Apple Polyphenols Extract (APE) Alleviated Dextran Sulfate Sodium Induced Acute Ulcerative Colitis and Accompanying Neuroinflammation via Inhibition of Apoptosis and Pyroptosis

Liu, Fang; Wang, Xinjing; Cui, Yuan; Yin, Yan; Qiu, D.; Li, Shilan; Li, Xinli

doi:10.3390/foods10112711

Cited by 25 publications

(10 citation statements)

References 49 publications

Supporting

Mentioning

Contrasting

Order By: Relevance

“…Based on the immunofluorescence analysis, a reduced protein level of IBα1 in the hippocampus and cortex was found after APE intervention. Meanwhile, our previous study also confirmed the alleviated depression and anxiety in acute colitis mice after APE intervention by reducing the mRNA expression of Cox-2 and GFAP in mouse brain tissue . Therefore, APE intervention ameliorated HFCD-induced atherosclerotic neuroinflammation in LDLR –/– mice.…”

Section: Discussionsupporting

confidence: 58%

Apple Polyphenol Extract Ameliorates Atherosclerosis and Associated Cognitive Impairment through Alleviating Neuroinflammation by Weakening TLR4 Signaling and NLRP3 Inflammasome in High-Fat/Cholesterol Diet-Fed LDLR^–/– Male Mice

Yang,

Song,

Xie

et al. 2023

J. Agric. Food Chem.

Self Cite

View full text Add to dashboard Cite

Although studies have supported the beneficial effects of the ingredients of apple polyphenol extract (APE), a polyphenol mixture being extracted from whole fresh apples, on neurodegenerative diseases, the role of APE in atherosclerosis-related cognitive impairment remains unclear. To clarify the role of APE in regulating cognitive dysfunction in mice with atherosclerosis and the underlying mechanisms, high-fat/cholesterol diet-fed male LDLR–/– mice were gavaged with 125 or 500 mg/(kg·bw·d) APE solution or sterile double-distilled water for consecutive 8 weeks, and age-matched C57BL/6 male mice were employed as normal control. APE intervention increased the serum concentration of high-density apolipoprotein cholesterol, improved atherosclerosis, and ameliorated cognitive function of mice by inhibiting the phosphorylation of tau protein, supporting with significantly reduced platform latency and obviously increased swimming distance in the target quadrant according to the Morris water maze test. APE intervention alleviated neuroinflammation by attenuating the activation of microglia and astrocytes and inhibiting TLR4 signaling with reduced protein expression of NF-κB, MyD88, TRIF, and IKKβ. Meanwhile, APE intervention inactivated NLRP3 inflammasome with downregulated protein expression of caspase-1, IL-18, and IL-1β. Additionally, APE intervention improved the damaged brain barrier structure by upregulating the protein expression of ZO-1 and occludin. Therefore, our research supplemented new data, supporting the potential of APE as an effective dietary bioactive ingredient to improve atherosclerosis and associated cognitive impairment.

show abstract

Section: Discussionsupporting

confidence: 58%

Apple Polyphenol Extract Ameliorates Atherosclerosis and Associated Cognitive Impairment through Alleviating Neuroinflammation by Weakening TLR4 Signaling and NLRP3 Inflammasome in High-Fat/Cholesterol Diet-Fed LDLR^–/– Male Mice

Yang,

Song,

Xie

et al. 2023

J. Agric. Food Chem.

Self Cite

View full text Add to dashboard Cite

show abstract

“…In conclusion, AP, the main secondary metabolites extracted [16][17][18] Therefore, AP possesses a good prospect for the development of anti-UC health food and drugs. It is believed that with the continuous development of research, AP would achieve promising results in clinical treatment.…”

Section: Discussionmentioning

confidence: 90%

“…15) However, as far as we know, there are not many related reports on AP treatment for UC. [16][17][18] Caco-2 cells, which could mimic human intestinal epithelial cells in the body when cultured in monolayer, have been widely used as a typical in vitro UC model for antioxidant study. [19][20][21][22] Hydrogen peroxide (H 2 O 2 ) which is an important ROS, could induce the oxidative stress damage and apoptosis of many cells.…”

Section: Introductionmentioning

confidence: 99%

Protective Effect of Apple Polyphenols on H<sub>2</sub>O<sub>2</sub>-Induced Oxidative Stress Damage in Human Colon Adenocarcinoma Caco-2 Cells

2023

View full text Add to dashboard Cite

Apple is an important dietary agent for human and apple polyphenols (AP) are the main secondary metabolites of apples. In this study, the protective effects of AP on hydrogen peroxide (H 2 O 2 )-induced oxidative stress damage in human colon adenocarcinoma Caco-2 cells were investigated by cell viability, oxidative stress change as well as cell apoptosis. Pre-adding AP could significantly increase the survival rate of H 2 O 2treated Caco-2 cells. Besides, the activities of antioxidant enzymes superoxide dismutase (SOD), glutathione peroxidase (GSH-PX) and catalase (CAT) were elevated. While the malondialdehyde (MDA) content which is the major oxidant products of polyunsaturated fatty acids (PUFA) reduced after AP treatment. In addition, AP also suppressed the emergence of DNA fragment and decreased the expression of apoptosis-related protein Caspase-3. These results demonstrated that AP could ameliorate H 2 O 2 -induced oxidative stress damage in Caco-2 cells, which could serve as a reference for further studies of apple natural active products and deep study of the anti-oxidative stress mechanism. Key words apple polyphenol (AP), Caco-2 cell, hydrogen peroxide (H 2 O 2 ), oxidative stress damage

show abstract

“…Until now, there is little research about effect of plant polyphenols especially PCA or Que on pyroptosis signals. Only Liu et al reported that apple polyphenols extract ameliorated dextran sulfate sodium-induced acute ulcerative colitis through inhibiting intestinal epithelial cell apoptosis and pyroptosis pathway [62]. Luo et al reported that Que possessed a protective effect on macrophages pyroptosis via TLR2/Myd88/ NF-ΚB pathway [63].…”

Section: Discussionmentioning

confidence: 99%

Protocatechuic acid and quercetin attenuate ETEC-caused IPEC-1 cell inflammation and injury associated with inhibition of necroptosis and pyroptosis signaling pathways

Xiao

Zhou

et al. 2023

J Animal Sci Biotechnol

View full text Add to dashboard Cite

Background Necroptosis and pyroptosis are newly identified forms of programmed cell death, which play a vital role in development of many gastrointestinal disorders. Although plant polyphenols have been reported to protect intestinal health, it is still unclear whether there is a beneficial role of plant polyphenols in modulating necroptosis and pyroptosis in intestinal porcine epithelial cell line (IPEC-1) infected with enterotoxigenic Escherichia coli (ETEC) K88. This research was conducted to explore whether plant polyphenols including protocatechuic acid (PCA) and quercetin (Que), attenuated inflammation and injury of IPEC-1 caused by ETEC K88 through regulating necroptosis and pyroptosis signaling pathways. Methods IPEC-1 cells were treated with PCA (40 μmol/L) or Que (10 μmol/L) in the presence or absence of ETEC K88. Results PCA and Que decreased ETEC K88 adhesion and endotoxin level (P < 0.05) in cell supernatant. PCA and Que increased cell number (P < 0.001) and decreased lactate dehydrogenases (LDH) activity (P < 0.05) in cell supernatant after ETEC infection. PCA and Que improved transepithelial electrical resistance (TEER) (P < 0.001) and reduced fluorescein isothiocyanate-labeled dextran (FD4) flux (P < 0.001), and enhanced membrane protein abundance of occludin, claudin-1 and ZO-1 (P < 0.05), and rescued distribution of these tight junction proteins (P < 0.05) after ETEC infection. PCA and Que also declined cell necrosis ratio (P < 0.05). PCA and Que reduced mRNA abundance and concentration of tumor necrosis factor-α (TNF-α), interleukin (IL)-6 and IL-8 (P < 0.001), and down-regulated gene expression of toll-like receptors 4 (TLR4) and its downstream signals (P < 0.001) after ETEC infection. PCA and Que down-regulated protein abundance of total receptor interacting protein kinase 1 (t-RIP1), phosphorylated-RIP1 (p-RIP1), p-RIP1/t-RIP1, t-RIP3, p-RIP3, mixed lineage kinase domain-like protein (MLKL), p-MLKL, dynamin- related protein 1 (DRP1), phosphoglycerate mutase 5 (PGAM5) and high mobility group box 1 (HMGB1) (P < 0.05) after ETEC infection. Moreover, PCA and Que reduced protein abundance of nod-like receptor protein 3 (NLRP3), nod-like receptors family CARD domain-containing protein 4 (NLRC4), apoptosis-associated speck-like protein containing a CARD (ASC), gasdermin D (GSDMD) and caspase-1 (P < 0.05) after ETEC infection. Conclusions In general, our data suggest that PCA and Que are capable of attenuating ETEC-caused intestinal inflammation and damage via inhibiting necroptosis and pyroptosis signaling pathways.

show abstract

Apple Polyphenols Extract (APE) Alleviated Dextran Sulfate Sodium Induced Acute Ulcerative Colitis and Accompanying Neuroinflammation via Inhibition of Apoptosis and Pyroptosis

Cited by 25 publications

References 49 publications

Apple Polyphenol Extract Ameliorates Atherosclerosis and Associated Cognitive Impairment through Alleviating Neuroinflammation by Weakening TLR4 Signaling and NLRP3 Inflammasome in High-Fat/Cholesterol Diet-Fed LDLR^–/– Male Mice

Apple Polyphenol Extract Ameliorates Atherosclerosis and Associated Cognitive Impairment through Alleviating Neuroinflammation by Weakening TLR4 Signaling and NLRP3 Inflammasome in High-Fat/Cholesterol Diet-Fed LDLR^–/– Male Mice

Protective Effect of Apple Polyphenols on H<sub>2</sub>O<sub>2</sub>-Induced Oxidative Stress Damage in Human Colon Adenocarcinoma Caco-2 Cells

Protocatechuic acid and quercetin attenuate ETEC-caused IPEC-1 cell inflammation and injury associated with inhibition of necroptosis and pyroptosis signaling pathways

Contact Info

Product

Resources

About

Apple Polyphenols Extract (APE) Alleviated Dextran Sulfate Sodium Induced Acute Ulcerative Colitis and Accompanying Neuroinflammation via Inhibition of Apoptosis and Pyroptosis

Cited by 25 publications

References 49 publications

Apple Polyphenol Extract Ameliorates Atherosclerosis and Associated Cognitive Impairment through Alleviating Neuroinflammation by Weakening TLR4 Signaling and NLRP3 Inflammasome in High-Fat/Cholesterol Diet-Fed LDLR–/– Male Mice

Apple Polyphenol Extract Ameliorates Atherosclerosis and Associated Cognitive Impairment through Alleviating Neuroinflammation by Weakening TLR4 Signaling and NLRP3 Inflammasome in High-Fat/Cholesterol Diet-Fed LDLR–/– Male Mice

Protective Effect of Apple Polyphenols on H<sub>2</sub>O<sub>2</sub>-Induced Oxidative Stress Damage in Human Colon Adenocarcinoma Caco-2 Cells

Protocatechuic acid and quercetin attenuate ETEC-caused IPEC-1 cell inflammation and injury associated with inhibition of necroptosis and pyroptosis signaling pathways

Contact Info

Product

Resources

About

Apple Polyphenol Extract Ameliorates Atherosclerosis and Associated Cognitive Impairment through Alleviating Neuroinflammation by Weakening TLR4 Signaling and NLRP3 Inflammasome in High-Fat/Cholesterol Diet-Fed LDLR^–/– Male Mice

Apple Polyphenol Extract Ameliorates Atherosclerosis and Associated Cognitive Impairment through Alleviating Neuroinflammation by Weakening TLR4 Signaling and NLRP3 Inflammasome in High-Fat/Cholesterol Diet-Fed LDLR^–/– Male Mice