Department of Pharmacy, Tongde Hospital Zhejiang Province, Hangzhou, Zhejiang, China (mainland).
Zhejiang Academy of Traditional Chinese Medicine, Hangzhou, Zhejiang, China (mainland).
Med Sci Monit. 2020 Jul 16;26:e921738. doi: 10.12659/MSM.921738.
BACKGROUND Liver fibrosis, defined as the aberrant accumulation of extracellular matrix (ECM) proteins such as collagen in the liver, is a common feature of chronic liver disease, and often culminates in portal hypertension, liver cirrhosis, and hepatic failure. Though therapeutically manageable, fibrosis is not always successfully treated by conventional antifibrotic agents. While the traditional Chinese medicine (TCM) Alisma Shugan Decoction (ASD) has several health benefits, including anti-inflammation, anti-oxidation, and limitation of cardiovascular and respiratory disorders, it remains unclear if it has any hepato-protective potential. MATERIAL AND METHODS The present study examined the therapeutic effect of ASD in thioacetamide (TAA)-induced liver injury and fibrosis rat models. RESULTS We demonstrated that 50 mg/kg ASD significantly reversed TAA-induced elevation of alanine or aspartate transaminase levels, elicited no dyscrasia, and conferred a 40% (p<0.01) or 20% (p<0.05) survival advantage, compared to rats treated with TAA or TAA+ASD, respectively. Treatment with ASD reversed TAA-induced liver injury and fibrogenesis via repression of alpha-SMA protein and reduction of the collagen area and fibrosis score. Concurrently, ASD markedly suppressed the mRNA expression of fibrogenic procollagen, ICAM-1, MMP2, MMP9, and MMP13, and production of TIMP-1, ICAM-1, CXCL7, or CD62L cytokine in rat liver injury models. Interestingly, ASD-elicited reduction of liver injury and fibrogenesis was mediated by dysregulated p65/NrF-2/JunD signaling, with a resultant 3.18-fold (p<0.05) increase in GSH/GSSH ratio, and a 3.61-fold (p<0.01) or 1.51-fold (p<0.01) reduction in the 4-hydroxynonenal and malondialdehyde (MDA) levels, respectively, indicating reduced oxidative stress in the ASD-treated rats, and suggesting an hepato-protective role for ASD. CONCLUSIONS In conclusion, the present study provides supplementary evidence of the therapeutic benefit of ASD as an efficient treatment option in cases of liver injury and fibrosis. Further large-cohort validation of these findings is warranted.
肝纤维化是指肝脏中细胞外基质(ECM)蛋白如胶原的异常积累,是慢性肝病的共同特征,常导致门静脉高压、肝硬化和肝衰竭。虽然可以通过治疗来控制,但纤维化并不总是能被传统的抗纤维化药物成功治疗。虽然传统中药(TCM)泽泻疏肝汤(ASD)有多种健康益处,包括抗炎、抗氧化和限制心血管和呼吸系统疾病,但它是否具有肝保护潜力尚不清楚。
本研究检查了 ASD 在硫代乙酰胺(TAA)诱导的肝损伤和纤维化大鼠模型中的治疗效果。
我们表明,与 TAA 或 TAA+ASD 治疗的大鼠相比,50mg/kg ASD 可显著逆转 TAA 诱导的丙氨酸或天冬氨酸转氨酶水平升高,无血液学异常,并分别提供 40%(p<0.01)或 20%(p<0.05)的生存优势。ASD 通过抑制α-SMA 蛋白和减少胶原面积和纤维化评分来逆转 TAA 诱导的肝损伤和纤维化。同时,ASD 显著抑制了纤维化前胶原、ICAM-1、MMP2、MMP9 和 MMP13 的 mRNA 表达以及大鼠肝损伤模型中 TIMP-1、ICAM-1、CXCL7 或 CD62L 细胞因子的产生。有趣的是,ASD 引起的肝损伤和纤维化减少是由 p65/NrF-2/JunD 信号通路的失调介导的,导致 GSH/GSSH 比率增加 3.18 倍(p<0.05),4-羟壬烯醛和丙二醛(MDA)水平分别降低 3.61 倍(p<0.01)或 1.51 倍(p<0.01),表明 ASD 治疗大鼠的氧化应激减少,并提示 ASD 具有肝保护作用。
总之,本研究为 ASD 作为肝损伤和纤维化的有效治疗选择提供了补充证据。需要进一步的大型队列验证这些发现。