Ampelopsin reduces endotoxic inflammation via repressing ROS-mediated activation of PI3K/Akt/NF-κB signaling pathways

Qi, Shimei; Xin, Yinqiang; Guo, Yingtao; Diao, Youxiang; Kou, Xianjuan; Luo, Lan; Yin, Zhengyu

doi:10.1016/j.intimp.2011.12.001

Cited by 191 publications

(124 citation statements)

References 38 publications

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“…The LPS-stimulated expressions of inflammatory markers inducible nitric oxide synthase (iNOS) and cyclooxygenase-2 (COX-2) were repressed in the presence of EMCDO ranging from 1.25 to 5 g/ml, and the repression efficiency was better than that of 7.5 g/ml curcumin, a well-known efficient natural anti-inflammation polyphenol compound (Wang, Sun, Huang, & Zheng, 2013) ( Figure 5C). LPS-treated RAW264.7 cells exhibited proinflammatory cytokines production and secretion, including TNF-, IL-6 and IL-1 (Qi et al, 2012). As expected, the three proinflammatory cytokines were dramatically repressed in the presence of EMCDO in a dose-dependent manner.…”

Section: Inhibition Of Inflammatory Mediators By Emcdosupporting

confidence: 75%

Suppression of Hepatitis B Virus Production and Inflammatory Response in vitro and in vivo by Mormodica charantia Compound EMCDO

Chang¹,

Chen²,

Chen³

et al. 2015

JAS

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Eight compounds were purified from Mormodica charanti, and their chemical structures were determined in this study. Their anti-HBV and anti-inflammation activities were investigated. Compound EMCDO exhibited the most efficient effect in terms of reducing HBV surface antigen, e antigen and viral DNA levels in HBV particles or surface antigen-producing cells 2.2.15 and PLC/PRF/5, respectively. Tumor suppressor p53 played a significant role in EMCDO-mediated anti-HBV effects. Pretreatment with EMCDO prevented 2.2.15 cells-induced tumor formation in a nude mice subcutaneous model. The anti-HBV and anti-tumor activities of EMCDO were better than those of oltipraz, an inhibitor of HBV transcription. EMCDO reduced the proinflammatory cytokines and mediators in LPS-treated RAW264.7 cells in a dose-dependent manner. The LPS-upregulated phosphorylation level of I was reduced in the presence of EMCDO. The transcription activity of NF-B was increased in cells treated with EMCDO. Utilization of a mouse ear edema model further confirmed the activity of EMCDO against TPA-elicited inflammation.

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Section: Inhibition Of Inflammatory Mediators By Emcdosupporting

confidence: 75%

Suppression of Hepatitis B Virus Production and Inflammatory Response in vitro and in vivo by Mormodica charantia Compound EMCDO

Chang¹,

Chen²,

Chen³

et al. 2015

JAS

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“…Amp, a major component of Ampelopsis grossedentata, is reported to possess not only important pharmacological activities, such as anti-inflammatory and hepatoprotective properties (25,26), but also anti-cancer activity. The anti-tumor activity of Amp is associated with the induction of apoptosis (27)(28)(29)(30) and the inhibition of metastasis (36).…”

Section: Discussionmentioning

confidence: 99%

“…ROS cause ER stress, which results in the generation of more ROS (45,47). Although Amp-mediated ROS trigger ER stress/AMPK activation and JNK/p38-MAPK signaling, leading to apoptosis in colon cancer cells, it is important to consider that Amp is not necessarily pro-ROS in all circumstances (25,48). In a previous study of lipopolysaccharide-activated macrophages, low doses of Amp effectively suppressed ROS generation and the release of inflammatory cytokines (25).…”

Section: Discussionmentioning

confidence: 99%

“…Although Amp-mediated ROS trigger ER stress/AMPK activation and JNK/p38-MAPK signaling, leading to apoptosis in colon cancer cells, it is important to consider that Amp is not necessarily pro-ROS in all circumstances (25,48). In a previous study of lipopolysaccharide-activated macrophages, low doses of Amp effectively suppressed ROS generation and the release of inflammatory cytokines (25). Low-dose Amp has also been demonstrated to inhibit phosphoinositide 3-kinase activation without attenuating MAPK (ERK, JNK and p38-MAPK) activation (25), and Amp-mediated ROS reduction has been identified to trigger the apoptosis of hepatocellular carcinoma cells (48).…”

Section: Discussionmentioning

confidence: 99%

“…A mpelopsi n (A mp), wh ich is ext racted f rom Ampelopsis grossedentata, is reported to have various biological functions, including anti-oxidative (25) and hepatoprotective effects (26). This flavonoid, also called dihydromyricetin, has potent anti-cancer activities in several types of malignancy (27,28).…”

Section: Introductionmentioning

confidence: 99%

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Ampelopsin‑induced reactive oxygen species enhance the apoptosis of colon cancer cells by activating endoplasmic reticulum stress‑mediated AMPK/MAPK/XAF1 signaling

2017

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Abstract. Ampelopsin (Amp) is bioactive natural product and exerts anti-cancer effects against several cancer types. The present study investigated the anti-colon cancer activity of Amp and explored its mechanism of action. The treatment of colon cancer cells with Amp resulted in the dose-and time-dependent induction of apoptosis via the activation of endoplasmic reticulum (ER) stress, 5' adenosine monophosphate-activated protein kinase (AMPK), and c-Jun N-terminal protein kinase (JNK)/p38 mitogen-activated protein kinases (MAPKs). Salubrinal, an ER stress inhibitor, prevented the upregulation of ER stress-associated proteins, including phosphorylated protein kinase RNA-like ER kinase, phosphorylated eukaryotic translation initiation factor 2α, glucose-regulated protein 78, and CCAAT/enhancer-binding protein homologous protein, as well as suppressing AMPK activation and the MAPK signaling pathway. Knockdown of AMPK by RNA interference failed to block ER stress. Additionally, SP600125 (a JNK inhibitor) and SB203580 (a p38-MAPK inhibitor) effectively inhibited apoptosis and attenuated the expression of X-linked IAP-associated factor 1 (XAF1) and apoptotic Bcl-2 family proteins (BCL2 antagonist/killer 1 and BCL2-associated X protein) in Amp-treated colon cancer cells. Furthermore, reactive oxygen species (ROS)-mediated ER stress/AMPK apoptotic signaling pathway in Amp-treated colon cancer cells were markedly inhibited by treatment with N-acetyl-L-cysteine, a ROS scavenger. These results demonstrate that treatment with Amp induces the apoptotic death of colon cancer cells through ER stress-initiated AMPK/MAPK/XAF1 signaling. These results also provide experimental information for developing Amp as therapeutic drug against colon cancer.

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Dihydromyricetin inhibits NLRP3 inflammasome‐dependent pyroptosis by activating the Nrf2 signaling pathway in vascular endothelial cells

Zhang

et al. 2017

BioFactors

146

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Increasing evidence demonstrates that pyroptosis, pro-inflammatory programmed cell death, is linked to atherosclerosis; however, the underlying mechanisms remain to be elucidated. Dihydromyricetin (DHM), a natural flavonoid, was reported to exert anti-oxidative and anti-inflammatory bioactivities. However, the effect of DHM on atherosclerosis-related pyroptosis has not been studied. In the present study, palmitic acid (PA) treatment led to pyroptosis in human umbilical vein endothelial cells (HUVECs), as evidenced by caspase-1 activation, LDH release, and propidium iodide-positive staining; enhanced the maturation and release of proinflammatory cytokine IL-1β and activation of the NLRP3 inflammasome; and markedly increased intracellular reactive oxygen species (ROS) and mitochondrial ROS (mtROS) levels. Moreover, NLRP3 siRNA transfection or treatment with inhibitors efficiently suppressed PA-induced pyroptosis, and pretreatment with total ROS scavenger or mtROS scavenger attenuated PA-induced NLRP3 inflammasome activation and subsequent pyroptosis. However, DHM pretreatment inhibited PA-induced pyroptotic cell death by increasing cell viability, decreasing LDH and IL-1β release, improving cell membrane integrity, and abolishing caspase-1 cleavage and subsequent IL-1β maturation. We also found that DHM pre-treatment remarkably reduced the levels of intracellular ROS and mtROS and activated the Nrf2 signaling pathway. Moreover, knockdown of Nrf2 by siRNA abrogated the inhibitory effects of DHM on ROS generation and subsequent PA-induced pyroptosis. Together, these results indicate that the Nrf2 signaling pathway plays a role, as least in part, in the DHM-mediated improvement in PA-induced pyroptosis in vascular endothelial cells, which implies the underlying medicinal value of DHM targeting immune/inflammatory-related diseases, such as atherosclerosis. © 2017 BioFactors, 44(2):123-136, 2018.

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Ampelopsin reduces endotoxic inflammation via repressing ROS-mediated activation of PI3K/Akt/NF-κB signaling pathways

Cited by 191 publications

References 38 publications

Suppression of Hepatitis B Virus Production and Inflammatory Response in vitro and in vivo by Mormodica charantia Compound EMCDO

Suppression of Hepatitis B Virus Production and Inflammatory Response in vitro and in vivo by Mormodica charantia Compound EMCDO

Ampelopsin‑induced reactive oxygen species enhance the apoptosis of colon cancer cells by activating endoplasmic reticulum stress‑mediated AMPK/MAPK/XAF1 signaling

Dihydromyricetin inhibits NLRP3 inflammasome‐dependent pyroptosis by activating the Nrf2 signaling pathway in vascular endothelial cells

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