(−)-Epigallocatechin Gallate Targets Notch to Attenuate the Inflammatory Response in the Immediate Early Stage in Human Macrophages

Wang, Tengfei; Xiang, Zemin; Wang, Ya; Li, Xi; Fang, Chongye; Song, Shuang; Li, Chunlei; Huang, Yu; Wang, Han; Ling, Yan; Sheng, Hao; Sheng, Jun

doi:10.3389/fimmu.2017.00433

Cited by 30 publications

(28 citation statements)

References 37 publications

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“…To verify these results in mouse macrophages, we examined the expression of Notch-1/2 by Western blot analysis. Similar to previous results (18), EGCG attenuated the expression of Notch-1/2 (Fig. 4B, C).…”

Section: Egcg Could Target Notch To Inhibit the Inflammatory Responsesupporting

confidence: 91%

“…4A), and release from mouse macrophages of the cytokines induced by LPS was inhibited by EGCG. In our previous study (18), we found that EGCG attenuated the immediate early inflammatory response through the Notch pathway in human macrophages differentiated from THP-1 cells. To verify these results in mouse macrophages, we examined the expression of Notch-1/2 by Western blot analysis.…”

Section: Egcg Could Target Notch To Inhibit the Inflammatory Responsementioning

confidence: 80%

“…In our previous study, (2)-epigallocatechin gallate (EGCG), which is the most abundant catechin in tea (17), was found to attenuate the inflammatory response by shutting off Notch signaling. Further study showed that EGCG could inhibit the LPS-induced inflammation and turn off Notch signaling in human primary macrophages (18).…”

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confidence: 98%

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Wound healing can be improved by (—)‐epigallocatechin gallate through targeting Notch in streptozotocin‐induced diabetic mice

et al. 2018

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Delayed wound healing is one of the most prominent clinical manifestations of diabetes and lacks satisfactory treatment options. Persistent inflammation occurs in the late phase of wound healing and impairs the healing process in mice with diabetes mellitus (DM). In this study, we observed that the late wound healing in streptozotocin (STZ)-induced DM mice could be improved by (-)-epigallocatechin gallate (EGCG). The macrophage accumulation, inflammation response, and Notch signaling can be inhibited by EGCG in the skin wounds of DM mice. Furthermore, we found that the LPS-induced inflammation response including overactivated Notch signaling, was inhibited by EGCG in mouse macrophages. Moreover, we confirmed that EGCG could directly bind with mouse Notch-1. In addition, our studies indicated that diabetic wound healing was improved by EGCG treatment before or after the inflammation phase by targeting the Notch signaling pathway, which suggests that the pre-existing diabetic wound healing can be improved by EGCG. To summarize, wound healing can be improved by EGCG through targeting Notch in STZ-induced DM mice. Our findings provide insight into the therapeutic strategy for diabetic wounds and offer EGCG as a novel potential medicine to treat chronic wounds.-Huang, Y.-W., Zhu, Q.-Q., Yang, X.-Y., Xu, H.-H., Sun, B., Wang, X.-J., Sheng, J. Wound healing can be improved by (-)-epigallocatechin gallate through targeting Notch in streptozotocin-induced diabetic mice.

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Section: Egcg Could Target Notch To Inhibit the Inflammatory Responsesupporting

confidence: 91%

Section: Egcg Could Target Notch To Inhibit the Inflammatory Responsementioning

confidence: 80%

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Wound healing can be improved by (—)‐epigallocatechin gallate through targeting Notch in streptozotocin‐induced diabetic mice

et al. 2018

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“…Therefore, the inhibition of NF‐κB has been suggested as a main target for the treatment of intestinal inflammatory reactions and maintenance of intestinal barrier function (Suenaert et al, ). Many researches demonstrated that EGCG significantly reduced inflammation by inhibiting NF‐κB pathways (Wang et al, ). Present study also showed that supplementation of EGCG to heat‐stressed broiler diet presented positive effect on villus height, crypt depth and the villus/crypt ration, as well as expression of Muc2 and Claudin‐1 .…”

Section: Discussionmentioning

confidence: 99%

The effect of Epigallocatechin‐3‐gallate on small intestinal morphology, antioxidant capacity and anti‐inflammatory effect in heat‐stressed broilers

Song

Lei

Luo

et al. 2019

Animal Physiology Nutrition

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This study was to investigate the effects of Epigallocatechin‐3‐gallate (EGCG) on intestinal morphology, antioxidant capacity and anti‐inflammatory response in heat‐stressed broiler. A total of 192 2‐week‐old Arbour Acres broilers chickens were divided into four groups with six replicates per group and eight chickens per replicate: one thermoneutral control group (28°C, group TN), which was fed the basal diet; and three cyclic high‐temperature groups (35°C from 7:00 to 19:00 hr; 28°C from 19:00 hr to 7:00 hr, heat stress group), which were fed the basal diet supplementation with EGCG 0 mg/kg (group HS0), 300 mg/kg (group HS300) and 600 mg/kg (group HS600). The gut morphology and intestinal mucosal oxidative stress indicators, as well as intestinal barrier‐related gene expression, were analysed. The results showed that compared with group TN, heat stress reduced the villus height (VH), activities of glutathione peroxidase (GSH‐Px), superoxide dismutase (SOD)and catalase (CAT), increased the crypt depth (CD) and malondialdehyde (MDA)content at 21, 28 and 35 days (p < 0.05). After the heat‐stressed broilers were supplemented with EGCG, VH, VH/CD (V/C), and the activities of GSH‐Px, SOD and CAT were increased, and CD and MDA content were reduced compared with those in group HS0 without EGCG supplementation at 21, 28 and 35 days (p < 0.05). The EGCG supplementation promoted the gene expression of nuclear factor‐erythroid 2‐related factor 2 (Nrf2), Claudin‐1, Mucin 2 (Muc2) and alleviated the nuclear factor‐kappa B (NF‐κB) and lipopolysaccharide‐induced tumour necrosis factor (LITAF) gene expression compared with group HS0 (p < 0.05). Moreover, intestinal morphology was strongly correlated with antioxidant ability and inflammatory response. In conclusion, EGCG alleviated the gut oxidative injury of heat‐stressed broilers by enhancing antioxidant capacity and inhibiting inflammatory response.

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“…Natural compounds have received great attention for their purported anti‐cancer effects, frequently mediated via Notch inhibition. For instance, xanthohumol, butein, honokiol, diallyl trisulfide, quercetin, and (−)‐epigallocatechin gallate have all shown Notch inhibitory effects in vitro. Curcumin, an extensively studied component of turmeric, exerts Notch‐inhibiting effects by downregulating γ‐secretase component expression .…”

Section: Strategies For Notch Inhibitionmentioning

confidence: 99%

Perspectives on the discovery of NOTCH2‐specific inhibitors

et al. 2017

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The Notch pathway is a cell-cell communication system where membrane-bound ligands interact with the extracellular region of Notch receptors to induce intracellular, downstream effects on gene expression. Aberrant Notch signaling promotes tumorigenesis, and the Notch pathway has tremendous potential for novel targeting strategies in cancer treatment. While γ-secretase inhibitors as Notch-inhibiting agents are already promising in clinical trials, they are highly non-specific with adverse side-effects. One of the underlying challenges is that two of the four known human Notch paralogs, NOTCH1 and 2, share very high structural similarity but play opposing roles in some tumorigenesis pathways. This perspective explores the feasibility of developing Notch-specific small molecule inhibitors targeting the anti-NOTCH2 antibody-binding epitopes or the "S2-Leu-plug-binding site" using a computer-aided drug discovery approach.

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(−)-Epigallocatechin Gallate Targets Notch to Attenuate the Inflammatory Response in the Immediate Early Stage in Human Macrophages

Cited by 30 publications

References 37 publications

Wound healing can be improved by (—)‐epigallocatechin gallate through targeting Notch in streptozotocin‐induced diabetic mice

Wound healing can be improved by (—)‐epigallocatechin gallate through targeting Notch in streptozotocin‐induced diabetic mice

The effect of Epigallocatechin‐3‐gallate on small intestinal morphology, antioxidant capacity and anti‐inflammatory effect in heat‐stressed broilers

Perspectives on the discovery of NOTCH2‐specific inhibitors

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