Liensinine alleviates high fat diet (HFD)-induced non-alcoholic fatty liver disease (NAFLD) through suppressing oxidative stress and inflammation via regulating TAK1/AMPK signaling

2022 ◽  
Vol 104 ◽  
pp. 108306
Author(s):  
Liping Liang ◽  
Shiwei Ye ◽  
Ruilai Jiang ◽  
Xiao Zhou ◽  
Junjie Zhou ◽  
...  
2020 ◽  
Vol 11 (1) ◽  
pp. 1037-1048 ◽  
Author(s):  
Yuanyuan Hu ◽  
Fawen Yin ◽  
Zhongyuan Liu ◽  
Hongkai Xie ◽  
Yunsheng Xu ◽  
...  

Acerola polysaccharides ameliorate HFD-induced NAFLD by inhibiting lipogenesis, reducing oxidative stress and inflammation, and promoting the mitochondrial function in C57BL/6 mice.


2020 ◽  
Vol 11 (4) ◽  
pp. 2953-2968 ◽  
Author(s):  
Xiaobing Yang ◽  
Wenjing Mo ◽  
Chuanjin Zheng ◽  
Wenzhi Li ◽  
Jian Tang ◽  
...  

Non-alcoholic fatty liver disease is associated with gut microbiota, oxidative stress, and inflammation.


2021 ◽  
Author(s):  
Ankita Sharma ◽  
Sumit Kr Anand ◽  
Neha Singh ◽  
Akshay Dwarkanath ◽  
Upendra Nath Dwivedi ◽  
...  

Non-alcoholic fatty liver disease (NAFLD), a chronic metabolic disorder is concomitant with oxidative stress and inflammation.


Nutrients ◽  
2020 ◽  
Vol 12 (2) ◽  
pp. 480 ◽  
Author(s):  
Weixin Ke ◽  
Pan Wang ◽  
Xuehua Wang ◽  
Xiaolu Zhou ◽  
Xiaosong Hu ◽  
...  

The root of Platycodon grandiflorus (PG), with hepatoprotective and anti-oxidation effects, has a long history of being used as food and herbal medicine in Asia. However, the mechanism of PG against non-alcoholic fatty liver disease (NAFLD) is still not clear. The aim of this study was to investigate the mechanism of PG suppressing the development of NAFLD induced by a high-fat diet (HFD) in mice. Male C57BL/6J mice were fed with either a standard chow diet or a HFD, either supplemented with or without PG, for 16 weeks. Serum lipids, liver steatosis, oxidative stress and insulin sensitivity were determined. Expressions or activities of hepatic enzymes in the related pathways were analyzed to investigate the mechanisms. PG significantly reduced HFD-induced hepatic injury and hyperlipidemia, as well as hepatic steatosis via regulating phosphorylation of acetyl-CoA carboxylase (p-ACC) and expression of fatty acid synthase (FAS). In addition, PG ameliorated oxidative stress by restoring glutathione (GSH) content and antioxidant activities, and improved insulin sensitivity by regulating the PI3K/Akt/GSK3β signaling pathway. Our data showed that dietary PG have profound effects on hepatic insulin sensitivity and oxidative stress, two key factors in the pathogenesis of NAFLD, demonstrating the potential of PG as a therapeutic strategy for NAFLD.


2021 ◽  
Vol 11 (1) ◽  
Author(s):  
Takuya Kawamura ◽  
Hiroaki Tanaka ◽  
Ryota Tachibana ◽  
Kento Yoshikawa ◽  
Shintaro Maki ◽  
...  

AbstractWe aimed to investigate the effects of maternal tadalafil therapy on fetal programming of metabolic function in a mouse model of fetal growth restriction (FGR). Pregnant C57BL6 mice were divided into the control, L-NG-nitroarginine methyl ester (L-NAME), and tadalafil + L-NAME groups. Six weeks after birth, the male pups in each group were given a high-fat diet. A glucose tolerance test (GTT) was performed at 15 weeks and the pups were euthanized at 20 weeks. We then assessed the histological changes in the liver and adipose tissue, and the adipocytokine production. We found that the non-alcoholic fatty liver disease activity score was higher in the L-NAME group than in the control group (p < 0.05). Although the M1 macrophage numbers were significantly higher in the L-NAME/high-fat diet group (p < 0.001), maternal tadalafil administration prevented this change. Moreover, the epididymal adipocyte size was significantly larger in the L-NAME group than in the control group. This was also improved by maternal tadalafil administration (p < 0.05). Further, we found that resistin levels were significantly lower in the L-NAME group compared to the control group (p < 0.05). The combination of exposure to maternal L-NAME and a high-fat diet induced glucose impairment and non-alcoholic fatty liver disease. However, maternal tadalafil administration prevented these complications. Thus, deleterious fetal programming caused by FGR might be modified by in utero intervention with tadalafil.


2014 ◽  
Vol 10 (6) ◽  
pp. 2917-2923 ◽  
Author(s):  
XIANG WANG ◽  
QIAOHUA REN ◽  
TAO WU ◽  
YONG GUO ◽  
YONG LIANG ◽  
...  

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