Astragaloside IV inhibits protein tyrosine phosphatase 1B and improves insulin resistance in insulin-resistant HepG2 cells and triglyceride accumulation in oleic acid (OA)-treated HepG2 cells

Zhang, Xiao; Wang, Lin Lin; Tang, Wen Jing; Tang, Biao

doi:10.1016/j.jep.2020.113556

Cited by 33 publications

(21 citation statements)

References 24 publications

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“…Liu et al found that Astragaloside IV could inhibit the levels of pro-inflammatory cytokines through Toll-like receptor 4 (TLR4)/myeloid differentiation primary response gene 88 (MyD88)/nuclear factor kappa-B (NF-κB) signaling pathway, ultimately alleviating hepatic steatosis in mice induced by a high-fat diet [10]. Moreover, Astragaloside IV could inhibit the protein expression levels of protein tyrosine phosphatase 1B and sterol element regulatory binding protein-1c to block the triglyceride (TG) accumulation in HepG2 cells challenged on oleic acid [11]. It has been shown that Astragaloside IV exerts a beneficial function on mitigating diabetic nephropathy via suppressing oxidative stress, inflammatory response, epithelial-mesenchymal transition, as well as the Wnt/βcatenin signaling pathway [12].…”

Section: Introductionmentioning

confidence: 99%

“…Dong et al showed that AP could reduce the gene expression of inflammatory factors and chemokines by inhibiting the phosphorylation of NF-κB in lipopolysaccharide-stimulated porcine intestinal epithelial cells, and the alleviation of inflammatory response was verified in BALB/c mice after AP administration [14]. Studies have shown that AS and AP possess other biological activities, such as anti-tumor, anti-apoptosis, neuroprotection, and anti-Parkinson properties, as well as the improvement of insulin resistance [11,[15][16][17], whereas the role of AS and AP in attenuating ALD remains poorly understood. In view of these bioactive properties above, we wondered whether AS and AP were potentially of benefit for the management of ALD.…”

Section: Introductionmentioning

confidence: 99%

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Astragalus Polysaccharides and Saponins Alleviate Liver Injury and Regulate Gut Microbiota in Alcohol Liver Disease Mice

Zhou

Zhang

Zhao

et al. 2021

Foods

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Astragalus, a medical and edible plant in China, shows several bioactive properties. However, the role of astragalus in attenuating alcoholic liver disease (ALD) is less clear. The objective of this project is to investigate the improving effect of astragalus saponins (AS) and astragalus polysaccharides (AP), which are the two primary constituents in astragalus on hepatic injury induced by alcohol, and the potential mechanisms of action. Different doses of AS (50 and 100 mg/kg bw) and AP (300 and 600 mg/kg bw) were orally given to alcohol-treated mice for four weeks. The results demonstrated that both AP and AS could reverse the increase of the levels of TC, TG, FFA, and LDL-C in serum, and the decrease of serum HDL-C content, as well as the elevation of hepatic TC and TG levels induced by alcohol. The activities of AST, ALT, ALP, and γ-GT in ALD mice were raised after AP and AS supplementation. The antioxidant markers (SOD, CAT, GSH, and GSH-Px) were obviously augmented and the pro-inflammatory cytokines (TNF-α, IL-6 and IL-1β) and hepatic histological variations were alleviated by AP and AS, which was in line with the levels of oxidative stress-associated genes (Keap1, Nfe2l2, Nqo1, and Hmox1) and inflammation-associated genes (Tlr4, Myd88 and Nfkb1). In addition, AS exerted a more efficient effect than AP and the results presented dose proportionality. Moreover, AS and AP could modulate the intestinal microbiota disturbance induced by alcohol. Overall, AS and AP administration could ameliorate lipid accumulation in the serum and liver, as well as hepatic function, oxidative stress, inflammatory response, and gut flora disorders in mice as a result of alcohol.

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Section: Introductionmentioning

confidence: 99%

Section: Introductionmentioning

confidence: 99%

Astragalus Polysaccharides and Saponins Alleviate Liver Injury and Regulate Gut Microbiota in Alcohol Liver Disease Mice

Zhou

Zhang

Zhao

et al. 2021

Foods

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“…In addition, PTP1B levels were significantly elevated in the hepatocytes of fructose-fed hamsters, HFD-fed mice, and fatty liver and insulin-resistant animal models [ 50 ]. The overexpression of PTP1B in liver cells increased the expression level and transcriptional activity of SREBP1, which resulted in the increased synthesis of liver triacylglycerols and fatty acids [ 51 ]. This was due to the enhanced transcriptional activity of the recombinant SP1 site in the SREBP1 promoter by increasing the activity of PP2A when PTP1B was overexpressed [ 52 ].…”

Section: Discussionmentioning

confidence: 99%

Melatonin Alleviates PM2.5-Induced Hepatic Steatosis and Metabolic-Associated Fatty Liver Disease in ApoE-/- Mice

Liang

et al. 2022

Oxidative Medicine and Cellular Longevity

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Background. Exposure to fine particulate matter (PM2.5) is associated with the risk of developing metabolic-associated fatty liver disease (MAFLD). Melatonin is the main secreted product of the pineal gland and has been reported to prevent hepatic lipid metabolism disorders. However, it remains uncertain whether melatonin could protect against PM2.5-induced MAFLD. Methods and Results. The purpose of our study was to investigate the mitigating effects of melatonin on hepatic fatty degeneration accelerated by PM2.5 in vivo and in vitro. Histopathological analysis and ultrastructural images showed that PM2.5 induced hepatic steatosis and lipid vacuolation in ApoE-/- mice, which could be effectively alleviated by melatonin administration. Increased ROS production and decreased expression of antioxidant enzymes were detected in the PM2.5-treated group, whereas melatonin showed recovery effects after PM2.5-induced oxidative damage in both the liver and L02 cells. Further investigation revealed that PM2.5 induced oxidative stress to activate PTP1B, which in turn had a positive feedback regulation effect on ROS release. When a PTP1B inhibitor or melatonin was administered, SP1/SREBP-1 signalling was effectively suppressed, while Nrf2/Keap1 signalling was activated in the PM2.5-treated groups. Conclusion. Our study is the first to show that melatonin alleviates the disturbance of PM2.5-triggered hepatic steatosis and liver damage by regulating the ROS-mediated PTP1B and Nrf2 signalling pathways in ApoE-/- mice. These results suggest that melatonin administration might be a prospective therapy for the prevention and treatment of MAFLD associated with air pollution.

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“…PTP1B is a reported negative regulator of the insulin signaling pathway as illustrated in Figure 6 ( Ma et al, 2011 ; Zhou et al, 2021 ). The group studied the effect of PTP1B inhibitor CCF06240 on lipid metabolic abnormalities and insulin sensitivity in vitro and in vivo .…”

Section: Discussionmentioning

confidence: 99%

“…Several studies reported strong correlation between PTP1B expression and insulin resistant state ( Choi and Kim, 2010 ; Panzhinskiy et al, 2013 ; Zhou et al, 2021 ). Insulin-stimulated glucose disposal has been significantly improved in PTP1B deficient mice, thus reducing overexpression of PTP1B may enhance the insulin signaling pathway ( Klaman et al, 2000 ).…”

Section: Introductionmentioning

confidence: 99%

Evaluation of the Hypoglycemic Activity of Morchella conica by Targeting Protein Tyrosine Phosphatase 1B

et al. 2021

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Morchella conica (M. conica) Pers. is one of six wild edible mushrooms that are widely used by Asian and European countries for their nutritional value. The present study assessed the anti-diabetic potential of M. conica methanolic extract (100 mg/kg body weight) on streptozotocin (STZ)-induced diabetic mice. STZ was used in a single dose of 65 mg/kg to establish diabetic models. Body weights, water/food intake and fasting blood glucose levels were measured. Histopathological analysis of the pancreas and liver were performed to evaluate STZ-induced tissue injuries. In addition, in vitro assays such as α-amylase and protein tyrosine phosphatase 1B (PTP1B) inhibitory, antiglycation, antioxidant and cytotoxicity were performed. The in vitro study indicated potent PTP1B inhibitory potential of M. conica with an IC50 value of 26.5 μg/ml as compared to the positive control, oleanolic acid (IC50 36.2 μg/ml). In vivo investigation showed a gradual decrease in blood sugar level in M. conica-treated mice (132 mg/dl) at a concentration of 100 mg/kg as compared to diabetic mice (346 mg/dl). The extract positively improved liver and kidney damages as were shown by their serum glutamic pyruvic transaminase, serum glutamic oxaloacetate, alkaline phosphatase, serum creatinine and urea levels. Histopathological analysis revealed slight liver and pancreas improvement of mice treated with extract. Cytotoxicity assays displayed lower IC50 values. Based on the present results of the study, it may be inferred that M. conica are rich in bioactive compounds responsible for antidiabetic activity and this mushroom may be a potential source of antidiabetic drug. However, further studies are required in terms of isolation of bioactive compounds to validate the observed results.

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Astragaloside IV inhibits protein tyrosine phosphatase 1B and improves insulin resistance in insulin-resistant HepG2 cells and triglyceride accumulation in oleic acid (OA)-treated HepG2 cells

Cited by 33 publications

References 24 publications

Astragalus Polysaccharides and Saponins Alleviate Liver Injury and Regulate Gut Microbiota in Alcohol Liver Disease Mice

Astragalus Polysaccharides and Saponins Alleviate Liver Injury and Regulate Gut Microbiota in Alcohol Liver Disease Mice

Melatonin Alleviates PM2.5-Induced Hepatic Steatosis and Metabolic-Associated Fatty Liver Disease in ApoE-/- Mice

Evaluation of the Hypoglycemic Activity of Morchella conica by Targeting Protein Tyrosine Phosphatase 1B

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