血管内皮生长因子
血管生成
超氧化物歧化酶
化学
丙二醛
下调和上调
药理学
生长因子
内分泌学
生物
内科学
医学
生物化学
氧化应激
受体
血管内皮生长因子受体
基因
作者
Yanquan Han,Lingyu Pan,Shan Ran,Yan Song,Fangfang Sun,Yong‐Zhong Wang,Yan Hong
标识
DOI:10.3892/mmr.2019.10006
摘要
Previously, we demonstrated that Rhizoma Paridis saponins (RPS), the major active component of Rhizoma Paridis, may exhibit hepatoprotective effects. The present study aimed to identify the potential mechanism of RPS on hepatic injury and improvement in hepatic fibrosis (HF). A HF model was created in Sprague‑Dawley rats by administration of carbon tetrachloride. RPS was administered for treatment following creation of the HF model. The protein and mRNA expression of vascular endothelial growth factor (VEGF), platelet‑derived growth factor (PDGF), extracellular signal‑regulated kinase (ERK)1/2 and α‑smooth muscle actin (SMA) was detected by reverse transcription quantitative polymerase chain reaction and western blot analysis. RPS was demonstrated to improve hepatic inflammation and decrease HF severity according to hematoxylin and eosin and Masson trichrome staining. Following RPS treatment, the level of alanine aminotransferase, aspartate aminotransferase and malondialdehyde, and expression levels of the mRNA and protein of VEGF, ERK1/2, PDGF and α‑SMA in the model group was decreased. By contrast, the content of glutathione‑PX and superoxide dismutase was increased. These data suggest that RPS may treat HF primarily through downregulation of the expression levels of the mRNA and phosphorylated VEGF, ERK1/2, PDGF and α‑SMA proteins.
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