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Published on: June 7, 2016
ANG II-AT1 receptor pathway is involved in the anti-fibrotic effect of beta-elemene
1Department of Traditional Chinese Medicine, Huazhong University of Science and Technology, Wuhan, 430022, China. zhurui19830108@163.com
Abstract:
To investigate the effects of beta-elemene on the ANG II-AT1 receptor pathway in rats with liver fibrosis, a model of hepatic fibrosis was induced by hypodermical injection of carbon tetrachloride (CCl4) into Wistar male rats. beta-elemene was intraperitonealy administered into the rats for 8 weeks (0.1 mL/100 g body weight per day). Masson staining was used to observe the liver fibrosis of rats and liver functions were measured by enzymatic kinetic analysis. The content of hydroxyproline in liver tissues was detected by specimen alkaline hydrolysis. The level of plasma ANG in blood II plasma was detected by radioimmunoassay. The expression of AT1R in rat liver were measured using reverse transcriptional-polymerase chain reaction and immunohistochemistry respectively. The results showed that beta-elemene could reduce the collagen disposition in liver and inhibit the progression of liver fibrosis. In addition, the levels of plasma ANG II and the expression of hepatic AT1R in rats with liver fibrosis were also suppressed by beta-elemene. It is concluded that the ANG II-AT1 receptor pathway plays an important role in the development of hepatic fibrosis and beta-elemene could down-regulate the levels of plasma ANG II and the expression of hepatic AT1R in rats with liver fibrosis.
Insights
Beta-elemene treatment effectively inhibited liver fibrosis progression in rats. This natural compound reduced collagen deposition and suppressed the angiotensin II-AT1 receptor pathway, offering a potential therapeutic strategy for liver fibrosis.
Area of Science:
- Pharmacology
- Hepatology
- Biochemistry
Background:
- Liver fibrosis is a significant health concern characterized by excessive collagen deposition.
- The renin-angiotensin system, particularly angiotensin II (ANG II) and its AT1 receptor (AT1R), is implicated in the pathogenesis of liver fibrosis.
Purpose of the Study:
- To investigate the therapeutic effects of beta-elemene on the ANG II-AT1 receptor pathway in a rat model of carbon tetrachloride (CCl4)-induced liver fibrosis.
- To determine if beta-elemene can modulate key markers of liver fibrosis and the ANG II-AT1 receptor pathway.
Main Methods:
- Hepatic fibrosis was induced in Wistar male rats using CCl4.
- Beta-elemene was administered intraperitoneally for 8 weeks.
- Liver fibrosis was assessed using Masson staining, hydroxyproline content, and liver function tests.
- Plasma ANG II levels were measured by radioimmunoassay.
- Hepatic AT1R expression was quantified using reverse transcriptional-polymerase chain reaction and immunohistochemistry.
Main Results:
- Beta-elemene administration significantly reduced collagen deposition and inhibited the progression of liver fibrosis.
- Treatment with beta-elemene led to a decrease in plasma ANG II levels.
- The expression of hepatic AT1R was suppressed by beta-elemene in fibrotic rat livers.
Conclusions:
- The ANG II-AT1 receptor pathway plays a crucial role in the development and progression of hepatic fibrosis.
- Beta-elemene demonstrates antifibrotic effects by down-regulating plasma ANG II levels and hepatic AT1R expression.
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