Introduction
This study aimed to investigate the mechanism of action of cordyceps polysaccharide on rat acute liver failure (ALF).

Material and methods
Sixty rats were randomly divided into five groups: a normal group, a model group without cordyceps polysaccharide and groups with cordyceps polysaccharide in three different doses (5, 10 and 20 mg/ml). Serum alanine aminotransferase (ALT), aspartate transaminase (AST), alkaline phosphatase (ALP), and total bilirubin (TBIL) contents were measured for assessing liver function. Hematoxylin and eosin (HE) staining was used for observing liver pathology. Apoptosis was detected through the method of terminal-deoxynucleotidyl transferase mediated nick end labeling (TUNEL) staining. Protein expression levels of caspase-1, interleukin-18 (IL-18), IL-10, vascular endothelial growth factor (VEGF), and stromal cell-derived factor-1α (SDF-1α) in liver tissue were detected by Western blot. Proliferating cell nuclear antigen (PCNA) and signal regulatory protein-α1 (SIRPα1) contents were measured by PCR.

Results
The rat ALF model was established with D-galactosamine induced by lipopolysaccharide (LPS). After modelling, tissue HE staining showed typical manifestation of acute liver injury that emerged in the rat ALF model. The liver failure group showed higher levels of serum ALT and AST, as well as hepatocyte apoptosis, than the groups treated with cordyceps polysaccharide. Cordyceps polysaccharide can effectively suppress the protein expression of caspase-1, IL-18, and IL-10, while simultaneously increasing the protein expression of VEGF and SDF-1α, as well as the mRNA expression of PCNA and SIRPα1.

Conclusions
Cordyceps polysaccharide can alleviate the immune response and inflammatory injury in ALF by regulating the balance of pro-inflammatory and anti-inflammatory factors and reducing the apoptosis.



中文翻译：

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虫草多糖对大鼠急性肝功能衰竭作用机制的评价。

引言
本研究旨在探讨虫草多糖对大鼠急性肝功能衰竭（ALF）的作用机制。

材料与方法
将60只大鼠随机分为5组：正常组、未添加虫草多糖的模型组和3个不同剂量（5、10和20mg/ml）的虫草多糖组。测定血清丙氨酸氨基转移酶 (ALT)、天冬氨酸转氨酶 (AST)、碱性磷酸酶 (ALP) 和总胆红素 (TBIL) 含量以评估肝功能。苏木精和伊红（HE）染色用于观察肝脏病理学。通过末端脱氧核苷酸转移酶介导的缺口末端标记（TUNEL）染色法检测细胞凋亡。肝组织中 caspase-1、白细胞介素 18 (IL-18)、IL-10、血管内皮生长因子 (VEGF) 和基质细胞衍生因子-1α (SDF-1α) 的蛋白表达水平通过以下方法检测蛋白质印迹。

结果
用脂多糖(LPS)诱导的D-半乳糖胺建立大鼠ALF模型。造模后组织HE染色显示大鼠ALF模型出现急性肝损伤的典型表现。肝功能衰竭组的血清ALT和AST水平高于冬虫夏草多糖组，肝细胞凋亡水平也高于冬虫夏草多糖组。虫草多糖能有效抑制caspase-1、IL-18和IL-10的蛋白表达，同时增加VEGF和SDF-1α的蛋白表达，以及PCNA和SIRPα1的mRNA表达。

结论
虫草多糖可通过调节促炎和抗炎因子的平衡，减少细胞凋亡来缓解ALF的免疫反应和炎症损伤。