Silibinin Alleviates Lipopolysaccharide Induced Inflammation in Porcine Mammary Epithelial Cells via mTOR/NF‐κB Signaling Pathway

Xu, Shengyu; Jiang, Xiaojun; Liu, Yalei; Jiang, Xuemei; Che, Lianqiang; Lin, Yan; Feng, Bin; Fang, Zhengfeng; Hua, Lun; Li, Jian; Wang, Jianping; Ren, Zhihua; Sun, Mengmeng; Zhuo, Yong

doi:10.1002/mnfr.202200715

Cited by 2 publications

(1 citation statement)

References 42 publications

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“…Of interest, the pretreatment of human umbilical vein endothelial cells (HUVECs) with SB was observed to reduce the TNF-α-induced gene expression of such proinflammatory genes as IL-6 and MCP-1 [64]. Silibinin was demonstrated to mitigate LPS-induced inflammation (TNF-α) in porcine mammary epithelial cells via the regulation of the mTOR/NF-κB signalling pathway, including the attenuation of increased expression of (phosphorylated) p-NF-κB p65, p-IκB-α and p-MAPK p38 [65].…”

Section: Epithelial Cellsmentioning

confidence: 98%

Silymarin and Inflammation: Food for Thoughts

Surai,

Earle-Payne

2024

Antioxidants

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Inflammation is a vital defense mechanism, creating hostile conditions for pathogens, preventing the spread of tissue infection and repairing damaged tissues in humans and animals. However, when inflammation resolution is delayed or compromised as a result of its misregulation, the process proceeds from the acute phase to chronic inflammation, leading to the development of various chronic illnesses. It is proven that redox balance disturbances and oxidative stress are among major factors inducing NF-κB and leading to over-inflammation. Therefore, the anti-inflammatory properties of various natural antioxidants have been widely tested in various in vitro and in vivo systems. Accumulating evidence indicates that silymarin (SM) and its main constituent silibinin/silybin (SB) have great potential as an anti-inflammation agent. The main anti-inflammatory mechanism of SM/SB action is attributed to the inhibition of TLR4/NF-κB-mediated signaling pathways and the downregulated expression of pro-inflammatory mediators, including TNF-α, IL-1β, IL-6, IL-12, IL-23, CCL4, CXCL10, etc. Of note, in the same model systems, SM/SB was able to upregulate anti-inflammatory cytokines (IL-4, IL-10, IL-13, TGF-β, etc.) and lipid mediators involved in the resolution of inflammation. The inflammatory properties of SM/SB were clearly demonstrated in model systems based on immune (macrophages and monocytes) and non-immune (epithelial, skin, bone, connective tissue and cancer) cells. At the same time, the anti-inflammatory action of SM/SB was confirmed in a number of in vivo models, including toxicity models, nonalcoholic fatty liver disease, ischemia/reperfusion models, stress-induced injuries, ageing and exercising models, wound healing and many other relevant model systems. It seems likely that the anti-inflammatory activities of SM/SB are key elements on the health-promoting properties of these phytochemicals.

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Section: Epithelial Cellsmentioning

confidence: 98%

Silymarin and Inflammation: Food for Thoughts

Surai,

Earle-Payne

2024

Antioxidants

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Silibinin Suppresses Inflammatory Responses Induced by Exposure to Asian Sand Dust

Lee,

Pak,

Kim

et al. 2024

Antioxidants

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Asian sand dust (ASD), generated from the deserts of China and Mongolia, affects Korea and Japan during spring and autumn, causing harmful effects on various bio-organs, including the respiratory system, due to its irritants such as fine dust, chemicals, and toxic materials. Here, we investigated the therapeutic effects of silibinin against ASD-induced airway inflammation using mouse macrophage-like cell line RAW264.7 and a murine model. ASD was intranasally administered to mice three times a week and silibinin was administered for 6 days by oral gavage. In ASD-stimulated RAW264.7 cells, silibinin treatment decreased tumor necrosis factor-α production and reduced the expression of p-p65NF-κB, p-p38, and cyclooxygenase (COX)-2, while increasing heme oxygenase (HO)-1 expression. In ASD-exposed mice, silibinin administration reduced inflammatory cell count and cytokines in bronchoalveolar lavage fluid and decreased inflammatory cell infiltration in lung tissue. Additionally, silibinin lowered oxidative stress, as evidenced by decreased 8-hydroxy-2’-deoxyguanosin (8-OHdG) expression and increased HO-1 expression. The expression of inflammatory-related proteins, including p-p65NF-κB, COX-2, and p-p38, was markedly reduced by silibinin administration. Overall, silibinin treatment reduced the expression of p-p65NF-κB, COX-2, and p-p38 in response to ASD exposure, while increasing HO-1 expression both in vitro and in vivo. These findings suggest that silibinin mitigates pulmonary inflammation caused by ASD exposure by reducing inflammatory signaling and oxidative stress, indicating its potential as a therapeutic agent for ASD-induced pulmonary inflammation.

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Silibinin Alleviates Lipopolysaccharide Induced Inflammation in Porcine Mammary Epithelial Cells via mTOR/NF‐κB Signaling Pathway

Cited by 2 publications

References 42 publications

Silymarin and Inflammation: Food for Thoughts

Silymarin and Inflammation: Food for Thoughts

Silibinin Suppresses Inflammatory Responses Induced by Exposure to Asian Sand Dust

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