Wang Xiufeng, Zhong Yunqing, Zhang Rongzhen, Chen Yueqiao, Wang Minggang, Lv Chao, Mao Dewen
Department of Liver Disease Area 1, The First Affiliated Hospital of Guangxi University of Chinese Medicine, Nanning 530201, China.
Department of Pulmonary Disease, Guangxi International Zhuang Medicine Hospital, Nanning, China.
Evid Based Complement Alternat Med. 2022 Mar 30;2022:5652172. doi: 10.1155/2022/5652172. eCollection 2022.
Acute-on-chronic liver failure (ACLF) is a group of chronic liver diseases and caused by acute internal and external liver injury. Wenyang Huazhuo Tuihuang (WYHZTH) formula had a good clinical effect on promoting the resolution of jaundice. The aim of this study is to further investigate the mechanism of the WYHZTH formula in the ACLF rat model.
The ACLF rat model was constructed by combining human serum albumin with LPS and D-gal. WYHZTH was used to intervene and treat. The cytokines IL-17, IL-23, IL-10, and TGF- were detected by ELISA and fluorescence-quantitative PCR. Flow cytometry was used to detect the percentage of Th17 and Treg cells in the peripheral blood and liver tissues of each group of rats. The pathological changes in the liver tissue were detected by hematoxylin-eosin staining, immunohistochemistry, and electron microscopy.
Compared with the ACLF group, the WYHZTH formula and Thy significantly decreased the levels of ALT, AST, and CHE in the ACLF group. After drug intervention, apoptosis was significantly reduced. The PCNA expression decreased in the ACLF model group but increased in the WYHZTH or Thy group. Under transmission electron microscope, hepatocytes in the ACLF group showed obvious necrosis. After drug intervention, hepatocyte necrosis was reduced with most of the structure returning to normal.
This present study demonstrated that WYHZTH formula may protect against acute-on-chronic liver failure, which may be related to the inhibition of Th17/Treg cell imbalance.
慢加急性肝衰竭（ACLF）是一组慢性肝病，由急性内源性和外源性肝损伤引起。温阳化浊退黄（WYHZTH）方在促进黄疸消退方面具有良好的临床效果。本研究旨在进一步探讨WYHZTH方在ACLF大鼠模型中的作用机制。
将人血清白蛋白与脂多糖和D-半乳糖联合使用构建ACLF大鼠模型。采用WYHZTH方进行干预治疗。通过酶联免疫吸附测定（ELISA）和荧光定量聚合酶链反应（PCR）检测细胞因子白细胞介素-17（IL-17）、白细胞介素-23（IL-23）、白细胞介素-10（IL-10）和转化生长因子（TGF-）。采用流式细胞术检测各组大鼠外周血和肝组织中辅助性T细胞17（Th17）和调节性T细胞（Treg）的百分比。通过苏木精-伊红染色、免疫组织化学和电子显微镜检测肝组织的病理变化。
与ACLF组相比，WYHZTH方和胸腺肽显著降低了ACLF组谷丙转氨酶（ALT）、谷草转氨酶（AST）和胆碱酯酶（CHE）的水平。药物干预后，细胞凋亡明显减少。增殖细胞核抗原（PCNA）表达在ACLF模型组降低，但在WYHZTH方组或胸腺肽组升高。在透射电子显微镜下，ACLF组肝细胞显示明显坏死。药物干预后，肝细胞坏死减少，大部分结构恢复正常。
本研究表明，WYHZTH方可能对慢加急性肝衰竭具有保护作用，这可能与抑制Th17/Treg细胞失衡有关。
