Qushi Huayu Decoction Ameliorates Non-Alcoholic Steatohepatitis Induced by High-Fat Diet in Mouse Associated with Regulation on Microbiota Composition and Mitogen-Activated Protein Kinase Pathways in the Intestine

2019 ◽  
Author(s):  
Jing Leng ◽  
Fu Huang ◽  
Yamei Hai ◽  
Huajie Tian ◽  
Wei Liu ◽  
...  
PLoS ONE ◽  
2014 ◽  
Vol 9 (9) ◽  
pp. e106300 ◽  
Author(s):  
Jan Freark de Boer ◽  
Arne Dikkers ◽  
Angelika Jurdzinski ◽  
Johann von Felden ◽  
Matthias Gaestel ◽  
...  

2021 ◽  
Vol 13 (9) ◽  
pp. 1666-1673
Author(s):  
Zhidong Chen ◽  
Kankai Tang ◽  
Wei Xu ◽  
Fengqi Liu ◽  
Bingnan Zhu ◽  
...  

This study aimed at elucidating the effect of astragaloside on atherosclerosis coupled inflammation and potential mechanism in mice. C57BL/6J mice were maintained in high-fat diet (HFD) for 12 weeks to induce atherosclerosis, with or without treatment with astragaloside (50 mg/kg). In turn, serum biochemical parameters in mice were also evaluated. Multiple tissue stain assay, including HE, were employed to assess the pathological alterations in arteries, and blood inflammation mediators were examined using ELISA. Expressions of microRNA101 (miR-101), p-p38 and mitogen-activated protein kinase phosphatase-1 (MKP-1) in the arteries were evaluated by qPCR and Western blot. Finally, AML-193 cells were transfected by miR-101 mimics and inhibitors. Expression of miR-101, MKP-1 and downstream inflammation cytokines were then analyzed. High-fat diet (HFD) mice with astragaloside treatment exhibited reduced atherosclerotic plaques size evaluated by oil red o, improved hepatocyte steatosis, and increased collagen fibers in atherosclerotic plaques for more stable plaque. Further, astragaloside treatment suppressed miR-101 transcription and enhanced MKP-1 expression, thus restraining the secretion of inflammation factors in vitro. Moreover, the inhibited impact of astragaloside in inflammatory factors production was ineffective in the presence of miR-101 mimics in AML-193 cells stimulated by LPS. Astragaloside exerted an anti-inflammatory role through miR-101/MKP-1/p38 signaling, for reducing atherosclerotic plaques and alleviate inflammation damage in mice and AML-193 cell.


2014 ◽  
Vol 35 (1) ◽  
pp. 26-40 ◽  
Author(s):  
Ahmed Lawan ◽  
Lei Zhang ◽  
Florian Gatzke ◽  
Kisuk Min ◽  
Michael J. Jurczak ◽  
...  

The liver plays a critical role in glucose metabolism and communicates with peripheral tissues to maintain energy homeostasis. Obesity and insulin resistance are highly associated with nonalcoholic fatty liver disease (NAFLD). However, the precise molecular details of NAFLD remain incomplete. The p38 mitogen-activated protein kinase (MAPK) and c-Jun NH2-terminal kinase (JNK) regulate liver metabolism. However, the physiological contribution of MAPK phosphatase 1 (MKP-1) as a nuclear antagonist of both p38 MAPK and JNK in the liver is unknown. Here we show that hepatic MKP-1 becomes overexpressed following high-fat feeding. Liver-specific deletion of MKP-1 enhances gluconeogenesis and causes hepatic insulin resistance in chow-fed mice while selectively conferring protection from hepatosteatosis upon high-fat feeding. Further, hepatic MKP-1 regulates both interleukin-6 (IL-6) and fibroblast growth factor 21 (FGF21). Mice lacking hepatic MKP-1 exhibit reduced circulating IL-6 and FGF21 levels that were associated with impaired skeletal muscle mitochondrial oxidation and susceptibility to diet-induced obesity. Hence, hepatic MKP-1 serves as a selective regulator of MAPK-dependent signals that contributes to the maintenance of glucose homeostasis and peripheral tissue energy balance. These results also demonstrate that hepatic MKP-1 overexpression in obesity is causally linked to the promotion of hepatosteatosis.


2021 ◽  
Vol 11 (1) ◽  
Author(s):  
Onrapak Reamtong ◽  
Tipparat Thiangtrongjit ◽  
Nathamon Kosoltanapiwat ◽  
Watanalai Panbangred ◽  
Pattaneeya Prangthip

AbstractSeveral studies have shown that probiotics and synbiotics ameliorate dyslipidemia. However, the molecular mechanisms mediating their effects remain to be determined. Therefore, we aimed to compare the effects of a probiotic, a prebiotic, and a synbiotic in dyslipidemic Sprague–Dawley rats, and explore the mechanisms involved using a proteomic approach. The rats were allocated to five groups: a control group that was fed normal chow, and four high-fat diet-fed groups, three of which were administered a probiotic (Lactobacillus acidophilus), a prebiotic (inulin), or a combination of the two (a synbiotic) for 30 days. We showed that the administration of inulin, and especially L. acidophilus, improved the lipid profile and reduced the serum concentrations of inflammatory markers in high-fat diet-fed rats. Proteomic analysis showed changes in lipid elongation, glycerolipid metabolism, activation of antioxidants, and a reduction in the activation of the mitogen-activated protein kinase signaling pathway in the livers of rats administered L. acidophilus, which likely mediate its beneficial effects on inflammation and dyslipidemia by reduced the levels of 18.56% CRP, 35.71% TNF-α 25.6% LDL-C and 28.57% LDL-C/HDL-C ratio when compared to HF group. L. acidophilus and inulin may represent effective natural means of maintaining inflammation and dyslipidemia.


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