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Study on the Hepatoprotection of Caulis Polysaccharides in Nonalcoholic Fatty Liver Disease in Rats Based on Metabolomics

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Journal Front Pharmacol
Date 2021 Oct 8
PMID 34621168
Citations 7
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Abstract

The aim of this study was to investigate the hepatoprotection of Caulis polysaccharides (SCPs) in the nonalcoholic fatty liver disease (NAFLD) induced by high-fat diet (HFD) in rats. A total of 30 Wistar rats were randomly divided into the control group (CON), model group (MOD), and caulis polysaccharide (SCP) group. Except for those in the CON group, the other rats were fed with high-fat diet for 4 weeks to establish an NAFLD model. From the 5th week, rats in the SCP group were given SCP solution (100 mg kg) by gavage for 6 weeks, and those in the CON and MOD groups were given an equal volume of distilled water in the same way. Aspartate aminotransferase (AST), alanine aminotransferase (ALT), triglyceride (TG), total cholesterol (TC), low-density lipoprotein cholesterol (LDL-C), high-density lipoprotein cholesterol (HDL-C) levels in serum, the malondialdehyde (MDA) level, glutathione peroxidase (GSH-Px), and superoxide dismutase (SOD) activities in the liver tissue were detected. The small molecular metabolites in the blood of rats were determined by the metabolomics method of ultra-high-performance liquid chromatography-quadrupole/electrostatic field orbitrap high-resolution mass spectrometry (UHPLC-Q-Orbitrap-MS/MS) combined with multivariate analysis. The enrichment analysis and pathway analysis of the different metabolites were carried out. The therapeutic mechanism of SCP in NAFLD rats was verified by western blot. The results showed that the levels of AST, ALT, TG, TC, and LDL-C in the serum of rats in the SCP group were significantly lower, and the levels of HDL-C were significantly higher than those in the MOD group. The screening and analysis of the metabolic pathways showed that SCP could alleviate the development of NAFLD by regulating the expression of UDP-glucose pyrophosphorylase (UGP2), UDP-glucose 6-dehydrogenase (UGDH), acetyl CoA carboxylase (ACC), and fatty acid synthase (FAS) in the liver of NAFLD rats. This study may provide a theoretical basis for the development and utilization of SCP.

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References
1.
Watt M, Miotto P, De Nardo W, Montgomery M . The Liver as an Endocrine Organ-Linking NAFLD and Insulin Resistance. Endocr Rev. 2019; 40(5):1367-1393. DOI: 10.1210/er.2019-00034. View

2.
Zhang L, Qi Y, Aluo Z, Liu S, Zhang Z, Zhou L . Betaine increases mitochondrial content and improves hepatic lipid metabolism. Food Funct. 2018; 10(1):216-223. DOI: 10.1039/c8fo02004c. View

3.
Luangmonkong T, Suriguga S, Mutsaers H, Groothuis G, Olinga P, Boersema M . Targeting Oxidative Stress for the Treatment of Liver Fibrosis. Rev Physiol Biochem Pharmacol. 2018; 175:71-102. DOI: 10.1007/112_2018_10. View

4.
Baumann A, Jin C, Brandt A, Sellmann C, Nier A, Burkard M . Oral Supplementation of Sodium Butyrate Attenuates the Progression of Non-Alcoholic Steatohepatitis. Nutrients. 2020; 12(4). PMC: 7231312. DOI: 10.3390/nu12040951. View

5.
Kim H . Recent advances in nonalcoholic fatty liver disease metabolomics. Clin Mol Hepatol. 2021; 27(4):553-559. PMC: 8524071. DOI: 10.3350/cmh.2021.0127. View