Qinggan Huoxue Recipe Protects against Experimental Alcoholic Liver Fibrosis through CXCL16 Inhibition

Ling Tang; Xiao Yu; Lu Zou; Shaobin Li; Yanqi Cheng; Yuqin Wu; Lianjun Xing; Hong Fang

doi:10.1155/2023/5642713

Qinggan Huoxue Recipe Protects against Experimental Alcoholic Liver Fibrosis through CXCL16 Inhibition

Evid Based Complement Alternat Med. 2023 Jan 3:2023:5642713. doi: 10.1155/2023/5642713. eCollection 2023.

Authors

Ling Tang¹, Xiao Yu², Lu Zou³, Shaobin Li¹, Yanqi Cheng¹, Yuqin Wu¹, Lianjun Xing², Hong Fang¹

Affiliations

¹ Preventive Health Department of Traditional Chinese Medicine, Longhua Hospital, Shanghai University of Traditional Chinese Medicine, No. 725, Wanping South Road, Xuhui District, Shanghai 200032, China.
² Department II of Digestive Diseases, Longhua Hospital, Shanghai University of Traditional Chinese Medi-cine, No. 725, Wanping South Road, Xuhui District, Shanghai 200032, China.
³ Experiment Center for Teaching & Learning, Shanghai University of Traditional Chinese Medicine, No. 1200, Cailun Road, Shanghai 201203, China.

Abstract

Background: Qinggan Huoxue recipe (QGHXR), a traditional Chinese medicinal formula, has a protective effect against liver fibrosis. However, the underlying mechanisms remain unclear.

Objective: This study investigated the antifibrotic role of QGHXR and its underlying mechanisms.

Methods: The composition of QGHXR was determined using ultra performance liquid chromatography-tandem mass spectrometry (UPLC-MS/MS). Female C57BL/6J mice were fed either a Lieber-DeCarli liquid diet or pair-fed control diet and intraperitoneally injected with CCl₄ for 8 weeks (n = 8). In week 5, the mice were administered 100, 200, and 400 mg/kg QGHXR via oral gavage daily for 4 weeks.

Results: UPLC-MS result showed that QGHXR contained 45 compounds including salvianolic acid A, scutellarin, baicalin, rutin, and chai saponin D. QGHXR alleviated pathological alterations in the liver. The alanine aminotransferase (ALT) level was reduced to 44.88 ± 4.39 U/L, aspartate aminotransferase (AST) to 76.25 ± 4.17 U/L, alkaline phosphatase (ALP) to 60.75 ± 5.41 U/L, and acetaldehyde to 38.54 ± 1.01 U/L compared with that of the control group (ALT 72.38 ± 5.19 U/L, AST 119.63 ± 9.82 U/L, and ALP 98.63 ± 6.71 U/L and acetaldehyde 64.86 ± 4.70 U/L). QGHXR inhibited lipid overproduction and fibrotic gene expression. The serum concentration of chemokine C-X-C ligand 16 (CXCL16) was reduced to 62.83 ± 6.80 pg/ml compared with that of the control group (130.91 ± 13.72 pg/mL). QGHXR downregulated CXCL16 mRNA and protein expressions. Pharmacological CXCL16 treatment reversed the QGHXR-induced protective effects in ethanol plus CCl₄ fed mice. QGHXR reduced CXCL16 levels (91.97 ± 5.86 pg/ml) in LPS-stimulated RAW264.7 cells compared with that of the control group (148.68 ± 8.62 pg/ml) and inhibited toll-like receptor 4 and nuclear factor-kappa B phosphorylation.

Conclusions: This study demonstrated that QGHXR mitigates experimental alcoholic liver fibrosis by CXCL16 inhibition, and may be considered a potential therapeutic agent for treating liver fibrosis.