucleus. All-trans-retinoic acid (ATRA), an inhibitor of Nrf2, abolished zedoarondiol-mediated anti-oxidative effect. Conclusion: Zedoarondiol attenuates ox-LDL-induced endothelial cells injury by inhibiting oxidative stress and inflammation via Nrf2/HO-1 pathway, suggesting that zedoarondiol might be meaningful on prevention and treatment of atherosclerosis.

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Section: Cell Culture and Treatmentmentioning

confidence: 99%

Zedoarondiol Attenuates Endothelial Cells Injury Induced by Oxidized Low-Density Lipoprotein via Nrf2 Activation

Mao

Tao

Wang

et al. 2018

Cell Physiol Biochem

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“…Wedelolactone (7-Methoxy-5, 11, 12-trihydroxycoumestan, mol wt. 314.2), the principle active polyphenolic compound found in extracts of Wedelia calandulaceae and Eclipta prostrata (9) is known for treatment of liver diseases, viral infections, human bronchial epithelial cell injury, and snake bites (10). Wedelolactone also regulates osteoclastogenesis in breast cancer (11)(12)(13), inhibits androgen-independent prostate cancer (14), and endometrial and ovarian cancer cell growth (15).…”

Section: Introductionmentioning

confidence: 99%

Enhancing Chemosensitivity of Breast Cancer Stem Cells by Downregulating SOX2 and ABCG2 Using Wedelolactone-encapsulated Nanoparticles

Das

Mukherjee

Chatterjee

et al. 2019

Molecular Cancer Therapeutics

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A major caveat in the treatment of breast cancer is disease recurrence after therapeutic regime at both local and distal sites. Tumor relapse is attributed to the persistence of chemoresistant cancer stem cells (CSC), which need to be obliterated along with conventional chemotherapy. Wedelolactone, a naturally occurring coumestan, demonstrates anticancer effects in different cancer cells, although with several limitations, and is mostly ineffective against CSCs. To enhance its biological activity in cancer cells and additionally target the CSCs, wedelolactone-encapsulated PLGA nanoparticles (nWdl) were formulated. Initial results indicated that nanoformulation of wedelolactone not only increased its uptake in breast cancer cells and the CSC population, it enhanced drug retention and sustained release within the cells. Enhanced drug retention was achieved by downregula-tion of SOX2 and ABCG2, both of which contribute to drug resistance of the CSCs. In addition, nWdl prevented epithelialto-mesenchymal transition, suppressed cell migration and invasion, and reduced the percentage of breast cancer stem cells (BCSC) in MDA-MB-231 cells. When administered in combination with paclitaxel, which is known to be ineffective against BCSCs, nWdl sensitized the cells to the effects of paclitaxel and reduced the percentage of ALDH þ BCSCs and mammospheres. Furthermore, nWdl suppressed growth of solid tumors in mice and also reduced CD44 þ /CD24 À/low population. Taken together, our data imply that nWdl decreased metastatic potential of BCSCs, enhanced chemosensitivity through coordinated regulation of pluripotent and efflux genes, and thereby provides an insight into effective drug delivery specifically for obliterating BCSCs.

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“…The evidence showed that CS‐induced regulatory elements implicated in carcinogenesis was associated with the pathogenesis of lung cancer . In our previous study, Eclipta prostrata L., (Asteraceae) has a potential protection human bronchial epithelial cell injury against CSE‐induced oxidant stress and inflammation responses . This function has been shown to be an activation of Nrf2 pathway.…”

Section: Discussionmentioning

confidence: 96%

“…In our previous study, we found that the components of Eclipta prostrata L. (CCE) has a protective effect against CSE‐induced stress of normal human bronchial epithelial (NHBE) cells . The major compound Wedelolactone of CCE can increase the cell viability of CSE‐induced NHBE cells through Nrf2 pathway . However, the underlying molecular basis for this action remains incompletely understood.…”

Section: Introductionmentioning

confidence: 99%

Regulation of Eclipta prostrata L. components on cigarette smoking‐induced autophagy of bronchial epithelial cells via keap1‐Nrf2 pathway

Ding

Hou

Wang

et al. 2018

Environmental Toxicology

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Cigarette smoking extract (CSE)-induced autophagic injury has been regarded as an important contributor to the pathogenesis of lung cancer. We previously found that Eclipta prostrata L. component (CCE) reduced CSE-induced bronchial epithelial cells damage. However, the mechanism remains unknown. Human normal bronchial epithelial cells (NHBE) were exposed to CSE to establish stress model. Nrf2-siRNA and Keap1-siRNA transfection were performed. mRFP-GFP-LC3 dual fluorescence and transmission electron microscopy were used to observe the autophagic characteristics. CCE prevented CSE-induced Nrf2 transfer into cytoplasm and up-regulated Keap1 level of NHBE cells. Furthermore, CCE significantly increased p-p16, p-p21 and p-p53 phosphorylation levels in Nrf2-siRNA- or Keap1-siRNA-transfected cells. As demonstrated by transmission electron microscopy and mRFP-GFP-LC3 dual fluorescence assays, CCE mitigated autophagic injury, and also down-regulated autophagy-related Beclin-1, LC3II/LC3I ratio, Atg5 and ATF4 levels. Our findings showed the attenuation of CCE on CSE-induced NHBE cells injury was associated with Nrf-2-mediated oxidative signaling pathway.

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Wedelolactone protects human bronchial epithelial cell injury against cigarette smoke extract-induced oxidant stress and inflammation responses through Nrf2 pathway

Cited by 37 publications

References 35 publications

Zedoarondiol Attenuates Endothelial Cells Injury Induced by Oxidized Low-Density Lipoprotein via Nrf2 Activation

Zedoarondiol Attenuates Endothelial Cells Injury Induced by Oxidized Low-Density Lipoprotein via Nrf2 Activation

Enhancing Chemosensitivity of Breast Cancer Stem Cells by Downregulating SOX2 and ABCG2 Using Wedelolactone-encapsulated Nanoparticles

Regulation of Eclipta prostrata L. components on cigarette smoking‐induced autophagy of bronchial epithelial cells via keap1‐Nrf2 pathway

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