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从桑椹果实（Morus nigra L.）中提取的多糖：改善 HO 诱导的 HepG2 细胞肝损伤的抗氧化作用。

Polysaccharides extracted from mulberry fruits (Morus nigra L.): antioxidant effect of ameliorating HO-induced liver injury in HepG2 cells.

机构信息

Key Laboratory of Characteristic Chinese Medicine Resources in Southwest China, College of Pharmacy, Chengdu University of Traditional Chinese Medicine, Chengdu, P. R. China.

College of Medical Technology, Chengdu University of Traditional Chinese Medicine, Chengdu, P. R. China.

出版信息

BMC Complement Med Ther. 2023 Apr 12;23(1):112. doi: 10.1186/s12906-023-03925-w.

DOI:10.1186/s12906-023-03925-w
PMID:37046263
原文链接:https://pmc.ncbi.nlm.nih.gov/articles/PMC10091537/
Abstract

BACKGROUND

Mori Fructus is an economical and readily available traditional Chinese medicine and food. Polysaccharides in Mori Fructus have clear antioxidant activity and have been found to alleviate oxidative stress (OS)-induced liver damage in experimental studies. The mechanism of regulation of cellular antioxidant activity by mulberry polysaccharides has been suggested to be Nrf2, but it is not clear whether the Nrf2 pathway is mediated by activation of other targets, and the exact process of effects in hepatocytes has yet to be elucidated.

METHODS

In this study, the basic characterization of total polysaccharides extracted from mulberry fruits (Morus nigra Linn.) was analyzed. A model of oxidative damage induced by HO in HepG2 cells was established. The levels of cellular oxidation-related markers, including ROS, SOD and Gpx, were then examined. Furthermore, Q-PCR and Western-blot were used to detect the expression of genes and proteins related to the PI3K/Akt-mediated Nrf2 signaling pathway.

RESULTS

The results showed that a total mulberry polysaccharides (TMP) has a molecular weight of 57.5 kDa with a pyranose ring mainly composed of glucose (48.81%), galactose (22.79%) and mannose (18.2%). TMP reduced the accumulation of ROS in HepG2 cells after HO treatment and modulated the activity of SOD and Gpx. Q-PCR and Western-blot showed that TMP could up-regulate the expression of p-PI3K, p-AKT, Nrf2, NQO1 and HO-1.

CONCLUSIONS

This study demonstrates that TMP can reduce ROS accumulation in HO-treated HepG2 cells and restore cell viability by activating the PI3K/AKT-mediated Nrf2 pathway. TMP may be a potent antioxidant agent that could slow down oxidative damage to the liver.

摘要

背景

桑椹是一种经济且易得的中药和食品。桑椹多糖具有明确的抗氧化活性，已在实验研究中发现可减轻氧化应激（OS）诱导的肝损伤。调节细胞抗氧化活性的桑椹多糖的机制被认为是 Nrf2，但尚不清楚 Nrf2 途径是否通过其他靶点的激活来介导，并且其在肝细胞中的确切作用过程仍有待阐明。

方法

本研究分析了从桑椹果实（Morus nigra Linn.）中提取的总多糖的基本特性。建立了 HO 诱导 HepG2 细胞氧化损伤的模型。然后检测细胞氧化相关标志物，包括 ROS、SOD 和 Gpx 的水平。此外，使用 Q-PCR 和 Western-blot 检测与 PI3K/Akt 介导的 Nrf2 信号通路相关的基因和蛋白的表达。

结果

结果表明，总桑椹多糖（TMP）的分子量为 57.5 kDa，吡喃糖环主要由葡萄糖（48.81%）、半乳糖（22.79%）和甘露糖（18.2%）组成。TMP 可减少 HO 处理后 HepG2 细胞中 ROS 的积累，并调节 SOD 和 Gpx 的活性。Q-PCR 和 Western-blot 表明，TMP 可以上调 p-PI3K、p-AKT、Nrf2、NQO1 和 HO-1 的表达。

结论

本研究表明，TMP 可以通过激活 PI3K/AKT 介导的 Nrf2 通路减少 HO 处理的 HepG2 细胞中 ROS 的积累并恢复细胞活力。TMP 可能是一种有效的抗氧化剂，可以减缓肝脏的氧化损伤。

https://cdn.ncbi.nlm.nih.gov/pmc/blobs/eeb0/10091537/d85baa4c55bf/12906_2023_3925_Fig8_HTML.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/eeb0/10091537/d0b6190b9d65/12906_2023_3925_Fig1_HTML.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/eeb0/10091537/770ea98c3129/12906_2023_3925_Fig2_HTML.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/eeb0/10091537/694e3348fabc/12906_2023_3925_Fig3_HTML.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/eeb0/10091537/c098bd2e060b/12906_2023_3925_Fig4_HTML.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/eeb0/10091537/1aec6647f521/12906_2023_3925_Fig5_HTML.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/eeb0/10091537/0203e639b927/12906_2023_3925_Fig6_HTML.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/eeb0/10091537/7a2c2695f115/12906_2023_3925_Fig7_HTML.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/eeb0/10091537/d85baa4c55bf/12906_2023_3925_Fig8_HTML.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/eeb0/10091537/d0b6190b9d65/12906_2023_3925_Fig1_HTML.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/eeb0/10091537/770ea98c3129/12906_2023_3925_Fig2_HTML.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/eeb0/10091537/694e3348fabc/12906_2023_3925_Fig3_HTML.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/eeb0/10091537/c098bd2e060b/12906_2023_3925_Fig4_HTML.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/eeb0/10091537/1aec6647f521/12906_2023_3925_Fig5_HTML.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/eeb0/10091537/0203e639b927/12906_2023_3925_Fig6_HTML.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/eeb0/10091537/7a2c2695f115/12906_2023_3925_Fig7_HTML.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/eeb0/10091537/d85baa4c55bf/12906_2023_3925_Fig8_HTML.jpg

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