Effect of Polygonum Multiflorum Thunb on liver fatty acid content in aging mice induced by D-galactose

Abstract

Background Polygonum Multiflorum Thunb (PMT) has multiple biological effects, such as anti-inflammatory, lipid-lowering, anti-aging and so on. Therefore, D-galactose-induced aging mice were used to study the effect of PMT on fatty acid metabolism and its underlying mechanism. Methods C57BL/6 male mice were randomly divided into normal group, aging model group, PMT intragastrical administration group (high, Medium, low); model group and PMT intragastrical administration group Daily intraperitoneal injection D-galactose 800 mg·ml − 1 ·Kg − 1 to establish subacute aging model; PMT intragastrical administration group at the same time to intragastrical PMT extract (1 g·ml − 1 ·Kg − 1 , 0.6 g·ml − 1 ·Kg − 1 , 0.3 g·ml − 1 ·Kg − 1 ), normal group injection and intragastrical equivalent saline for 60 consecutive days. By detecting the oxidation index of liver to judge the efficacy of PMT, gas chromatography-mass spectrometry (GC-MS) analysis was used to quantitatively analyze the fatty acid content in liver. Results Finally, we found that PMT improved the enzyme activity of superoxide dismutase (SOD) and glutathione peroxidase (GSH-Px) in aging mice, and reduce the enzyme activity of malondialdehyde (MDA), aspartate aminotransferase (AST) and alanine aminotransferase (ALT). The content of fatty acids such as C18:1, C18:2, C18:3 N3, C20:2 and C20:3 N3 decreased significantly in senescent mice ( P < 0.05) as evidenced by GC-MS analysis, whereas, these fatty acids increased significantly after treatment of PMT ( P < 0.05). Conclusion PMT improves the content of liver fatty acids in aging mice induced by D-galactose through, enhancing the activity of anti-oxidant enzymes.

Pathophysiological study of atorvastatin drug on toxicity induced by D-galactose in liver of experimental rats

“…The activity of these enzymes rises when the liver is inflamed or dysfunctional. ALT, AST, and ALP levels in the serum and liver of animals treated with D-galactose were found to be significantly elevated in previous studies (Chen et al, 2011(Chen et al, , 2018Huang et al, 2013;Kong et al, 2018;Lin et al, 2018;Liu et al, 2019;Mo et al, 2017;Mohammadi et al 2018;Shahroudi et al 2017;Taghipour et al, 2019;Wang et al, 2018;Yang et al, 2019). However, our results reveal that coadministration of atorvastatin 10,20, and 40 mg per kg with Dgalactose reduce the toxic effects of D-galactose on hepatocytes by a decrease in both ALT and AST.…”

“…Because D-galactose is primarily processed in the liver, a high level of D-galactose in the body might hurt the liver. Treatment with Dgalactose has been shown to cause oxidative stress in the liver by increasing Nitric oxide, malondialdehyde, and 8-hydroxy-2-deoxyguanosine while decreasing Catalase, glutathione peroxidase, superoxide dismutase, nitric oxide synthase, reduced glutathione, and total antioxidant capacity in liver tissues (Chen et al, 2011(Chen et al, , 2018Feng et al, 2016;Ji et al, 2017;Kong et al, 2018;Lei et al, 2016;Li et al, 2005;Liu et al, 2018;Mo et al, 2017;Mohammadi et al, 2018;Noureen et al, 2019;Shahroudi et al, 2017;Xu et al, 2016;Yang et al, 2019;Zhuang et al, 2017). The intracellular (p38 mitogen-activated protein kinasenuclear factor erythroid 2-heme oxygenase-1) ( p38 MAPK-NRF2-HO-1) signaling pathway in the liver has been shown to activate by D-galactose therapy (Gao et al, 2018;Lin et al, 2018).…”

A Candidate Drug for Nonalcoholic Fatty Liver Disease: A Review of Pharmacological Activities of Polygoni Multiflori Radix

“…Besides, PMR upregulated mRNA expression in the nuclear factor erythroid 2-related factor 2 (Nrf2) signal pathway including heme oxygenase-1 (HO-1), NQO1, and glutamate-cysteine ligase catalytic subunit (GCLc) dose-dependently and influenced the nuclear translocation of Nrf2 as well as reduced the content of ROS in H 2 O 2 -and acetaminophen-(APAP-) induced cells [43]. The enzyme activities of SOD, GSH, GRD, GSH-Px, and GST were improved by PMR in Dgalactose-injected mice and CCl 4 -induced mice [44,46]. PMR and PMRP improved mitochondrial β-oxidation by increasing the activity of CPT1A enzyme in vivo and in vitro [47].…”

“…PMR could alleviate the damage to the liver and might become a hepatoprotective medicine to treat NAFLD. The extract of PMR reduced the contents of AST and ALT in serum [42][43][44]48] and the production of malondialdehyde (MDA) compared with CCl 4 -induced liver damage. In addition, the TNF-α was reduced and histopathology examination showed relieved adipose tissue and necrosis in the PMR treatment group [48].…”

Integration of lncRNA and mRNA profiles to reveal the protective effects of Codonopsis pilosula extract on the gastrointestinal tract of mice subjected to D‑galactose‑induced aging

“…Integration of lncRNA and mRNA profiles to reveal the protective effects of Codonopsis pilosula extract on the gastrointestinal tract of mice subjected to D-galactose-induced aging aging is often used for studies of aging and anti-aging (6)(7)(8).…”