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- Title
The Effect of Notoginsenoside R1 on TGF-β1/smad3 Signal Pathway in Hepatic Fibrosis Rats.
- Authors
PU Xian-hong; HE Yuan; HUANG Wei; RU Jin; YANG Jin-wei
- Abstract
Objective: To investigate the expression of transforming growth factor-β1 (TGF-β1) and Smad3 in liver and serum after hepatic fibrosis, and the protective effect ofNotoginsenoside R1 on hepatic fibrosis. Methods: 72 healthy male SD rats were randomly divided into control group, NDMA group and Notoginsenoside R1 group, according to the different time points of 1, 2, 4 weeks, 3 subgroups, each subgroup 8 animals. For NMDA group, NMDA was administrated by intraperitoneal injection (2 mL/kg); and for Notoginsenoside R1 group, Notoginsenoside R1 was administrated by intravenous injection with a dose of 100 mg/kg and the animals of control group was injected with equal amount normal saline. The expression of TGF-β1 and Smad3 in liver tissues and serum was detected at different time points using ELISA and RT-PCR. Results: Expression of TGF-β1 and Smad3 protein and mRNA was detectable in all groups. In the control group, the expression ofTGF-β1 and Smad3 at different time points had no statistical significance (P>0.05). Compared with that in the control group, the expression of TGF-β1 and Smad3 protein and mRNA in NMDA group gradually increased at each time point with the injury, and showed statistical significance (P<0.05). While in Notoginsenoside R1 group, expression of TGF-β1 and Smad3 at each time point was down-regulated, with statistical significance (P<0.05) compared with that in the NDMA group. Conclusions: TGF-β1/Smad3 signal was involved in the occurrence and development of liver fibrosis, and with the aggravation of injury, the expression of TGF-β1 and Smad3 gradually increased. Notoginsenoside R1 could reduce TGF-β1/Smad3 signal in liver tissues, then reduce liver fibrosis and protect the liver from injury.
- Publication
Progress in Modern Biomedicine, 2015, Vol 15, Issue 4, p622
- ISSN
1673-6273
- Publication type
Article
- DOI
10.13241/j.cnki.pmb.2015.04.006