Shen Baode, Deng Li, Liu Yuan, Li Ruisheng, Shen Chengying, Liu Xiao, Li Yinchao, Yuan Hailong
Department of Pharmacy, Air Force Medical Center, PLA, Beijing 100142, China.
College of Pharmaceutical Sciences, Zhengzhou University, Zhengzhou 450001, China.
Chin Herb Med. 2021 Dec 21;14(1):104-110. doi: 10.1016/j.chmed.2021.09.013. eCollection 2022 Jan.
Fufang Biejia Ruangan Tablet (FBRT) is widely used for the treatment of liver fibrosis. However, (HP), as an important adjuvant of FBRT, has been restricted for medicinal using due to the limited availability, ethical controversy and safety issues. The present study aimed to investigate the therapeutic effects of novel FBRT (N-FBRT) with sheep placenta (SP) as substitute for HP on liver fibrosis and explore its possible mechanisms. Different dosages of SP in N-FBRT were also evaluated.
Rats were subcutaneously injected with CCl to induce liver fibrosis and then treated with N-FBRT and FBRT. The anti-hepatic fibrosis effect was determined based on biomarkers analysis of liver function and hepatic fibrosis, and the liver pathology was visualized by H&E staining and Masson staining. The oxidative stress and inflammatory cytokines were also detected. Immunohistochemical staining of α-SMA, real time PCR and Western blotting were performed to evaluate hepatic stellate cells (HSCs) activation and TGF-β1/Smad signaling pathway.
N-FBRT and FBRT could ameliorate CCl-induced liver fibrosis and improve liver function, as evidenced by lowering serum biomarkers levels of liver function and hepatic fibrosis, and decreasing hepatic Hyp content and collagen deposition, and improving the hepatic morphology and architecture changes. Moreover, the anti-liver fibrosis effect was better when the dosage of SP used in N-FBRT was 1/2 of HP in FBRT. Administration of N-FBRT markedly alleviated oxidative stress and inflammatory cytokines, and inhibited α-SMA expression. Furthermore, the mRNA expression of , , and , and proteins expression of α-SMA, TGF-β1, Smad2/3 and p-Smad2/3 were significantly down-regulated by N-FBRT treatment.
SP can be used as substitute for HP to prepare N-FBRT for the treatment of liver fibrosis and the anti-liver fibrosis effect of N-FBRT is achieved by eliminating oxidative stress and inflammation, and inhibiting HSCs activation and ECM production by blocking TGF-β1/Smad signaling pathway.
复方鳖甲软肝片（FBRT）被广泛用于治疗肝纤维化。然而，羊胎盘（HP）作为FBRT的一种重要佐剂，由于其来源有限、伦理争议和安全问题，在药用方面受到限制。本研究旨在探讨以羊胎盘（SP）替代HP的新型复方鳖甲软肝片（N-FBRT）对肝纤维化的治疗作用，并探索其可能的机制。同时还评估了N-FBRT中不同剂量的SP。
大鼠皮下注射四氯化碳诱导肝纤维化，然后用N-FBRT和FBRT进行治疗。基于肝功能和肝纤维化的生物标志物分析确定抗肝纤维化作用，并通过苏木精-伊红（H&E）染色和Masson染色观察肝脏病理变化。还检测了氧化应激和炎性细胞因子。进行α-平滑肌肌动蛋白（α-SMA）的免疫组化染色、实时聚合酶链反应（PCR）和蛋白质印迹法，以评估肝星状细胞（HSCs）的活化及转化生长因子-β1（TGF-β1）/Smad信号通路。
N-FBRT和FBRT均可改善四氯化碳诱导的肝纤维化并改善肝功能，这通过降低肝功能和肝纤维化的血清生物标志物水平、降低肝脏羟脯氨酸含量和胶原沉积、改善肝脏形态和结构变化得以证明。此外，当N-FBRT中使用的SP剂量为FBRT中HP剂量的1/2时，抗肝纤维化效果更佳。给予N-FBRT可显著减轻氧化应激和炎性细胞因子，并抑制α-SMA表达。此外，N-FBRT治疗可使TGF-β1、Smad2、Smad3和Smad7的mRNA表达以及α-SMA、TGF-β1、Smad2/3和磷酸化Smad2/3的蛋白表达显著下调。
SP可替代HP制备N-FBRT用于治疗肝纤维化，N-FBRT的抗肝纤维化作用是通过消除氧化应激和炎症、阻断TGF-β1/Smad信号通路抑制HSCs活化和细胞外基质（ECM）产生来实现的。
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