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Restorative effects of hydroxysafflor yellow A on hepatic function in an experimental regression model of hepatic fibrosis induced by carbon tetrachloride

机译:在四氯化碳引起的肝纤维化实验回归模型中羟基红花黄色素A对肝功能的修复作用

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摘要

Hepatic fibrosis is a reversible pathological process, in which fibrotic tissue is excessively deposited in the liver during the repair process that follows hepatic injury. Early prevention or treatment of hepatic fibrosis has great significance on the treatment of chronic hepatic diseases. Hydroxysafflor yellow A (HSYA) is a water-soluble monomer extracted from safflower, which serves numerous pharmacological roles. However, it remains to be elucidated how HSYA regulates hepatic fibrogenesis. The aim of the present study was to reveal the possible mechanisms underlying the effects of HSYA on the prevention and treatment of hepatic fibrosis. A rat model of hepatic fibrosis was established in the present study, and the rats were administered various doses of HSYA. The effects of HSYA on pathological alterations of the liver tissue in rats with hepatic fibrosis were observed using hematoxylin-eosin staining and Masson staining. In order to explore the anti-hepatic fibrosis effects and underlying mechanisms of HSYA, serum levels, and hepatic function and hepatic fibrosis indices were evaluated. The results demonstrated that HSYA can improve the general condition of rats with hepatic fibrosis and relieve cellular swelling of the liver, fatty degeneration, necrosis, inflammatory cell infiltration and fibroplastic proliferation. Subsequent to administration of HSYA, globulin was increased during hepatic fibrosis caused by tetrachloromethane. However, total cholesterol, triglyceride, alanine aminotransferase, aspartate aminotransferase and levels of hyaluronic acid, laminin, procollagen III N-terminal peptide, collagen type IV and hydroxyproline were significantly reduced. The results additionally demonstrated that HSYA could enhance superoxide dismutase activity and reduce malondialdehyde levels, inhibiting lipid peroxidation caused by free radicals.
机译:肝纤维化是一种可逆的病理过程,其中在肝损伤后的修复过程中,肝纤维化组织过多沉积在肝脏中。肝纤维化的早期预防或治疗对慢性肝病的治疗具有重要意义。羟基红花黄A(HSYA)是从红花中提取的水溶性单体,具有许多药理作用。但是,尚需阐明HSYA如何调节肝纤维化。本研究的目的是揭示HSYA预防和治疗肝纤维化的潜在机制。在本研究中建立了大鼠肝纤维化模型,并且给大鼠施用了不同剂量的HSYA。用苏木精-伊红染色和Masson染色观察HSYA对肝纤维化大鼠肝组织病理改变的影响。为了探讨抗肝纤维化的作用及其对HSYA的潜在作用机制,评估了血清水平,肝功能和肝纤维化指标。结果表明,HSYA可以改善大鼠肝纤维化的一般状况,并减轻肝脏的细胞肿胀,脂肪变性,坏死,炎性细胞浸润和纤维增生。施用HSYA后,在由四氯甲烷引起的肝纤维化过程中,球蛋白增加。但是,总胆固醇,甘油三酸酯,丙氨酸转氨酶,天冬氨酸转氨酶和透明质酸,层粘连蛋白,前胶原III N端肽,IV型胶原和羟脯氨酸的水平均显着降低。结果还表明,HSYA可以增强超氧化物歧化酶活性并降低丙二醛水平,从而抑制自由基引起的脂质过氧化。

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