Seed oil of Rosa roxburghii Tratt against non-alcoholic fatty liver disease in vivo and in vitro through PPARα/PGC-1α-mediated mitochondrial oxidative metabolism

Ni, Haiyan; Yu, Liang; Zhao, Xuelian; Wang, Litao; Zhao, Chunjian; Huang, Han; Zhu, Han-Lin; Efferth, Thomas; Gu, Cheng‐Bo; Fu, Yujie

doi:10.1016/j.phymed.2021.153919

Cited by 21 publications

(7 citation statements)

References 41 publications

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“…Peroxisome proliferator activated receptor γ coactivator-1α ( PGC1α ) is abundantly found in tissues that are rich in mitochondria. It plays a crucial role in lipid metabolism by activating fatty acid oxidation and key enzymes involved in mitochondrial respiration ( Ni et al, 2022 ). The RNA—Seq results revealed that the expression of CPT1A and PGC1α were significantly up-regulated in the MG500 group compared to the HFD group, suggesting that magnolol has the potential to enhance fatty acid oxidation.…”

Section: Discussionmentioning

confidence: 99%

Dietary supplementation of magnolol alleviates fatty liver hemorrhage syndrome in postpeak Xinhua laying hens via regulation of liver lipid metabolism

Chu,

Zheng,

et al. 2024

Poultry Science

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Section: Discussionmentioning

confidence: 99%

Dietary supplementation of magnolol alleviates fatty liver hemorrhage syndrome in postpeak Xinhua laying hens via regulation of liver lipid metabolism

Chu,

Zheng,

et al. 2024

Poultry Science

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“…Oxidative stress is high in hepatic steatosis, and its level is related to the severity of nonalcoholic fatty liver disease (NAFLD). 30 After liver ischemia-reperfusion, a cascade causing oxidative stress is activated; however, the antioxidant system is inhibited. The clearance of reactive oxygen species (ROS) is reduced, leading to a sharp increase in ROS, which produces oxidized protein that acts as a ligand for NLRP3 activation.…”

Section: Discussionmentioning

confidence: 99%

Activation of NLRP3 Inflammasome via Drp1 Overexpression in Kupffer Cells Aggravates Ischemia-reperfusion Injury in Hepatic Steatosis

Zhang¹,

Wang²,

An³

et al. 2023

J Clin Transl Hepatol

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Background and Aims Donors with fatty livers are considered to address the shortage of livers for transplantation, but those livers are particularly sensitive to ischemia-reperfusion injury (IRI), and an increased incidence of graft failure is observed. Kupffer cells account for 20–35% of liver nonparenchymal cells, and have been shown to participate in the process of IRI and inflammatory reactions of hepatic steatosis. NOD-like receptor thermal protein domain-associated protein 3 (NLRP3) is an intracellular sensor activated by Kupffer cells to promote generation and participates in IRI. Dynamics-associated protein 1 (Drp1) is one of the main proteins regulating mitochondrial division and exacerbates IRI by affecting mitochondrial dynamics. The mechanism of interaction of Kupffer cells with Drp1 and NLRP3 to aggravate IRI has not been clarified. Methods A mouse model of hepatic steatosis was established by feeding the mice with a high-fat diet. In vitro experiments were performed using AML12 normal mouse liver cells and RAW264.7 mononuclear macrophage cells cultured in medium with palmitate and oleic acid. Western blotting and immunohistochemical (IHC) staining were used to detect the expression of NLRPP3 and Drp1 in IRI in the control and high-fat diet groups. The expression of F4/80+ cells during IRI in hepatic steatosis was verified by IHC staining, and the role of NLRPP3 and Drp1 in Kupffer-cell mediated IRI was investigated by targeting Drp-1 inhibition. Results Drp1 and NLRP3 expression was increased during IRI in hepatic steatosis, and the expression of Drp1 and NLRP3 were decreased after the elimination of Kupffer cells. That indicated Kupffer cells were involved in the process of IRI in hepatic steatosis through the action of Drp1 and NLRP3. After Drp1 inhibition, liver function was restored and NLRP3 expression level was reduced. Conclusions Kupffer cells aggravated IRI in hepatic steatosis via NLRP3 and Drp1. Drp1 inhibitors might be useful as specific therapeutics to alleviate IRI in hepatic steatosis and may have promise in case of liver donor shortage.

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“…When exposed to cold stress (12°C ± 1°C), the body's demand for energy increases ( Zhang et al, 2014 ), and the body may compensate for the increase in energy expenditure by raising the β-oxidation levels of fatty acids under cold exposure ( Hauton et al, 2006 ; Yang et al, 2011 ). The peroxisome proliferator-activated receptor alpha ( PPARα )/peroxisome-proliferator-activated receptor coactivator 1α ( PGC-1α ) signaling pathway is considered a key pathway for promoting fatty acid oxidation and enhancing cellular energy metabolism ( Ni et al, 2022 ). The activation of the PPARα/PGC-1α signaling pathway can induce the expression of carnitine palmitoyl transferase 1 ( CPT1 ), acyl-coenzyme oxidase ( ACO ) and Acyl CoA synthase long-chain family member 1 ( ACSL1 ), and under the influence of the coactivator PGC-1α, promote fatty acid β-oxidation ( Grabacka et al, 2016 ; Coleman, 2019 ; Zhang et al, 2023 ).…”

Section: Introductionmentioning

confidence: 99%

Intermittent cold stimulation affects energy metabolism and improves stress resistance in broiler heart

Li,

Wei,

Zhang

et al. 2024

Poultry Science

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Seed oil of Rosa roxburghii Tratt against non-alcoholic fatty liver disease in vivo and in vitro through PPARα/PGC-1α-mediated mitochondrial oxidative metabolism

Cited by 21 publications

References 41 publications

Dietary supplementation of magnolol alleviates fatty liver hemorrhage syndrome in postpeak Xinhua laying hens via regulation of liver lipid metabolism

Dietary supplementation of magnolol alleviates fatty liver hemorrhage syndrome in postpeak Xinhua laying hens via regulation of liver lipid metabolism

Activation of NLRP3 Inflammasome via Drp1 Overexpression in Kupffer Cells Aggravates Ischemia-reperfusion Injury in Hepatic Steatosis

Intermittent cold stimulation affects energy metabolism and improves stress resistance in broiler heart

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