Adiponectin alleviates non-alcoholic fatty liver injury via regulating oxidative stress in liver cells

Ma, Wenwen; Zhang, Shanshan; Li, Yang; Chen, Tansheng; Yang, Qin; Xue, Feng

doi:10.23736/s0026-4806.20.06734-8

Cited by 3 publications

(3 citation statements)

References 52 publications

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“…They are important biomarkers of oxidative stress [22]. Levels of SOD and MDA in liver tissue can reflect the extent of lipid peroxidation and the ability to eliminate free radicals [23]. As the primary end product of lipid peroxidation, MDA can directly activate Kupffer cells and hepatic stellate cells, ultimately leading to liver cell damage.…”

Section: Discussionmentioning

confidence: 99%

Protective Effects of Resveratrol on Cytotoxicity of Mouse Hepatic Stellate Cells Induced by PM2.5

Zhang,

Chen,

Bai

et al. 2024

Atmosphere

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The atmosphere’s fine particulate matter (PM2.5) can enter the liver through the circulatory system, leading to hepatic inflammation and fibrosis. As a non-flavonoid polyphenolic compound, resveratrol (RES) has anti-oxidant, anti-inflammatory and hepatoprotective effects, but the molecular mechanisms of liver fibrosis induced by PM2.5 exposure are still limited. In this study, we established an in vitro cell model to investigate the intervention effect of RES with different concentrations (5 and 20 μmol/mL) on mouse hepatic stellate cells (mHSCs) injury induced by PM2.5 (100 μg/mL). We determined the cell viability in mHSCs after treatment with PM2.5 or/and RES for 24 h. We investigated the intracellular oxidative stress by detecting the changes in reactive oxygen species (ROS), malondialdehyde (MDA), superoxide dismutase (SOD) and lactate dehydrogenase (LDH) levels. We also measured the protein expressions of fibrosis-related genes (α-SMA, Collagen I and Collagen III) and key genes (SIRT1, NF-κB, NLRP3, Cleaved-Caspase1, IL-1β) in the NLRP3 pathway in mHSCs exposed to PM2.5 with or without RES. The results showed that (1) PM2.5 has cytotoxic effects on mHSCs, whereas RES (5 μmol/L and 20 μmol/L) inhibited PM2.5-induced cytotoxicity and LDH leakage; (2) RES effectively reduces ROS and MDA production caused by PM2.5 while concurrently enhancing SOD levels, thereby improving cellular anti-oxidant capacity; (3) the expression of α-SMA, Collagen I and Collagen III were notably downregulated in the PM2.5 plus RES treatment group compared to the PM2.5-exposed group; (4) RES significantly increased SIRT1 expression and decreased the expression of NF-κB, NLRP3, Cleaved-Caspase1 and IL-1β in mHSCs exposure to PM2.5 compared to the PM2.5 group. These results demonstrate that RES can up-regulate SIRT1 and mitigate PM2.5-induced fibrosis by suppressing oxidative stress in mHSCs and the SIRT1/NF–κB/NLRP3 pathway activated by PM2.5.

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Section: Discussionmentioning

confidence: 99%

Protective Effects of Resveratrol on Cytotoxicity of Mouse Hepatic Stellate Cells Induced by PM2.5

Zhang,

Chen,

Bai

et al. 2024

Atmosphere

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“…In NAFLD patients, ADPN is reduced in the blood and liver, while a high level of ADPN reverses stress-induced decrease in SOD activity with increased MDA and TG [ 101 ]. ADPN also inhibits inflammasome activation in hepatocytes [ 102 ] and alleviates the injury of NAFLD cells by reducing oxidative stress [ 103 ]. Activation of ADPN receptors has a protective effect on fatty liver injury in HFD-fed goslings through regulating the AMPK and p38 MAPK signaling pathways, as well as the transcription factors such as PPARα, reducing the lipid content in blood and liver tissues, improving antioxidant capacity, and regulating apoptosis and autophagy [ 104 ].…”

Section: Molecular Mechanism Of Osteocalcin In Flhs Chickensmentioning

confidence: 99%

Osteocalcin and Its Potential Functions for Preventing Fatty Liver Hemorrhagic Syndrome in Poultry

Zhang

Jiang

et al. 2023

Animals

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Osteocalcin (OCN) is synthesized and secreted by differentiating osteoblasts. In addition to its role in bone, OCN acts as a hormone in the pancreas, liver, muscle, fat, and other organs to regulate multiple pathophysiological processes including glucose homeostasis and adipic acid metabolism. Fat metabolic disorder, such as excessive fat buildup, is related to non-alcoholic fatty liver disease (NAFLD) in humans. Similarly, fatty liver hemorrhage syndrome (FLHS) is a metabolic disease in laying hens, resulting from lipid accumulation in hepatocytes. FLHS affects hen health with significant impact on poultry egg production. Many studies have proposed that OCN has protective function in mammalian NAFLD, but its function in chicken FLHS and related mechanism have not been completely clarified. Recently, we have revealed that OCN prevents laying hens from FLHS through regulating the JNK pathway, and some pathways related to the disease progression have been identified through both in vivo and vitro investigations. In this view, we discussed the current findings for predicting the strategy for using OCN to prevent or reduce FLHS impact on poultry production.

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“…Adiponectin binds to receptors to participate in insulin-sensitizing, lipid metabolism, energy regulation, inflammation, and cancer development [22]. Circulating levels of adiponectin show an inverse correlation with multiple diseases, such as obesity, type 2 diabetes, atherosclerosis, hypertension, dyslipidemia, and nonalcoholic fatty liver disease [23][24][25][26][27]. It also negatively correlates with several cancers, one of which is MM [28,29].…”

Section: Adiponectinmentioning

confidence: 99%

Obesity as a risk factor for multiple myeloma: insight on the role of adipokines

Tie,

Ma,

et al. 2023

Pathol. Oncol. Res.

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Multiple myeloma (MM) is a hematologic disorder characterized by the accumulation of malignant plasma cells in the bone marrow. Genetic and environmental factors are contributed to the etiology of MM. Notably, studies have shown that obesity increases the risk of MM and worsens outcomes for MM patients. Adipokines play an important role in mediating the close association between MM and metabolic derangements. In this review, we summarize the epidemiologic studies to show that the risk of MM is increased in obese. Accumulating clinical evidence suggests that adipokines could display a correlation with MM. In vitro and in vivo studies have shown that adipokines are linked to MM, including roles in the biological behavior of MM cells, cancer-associated bone loss, the progression of MM, and drug resistance. Current and potential therapeutic strategies targeted to adipokines are discussed, proposing that adipokines can guide early patient diagnosis and treatment.

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Adiponectin alleviates non-alcoholic fatty liver injury via regulating oxidative stress in liver cells

Cited by 3 publications

References 52 publications

Protective Effects of Resveratrol on Cytotoxicity of Mouse Hepatic Stellate Cells Induced by PM2.5

Protective Effects of Resveratrol on Cytotoxicity of Mouse Hepatic Stellate Cells Induced by PM2.5

Osteocalcin and Its Potential Functions for Preventing Fatty Liver Hemorrhagic Syndrome in Poultry

Obesity as a risk factor for multiple myeloma: insight on the role of adipokines

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