Mangiferin inhibits mastitis induced by LPS via suppressing NF-ĸB and NLRP3 signaling pathways

Qu, Shihui; Wang, Wenqing; Li, Depeng; Li, Shumin; Zhang, Like; Fu, Yunhe; Zhang, Naisheng

doi:10.1016/j.intimp.2016.11.036

Cited by 38 publications

(29 citation statements)

References 30 publications

Supporting

Mentioning

Contrasting

Order By: Relevance

“…More and more studies focus on natural products and mastitis. Previous studies have shown that mangiferin can inhibit mastitis induced by LPS via suppressing NF-κB and NLRP3 signaling pathways, and resveratrol inhibits LPS-induced mice mastitis through attenuating the Mitogen-activated protein kinase (MAPK) and NF-κB signaling pathway [ 6 , 7 ]. Peiminine is a natural product of alkaloids, which comes from Fritillaria [ 8 ].…”

Section: Introductionmentioning

confidence: 99%

Peiminine Protects against Lipopolysaccharide-Induced Mastitis by Inhibiting the AKT/NF-κB, ERK1/2 and p38 Signaling Pathways

Gong

et al. 2018

IJMS

View full text Add to dashboard Cite

Peiminine, an alkaloid extracted from Fritillaria plants, has been reported to have potent anti-inflammatory properties. However, the anti-inflammatory effect of peiminine on a mouse lipopolysaccharide (LPS)-induced mastitis model remains to be elucidated. The purpose of this experiment was to investigate the effect of peiminine on LPS-induced mastitis in mice. LPS was injected through the canals of the mammary gland to generate the mouse LPS-induced mastitis model. Peiminine was administered intraperitoneally 1 h before and 12 h after the LPS injection. In vitro, mouse mammary epithelial cells (mMECs) were pretreated with different concentrations of peiminine for 1 h and were then stimulated with LPS. The mechanism of peiminine on mastitis was studied by hematoxylin-eosin staining (H&E) staining, western blotting, and enzyme-linked immunosorbent assay (ELISA). The results showed that peiminine significantly decreased the histopathological impairment of the mammary gland in vivo and reduced the production of pro-inflammatory mediators in vivo and in vitro. Furthermore, peiminine inhibited the phosphorylation of the protein kinase B (AKT)/ nuclear factor-κB (NF-κB), extracellular regulated protein kinase (ERK1/2), and p38 signaling pathways both in vivo and in vitro. All the results suggested that peiminine exerted potent anti-inflammatory effects on LPS-induced mastitis in mice. Therefore, peiminine might be a potential therapeutic agent for mastitis.

show abstract

Section: Introductionmentioning

confidence: 99%

Peiminine Protects against Lipopolysaccharide-Induced Mastitis by Inhibiting the AKT/NF-κB, ERK1/2 and p38 Signaling Pathways

Gong

et al. 2018

IJMS

View full text Add to dashboard Cite

show abstract

“…Several plant extracts are familiar to make as anti‐inflammatory properties, but the mechanism of action is mostly unknown. Mangiferin isolated from M. indica has been found to execute antioxidant and anti‐inflammatory properties through targeting NF‐κB signaling pathways 49 . Recent studies have determined that mangiferin protects against liver injury and endothelial dysfunction by inhibiting NLRP3 inflammasome activation in liver and endothelial cells 50,51 .…”

Section: Discussionmentioning

confidence: 99%

Mangiferin inhibits lipopolysaccharide‐induced epithelial‐mesenchymal transition (EMT) and enhances the expression of tumor suppressor gene PER1 in non‐small cell lung cancer cells

Lin

Tsai

Chen

et al. 2020

Environmental Toxicology

View full text Add to dashboard Cite

Non‐small cell lung cancer (NSCLC) is often complicated by pulmonary infection, which affects treatment and prognosis. Bacterial lipopolysaccharide (LPS) is an effective stimulator of inflammatory cytokine production, and previous studies have reported that LPS promotes tumor invasion and metastasis. Mangiferin is a plant‐derived C‐glucosylxanthone with many biological activities, such as antioxidation and anti‐inflammation. This research mainly explored the mechanism of its antitumor activities on LPS‐induced A549, NCI‐H460, and NCI‐H520 NSCLC cells. We determined that mangiferin exhibits growth inhibiting activity against LPS‐induced NSCLC cells through the 3‐(4, 5‐dimethylthiazol‐2‐yl)‐2, 5‐diphenyltetrazolium bromide (MTT) assay. In addition, mangiferin reversed the LPS‐induced downregulation of E‐cadherin (epithelial marker); conversely, it significantly inhibited the expression of raised vimentin (mesenchymal markers). Moreover, the ability of NSCLC cells to migrate, as evidenced by the wound healing and transwell migration assays, and the expression of CXCR4 increased by LPS were significantly repressed by mangiferin. In addition, mangiferin markedly mediated protein levels of PER1 and NLRP3 in LPS‐induced NSCLC cells and reduced the secretion of IL‐1β. These results indicate that mangiferin is not only a remarkable anti‐inflammatory compound but also an antitumor agent; thus, it has the potential for being developed into anti‐inflammatory and antitumor drugs in the future.

show abstract

“…Besides, previous investigations have demonstrated that MF was a xanthonoid with anti-inflammatory capacity, and it was reported to be a promising therapeutic drug for OA (Luczkiewicz et al, 2014;Saha et al, 2016;Qu et al, 2017b;Garrido-Suarez and Garrido, 2019). Previous investigations elucidated that MF markedly suppressed the productions of IL-6, IL-1b, and TNF-a in LPS-triggered primary hepatocytes, BALB/c mice mammary gland, and peritoneal macrophages (Jeong et al, 2014;Pan et al, 2016;Qu et al, 2017a). Furthermore, an earlier research revealed that PT-MF remarkably decreased the expression of Cox-2, iNOS and TNF-a, and the generation of ROS in LPS-evoked RAW 264.7 cells (Bulugonda et al, 2017).…”

Section: Discussionmentioning

confidence: 99%

“…A previous study revealed that suppression of NF-kB could effectively alleviate OA development (Roman-Blas and Jimenez, 2006). Besides, researchers have clarified that MF exposure could repress LPSinduced phosphorylation of NF-kB (Jeong et al, 2014;Tsubaki et al, 2015;Qu et al, 2017a). Earlier investigations demonstrated that the un-stimulated NF-kB was localized in the cytoplasm (Chen et al, 1999), while once stimulated NF-kB would be translocated into the nuclear and then activated its mediated transcription gene expression (Feng et al, 2012).…”

Section: Discussionmentioning

confidence: 99%

Mangiferin Relieves Lipopolysaccharide-Induced Injury by Up-Regulating miR-181a via Targeting PTEN in ATDC5 Cells

Liu

et al. 2020

Front. Pharmacol.

View full text Add to dashboard Cite

Background: Mangiferin (MF) was reported to possess anti-inflammatory activity. This investigation tried to probe into the underlying mechanism of MF in osteoarthritis.Methods: ATDC5 cells were pretreated with series concentrations of MF (0.1, 1, 5, 10, 15, 20 mM) for 2 h and then were exposed to lipopolysaccharide (LPS) (5 mg/ml) for 12 h to construct the inflammatory injury model. The cell viability, productions of pro-inflammatory cytokines and enzymes were respectively measured by employing CCK-8 assay, western blot, ELISA, and quantitative reverse-transcription (qRT)-PCR. miR-181a expression was altered by employing cell transfection. Dichloro-dihydro-fluorescein diacetate (DCFH-DA) method was employed for detection of reactive oxygen species (ROS) generation. Dual luciferase activity assay was conducted for analyzing the relationship between miR-181a and PTEN. The underlying mechanism was determined by employing western blot.Results: High doses of MF treatment (15 and 20 mM) noticeably induced inflammatory injury exhibiting as increased the productions of pro-inflammatory cytokines, enzymes and ROS, activated NF-kB pathway and deactivated PTEN/PI3K/AKT pathway in ATDC5 cells. Besides, MF treatment notably remitted LPS-induced inflammatory injury through deactivation of NF-kB pathway and activation of PTEN/PI3K/AKT pathway. PTEN was a target of miR-181a. Inhibition of miR-181a remarkably reversed MF-triggered impacts on ATDC5 cells.Conclusion: MF attenuated LPS-induced inflammatory damage through miR-181a/ PTEN axis and thereby inhibiting NF-kB pathway and activating PI3K/AKT pathway.

show abstract

Mangiferin inhibits mastitis induced by LPS via suppressing NF-ĸB and NLRP3 signaling pathways

Cited by 38 publications

References 30 publications

Peiminine Protects against Lipopolysaccharide-Induced Mastitis by Inhibiting the AKT/NF-κB, ERK1/2 and p38 Signaling Pathways

Peiminine Protects against Lipopolysaccharide-Induced Mastitis by Inhibiting the AKT/NF-κB, ERK1/2 and p38 Signaling Pathways

Mangiferin inhibits lipopolysaccharide‐induced epithelial‐mesenchymal transition (EMT) and enhances the expression of tumor suppressor gene PER1 in non‐small cell lung cancer cells

Mangiferin Relieves Lipopolysaccharide-Induced Injury by Up-Regulating miR-181a via Targeting PTEN in ATDC5 Cells

Contact Info

Product

Resources

About