Quercetin Pretreatment Attenuates Hepatic Ischemia Reperfusion-Induced Apoptosis and Autophagy by Inhibiting ERK/NF-<i>κ</i>B Pathway

Wu, Liwei; Dai, Weiqi; Li, Sainan; Jiao, Feng; Li, Jingjing; Liu, Tong; Xu, Shizan; Wang, Wenwen; Yu, Qiang; Chen, Kan; Xia, Yujing; Lü, Jie; Zhou, Yingqun; Fan, Xiaoming; Guo, Chuanyong

doi:10.1155/2017/9724217

Cited by 36 publications

(25 citation statements)

References 58 publications

(48 reference statements)

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“…Our study exhibited that the HI for 45 minutes followed by 3 hours of reperfusion led to the liver injury which is assessed by marked elevation of liver enzymes ALT and AST levels indicating damage in the cell membrane of the liver and this is in accordance with previous studies [ 25 , 35 , 36 ]. Moreover, hepatic necrosis, sinusoidal congestion, hemorrhage, and hepatocyte degeneration are the characteristic pathological changes seen after HIR [ 24 , 34 , 37 ].…”

Section: Discussionsupporting

confidence: 93%

Vildagliptin Attenuates Hepatic Ischemia/Reperfusion Injury via the TLR4/NF‐κB Signaling Pathway

Sherif

Al-Shaalan

2018

Oxidative Medicine and Cellular Longevity

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The Toll-like receptor-4 (TLR4)/nuclear factor kappa B (NF-κB) signaling pathway is vital in the pathogenesis of hepatic ischemia/reperfusion (HIR) injury. Dipeptidyl peptidase-4 (DPP4) inhibitors exert protective effects on IR injury of the kidney, heart, and lung; however, their effect on the liver is still unknown. Thus, the purpose of this study was to examine whether pretreatment with vildagliptin (Vilda), a DPP4 inhibitor, produces hepatic protection against IR injury and to investigate its influence on TLR4/NF-κB signaling in a rat model. Thirty male Wistar rats were divided into 3 groups: the sham group: subjected to a sham operation and received normal saline; the HIR group: subjected to HIR and received normal saline; and the Vilda + HIR group: subjected to HIR with pretreatment of 10 mg/kg/day Vilda for 10 days intraperitoneally. Hepatic ischemia lasted for 45 minutes followed by 3-hour reperfusion; then blood and liver samples were collected for biochemical and histopathological examination. The HIR group produced a significant increase in serum alanine aminotransferase (ALT), aspartate aminotransferase (AST), hepatic malondialdehyde (MDA), nitric oxide (NO), and tumor necrosis factor alpha (TNF-α) levels and a significant reduction in the hepatic catalase level in comparison to the sham group. Moreover, a significant upregulation of gene and protein expressions of TLR4, NF-κB, and high-mobility group box-1 (HMGB1) along with caspase-3 protein expression was observed in the HIR group when compared with the sham group. Histopathological examination of the liver from the HIR group showed necrosis, sinusoidal congestion, hemorrhage, and hepatocyte degeneration. Administration of Vilda ameliorated the biochemical and histopathological changes caused by HIR. Vildagliptin showed for the first time a hepatoprotective effect in HIR injury through downregulation of TLR4/NF-κB/HMGB1 and caspase-3 hepatic expressions.

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Section: Discussionsupporting

confidence: 93%

Vildagliptin Attenuates Hepatic Ischemia/Reperfusion Injury via the TLR4/NF‐κB Signaling Pathway

Sherif

Al-Shaalan

2018

Oxidative Medicine and Cellular Longevity

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“…The protective effects of many Chinese herbal medicines, such as quercetin, [51][52][53] oleanolic acid, 54 proanthocyanidin B2, 55 epigallocatechin-3-gallate, 56 isorhamnetin 57 and genistein, 58 in liver diseases have been confirmed by our studies.…”

Section: Ppa Rγ Agonis Ts From Natur Al Produc Tssupporting

confidence: 79%

Therapeutic potential of PPARγ natural agonists in liver diseases

Guo

2020

J Cellular Molecular Medi

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Peroxisome proliferator‐activated receptor gamma (PPARγ) is a vital subtype of the PPAR family. The biological functions are complex and diverse. PPARγ plays a significant role in protecting the liver from inflammation, oxidation, fibrosis, fatty liver and tumours. Natural products are a promising pool for drug discovery, and enormous research effort has been invested in exploring the PPARγ‐activating potential of natural products. In this manuscript, we will review the research progress of PPARγ agonists from natural products in recent years and probe into the application potential and prospects of PPARγ natural agonists in the therapy of various liver diseases, including inflammation, hepatic fibrosis, non‐alcoholic fatty liver and liver cancer.

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“…In addition, we also observed that sevoflurane significantly reduced the apoptosis of liver tissue cells. Apoptosis is a common phenomenon in the process of hepatic ischemia–reperfusion [ 25 , 26 ]. It has been reported that 50–70% of endothelial cells and 40–60% of hepatocytes underwent apoptosis during hepatic ischemia–reperfusion [ 27 ].…”

Section: Discussionmentioning

confidence: 99%

Sevoflurane relieves hepatic ischemia–reperfusion injury by inhibiting the expression of Grp78

Liu¹,

Jin²,

Zhang³

et al. 2018

Bioscience Reports

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Purpose: This article aimed to study the role of sevoflurane pre-conditioning in hepatic ischemia–reperfusion and its potential mechanism.Methods: Rat liver ischemia–reperfusion model was constructed. Serum TNF-α, IL-1β, IL-10, and IL-6 concentrations were detected by ELISA. Malondialdehyde (MDA), superoxide dismutase (SOD), and nitric oxide (NO) in liver homogenate were determined. Hematoxylin–Eosin (HE) staining, Tunel, and immunohistochemistry were performed. Ischemia–reperfusion hepatocyte model was established. Cells transfection was conducted. Apoptosis was observed by flow cytometry. Quantitative real-time PCR (qRT-PCR) and Western blotting analysis were used.Results: Compared with I/R group, liver damage degree, liver cell apoptosis, and glucose regulatory protein 78 (Grp78) expression was obviously reduced in rats of SEV group. TNF-α, IL-1β, and IL-6 concentrations were also significantly increased (P<0.01). MDA and NO concentrations were dramatically lower (P<0.01) and SOD concentration was significantly higher (P<0.01). Apoptosis rate, Grp78, PERK, eIF2α, and p-c-JNK/JNK expression was also significantly decreased (P<0.01). Sevoflurane significantly reduced apoptosis and expression of PERK, eIF2α, p-c-JNK/JNK by inhibiting the expression of Grp78 (P<0.01).Conclusion: Sevoflurane relieves hepatic ischemia–reperfusion injury by inhibiting the expression of Grp78.

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Quercetin Pretreatment Attenuates Hepatic Ischemia Reperfusion-Induced Apoptosis and Autophagy by Inhibiting ERK/NF-κB Pathway

Cited by 36 publications

References 58 publications

Vildagliptin Attenuates Hepatic Ischemia/Reperfusion Injury via the TLR4/NF‐κB Signaling Pathway

Vildagliptin Attenuates Hepatic Ischemia/Reperfusion Injury via the TLR4/NF‐κB Signaling Pathway

Therapeutic potential of PPARγ natural agonists in liver diseases

Sevoflurane relieves hepatic ischemia–reperfusion injury by inhibiting the expression of Grp78

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