The Dietary Supplement <i>γ</i>‐Oryzanol Attenuates Hepatic Ischemia Reperfusion Injury via Inhibiting Endoplasmic Reticulum Stress and HMGB1/NLRP3 Inflammasome

Du, Yichao; Zhong, Furui; Cheng, Huanli; Li, Tongxi; Chen, Yifan; Tan, Peng; Huang, Meizhou; Liang, Tiancheng; Liu, Yu; Fu, Wenguang

doi:10.1155/2021/4628050

Cited by 14 publications

(9 citation statements)

References 46 publications

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“…The results of the existing study showed that the ischemic reperfused animals exhibited an increase in the gene expression of HMGB1, TLR4, NFκB, and NLP3, suggesting amplified HMGB1/TLR4/NFκB/NLP3 pathways associated with ischemia reperfusion-induced damage. Previous reports have shown the detrimental roles of these pathways [ 26 , 30 , 31 ]. HMGB1 is released as an early mediator of ischemia-reperfusion [ 5 ].…”

Section: Discussionmentioning

confidence: 99%

Ameliorative Effect of D-Carvone against Hepatic Ischemia-Reperfusion-Induced Injury in Rats

Mohamed

Younis

2022

Life

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Background: D-carvone is a monoterpene that exists in the essential oils of several plant species. Hepatic ischemia-reperfusion (Hep I/R) takes place clinically during different scenarios of liver pathologies. The aim of the current investigation is to disclose the hepato-protective actions of carvone against Hep I/R-induced damage and to reveal the underlying mechanism. Material and methods: Rats were assigned into five groups: sham and carvone plus sham groups, in which rats were administered either saline or carvone orally for three weeks prior to the induction of Hep I/R. In the Hep I/R group, rats were administered saline orally prior to the Hep I/R induction operation. The carvone 25 plus Hep I/R and Carvone 50 plus Hep I/R groups were administered carvone (25 and 50 mg/kg, respectively) for three weeks, followed by the induction of Hep I/R. Results: Liver ischemic animals demonstrated impaired liver function, several histopathological variations, and reduced levels of antioxidant enzyme activities. Furthermore, the Hep I/R groups showed the elevated gene expression of high-mobility group box 1 (HMGB1), toll-like receptors 4 (TLR4), nuclear factor kappa B (NFκB), and LR family pyrin domain containing 3 (NLP3), with subsequent escalated adhesion molecule 1 (ICAM-1), neutrophil infiltration, and several inflammatory mediators, including interleukin 1 beta (IL-1β), interleukin 6 (IL-6), and tumor necrosis factor α (TNF-α), as well as apoptotic markers. Pretreatment with D-carvone alleviated ischemia/reperfusion-induced impaired liver function, diminished the histopathological deviations, and augmented the antioxidant enzymes. In addition, D-carvone mitigated the gene expression of HMGB1, TLR4, NFκB, and NLP3, with a subsequent reduction in ICAM-1, neutrophils infiltration, inflammatory mediators, and apoptotic markers. Conclusion: Rats pretreated with D-carvone exhibited hepato-protective actions against Hep I/R-induced damage via the downregulation of HMGB1, TLR4, NFκB, NLP3, associated inflammatory mediators, and apoptotic markers.

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Section: Discussionmentioning

confidence: 99%

Ameliorative Effect of D-Carvone against Hepatic Ischemia-Reperfusion-Induced Injury in Rats

Mohamed

Younis

2022

Life

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“…γ- Oryzanol (ORY), an important bioactive ingredient isolated from rice bran oil, has anti-inflammation and anti-oxidation properties and can exert protective effects in a variety of liver disease models [ 140 , 141 ]. Du et al found that ORY protected the liver from I/R-induced inflammasome activation and apoptosis by inhibiting the HMGB1/NLRP3/IL-1β signaling pathway by establishing a hepatic 70% warm ischemia-reperfusion model after mice were fed ORY for seven days [ 142 ]. Studies have also shown that dietary restrictions exert protective effects in IRI in multiple organs, including the liver [ 143 , 144 ].…”

Section: Nlrp3 Inflammasome and Programmed Cell Death In Alimentioning

confidence: 99%

The Role of the NLRP3 Inflammasome and Programmed Cell Death in Acute Liver Injury

Chen

Miao

et al. 2023

IJMS

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Acute liver injury (ALI) is a globally important public health issue that, when severe, rapidly progresses to acute liver failure, seriously compromising the life safety of patients. The pathogenesis of ALI is defined by massive cell death in the liver, which triggers a cascade of immune responses. Studies have shown that the aberrant activation of the nod-like receptor protein 3 (NLRP3) inflammasome plays an important role in various types of ALI and that the activation of the NLRP3 inflammasome causes various types of programmed cell death (PCD), and these cell death effectors can in turn regulate NLRP3 inflammasome activation. This indicates that NLRP3 inflammasome activation is inextricably linked to PCD. In this review, we summarize the role of NLRP3 inflammasome activation and PCD in various types of ALI (APAP, liver ischemia reperfusion, CCl4, alcohol, Con A, and LPS/D-GalN induced ALI) and analyze the underlying mechanisms to provide references for future relevant studies.

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“…Similar results were obtained in AML12 cells (mouse normal hepatocytes) in vitro. Collectively, ORY improved HIRI by suppressing the NLRP3 inflammasome and ER stress [ 75 ]. Studies have revealed that the massive production of ROS is closely related to HIRI [ 76 ].…”

Section: The Role Of Endoplasmic Reticulum Stress and The Nlrp3 Infla...mentioning

confidence: 99%

The Role of Endoplasmic Reticulum Stress and NLRP3 Inflammasome in Liver Disorders

Lü

Huang

et al. 2022

IJMS

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The endoplasmic reticulum (ER) is a key organelle responsible for the synthesis, modification, folding and assembly of proteins; calcium storage; and lipid synthesis. When ER homeostatic balance is disrupted by a variety of physiological and pathological factors—such as glucose deficiency, environmental toxins, Ca2+ level changes, etc.—ER stress can be induced. Abnormal ER stress can be involved in many diseases. NOD-like receptor family pyrin domain-containing 3 (NLRP3), an intracellular receptor, can perceive internal and external stimuli. It binds to apoptosis-associated speck-like protein containing a CARD (ASC) and caspase-1 to assemble into a protein complex called the NLRP3 inflammasome. Evidence indicates that ER stress and the NLRP3 inflammasome participate in many pathological processes; however, the exact mechanism remains to be understood. In this review, we summarized the role of ER stress and the NLRP3 inflammasome in liver disorders and analyzed the mechanisms, to provide references for future related research.

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The Dietary Supplement γ‐Oryzanol Attenuates Hepatic Ischemia Reperfusion Injury via Inhibiting Endoplasmic Reticulum Stress and HMGB1/NLRP3 Inflammasome

Cited by 14 publications

References 46 publications

Ameliorative Effect of D-Carvone against Hepatic Ischemia-Reperfusion-Induced Injury in Rats

Ameliorative Effect of D-Carvone against Hepatic Ischemia-Reperfusion-Induced Injury in Rats

The Role of the NLRP3 Inflammasome and Programmed Cell Death in Acute Liver Injury

The Role of Endoplasmic Reticulum Stress and NLRP3 Inflammasome in Liver Disorders

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