Background

Ginseng polysaccharides (GP) have been found to exhibit significant immune regulatory effects, making them a promising candidate for treating immune-related diseases. However, their mechanism of action in immune liver injury is not yet clear. The innovation of this study lies in exploring the mechanism of action of ginseng polysaccharides (GP) in immune liver injury. While GP has been previously identified for its immune regulatory effects, this study aims to provide a clearer understanding of its therapeutic potential for immune-related liver diseases.

Purpose

The purpose of this study is to characterize low molecular weight gingeng polysaccharides (LGP), investigate their effect on ConA-induced autoimmune hepatitis (AIH), and identify their potential molecular mechanisms.

Methods

LGP was extracted and purified using water-alcohol precipitation, DEAE-52 cellulose column, and Sephadex G200. And its structure was analyzed. It was then evaluated for anti-inflammatory and hepatoprotective effects in ConA-induced cells and mice, assessing cellular viability and inflammation with Cell Counting Kit-8 (CCK-8), Reverse Transcription-polymerase Chain Reaction (RT-PCR), and Western Blot, and hepatic injury, inflammation, and apoptosis with various biochemical and staining methods.

Results

LGP is a polysaccharide composed of glucose (Glu), galactose (Gal), and arabinose (Ara), with a molar ratio of 12.9:1.6:1.0. LGP has a low crystallinity amorphous powder structure and is free from impurities. LGP enhances cell viability and reduces inflammatory factors in ConA-induced RAW264.7 cells and inhibits inflammation and hepatocyte apoptosis in ConA-induced mice. LGP inhibits Phosphoinositide 3-kinase/protein kinase B (PI3K/AKT) and Toll-like receptors/Nuclear factor kappa B (TLRs/NF-κB) signaling pathways in vitro and in vivo to treat AIH.

Conclusions

LGP was successfully extracted and purified, exhibiting potential as a treatment for ConA-induced autoimmune hepatitis due to its ability to inhibit the PI3K/AKT and TLRs/NF-κB signaling pathways and protect liver cells from damage.

中文翻译：

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人参多糖通过抑制PI3K/AKT和TLRs/NF-κB信号通路降低自身免疫性肝炎炎症反应

背景

人参多糖 (GP) 已被发现具有显着的免疫调节作用，使其成为治疗免疫相关疾病的有前途的候选者。但其在免疫性肝损伤中的作用机制尚不明确。本研究的创新点在于探索人参多糖（GP）在免疫性肝损伤中的作用机制。虽然 GP 之前已被确定具有免疫调节作用，但本研究旨在更清楚地了解其对免疫相关肝病的治疗潜力。

目的

本研究的目的是表征低分子量人参多糖 (LGP)，研究其对 ConA 诱导的自身免疫性肝炎 (AIH) 的影响，并确定其潜在的分子机制。

方法

使用水醇沉淀、DEAE-52 纤维素柱和 Sephadex G200 提取和纯化 LGP。并对其结构进行了分析。然后评估它在 ConA 诱导的细胞和小鼠中的抗炎和保肝作用，使用细胞计数试剂盒 8 (CCK-8)、逆转录聚合酶链反应 (RT-PCR) 和西方评估细胞活力和炎症用各种生化和染色方法进行印迹和肝损伤、炎症和细胞凋亡。

结果

LGP是由葡萄糖(Glu)、半乳糖(Gal)和阿拉伯糖(Ara)组成的多糖，摩尔比为12.9:1.6:1.0。导光板具有低结晶度的无定形粉末结构，不含杂质。LGP 增强细胞活力并减少 ConA 诱导的 RAW264.7 细胞中的炎症因子，并抑制 ConA 诱导的小鼠的炎症和肝细胞凋亡。LGP在体外和体内抑制磷酸肌醇 3-激酶/蛋白激酶 B (PI3K/AKT) 和 Toll 样受体/核因子 kappa B (TLRs/NF-κB) 信号通路以治疗AIH 。

结论

LGP 被成功提取和纯化，由于其能够抑制 PI3K/AKT 和 TLRs/NF-κB 信号通路并保护肝细胞免受损伤，因此具有治疗 ConA 诱导的自身免疫性肝炎的潜力。