Rosmarinic acid displays antifibrotic effects on liver tissue.
Article Type: Report
Subject: Rosemary (Research)
Rosemary (Health aspects)
Medicinal plants (Health aspects)
Medicinal plants (Research)
Liver failure (Care and treatment)
Liver failure (Research)
Author: Finney-Brown, Tessa
Pub Date: 03/22/2010
Publication: Name: Australian Journal of Medical Herbalism Publisher: National Herbalists Association of Australia Audience: Academic Format: Magazine/Journal Subject: Health Copyright: COPYRIGHT 2010 National Herbalists Association of Australia ISSN: 1033-8330
Issue: Date: Spring, 2010 Source Volume: 22 Source Issue: 1
Topic: Event Code: 310 Science & research
Product: Product Code: 0139913 Medicinal Plants NAICS Code: 1119 Other Crop Farming SIC Code: 2833 Medicinals and botanicals
Accession Number: 223823994
Full Text: Li G, Jiang W, Tian J, Qu G, Zhu H, Fu F. 2010. In vitro and in vivo antifibrotic effects of rosmarinic acid on experimental liver fibrosis. Phytomed 17;282-8.

Rosemary, via one of its active constituents rosamarinic acid (RA), is often used by herbalists and naturopaths for its beneficial effects on the liver. This recent Chinese study investigated the potential effects of this compound on hepatic fibrosis, the consequence of sustained wound healing responses by the liver. Cultures of hepatic stellate cells (HSCs) were used for in vitro assessment and tetrachloride treated rats as in vivo subjects.

One proposed therapeutic target against hepatic fibrosis is suppression of the HSCs, possibly via inhibition of transforming growth factor [beta] (TGF-[beta]) or blockage of its downstream signalling pathway. Another potential target is connective tissue growth factor (CTGF), a mediator of TGF-[beta]1 induced fibrosis. Reduction of this compound results in reduced fibrotic tissue deposition. In the cultured HSCs in this study, treatment with RA was shown to inhibit TGF-[beta]1, CTGF and [alpha]-smooth muscle actin.

The in vivo segment of the trial was carried out in 75 male Sprague-Dawley rats. Ten were an untreated control group and the remainder were given tetrachloride to induce liver damage. These were then further divided into five subgroups by body weight and serum alkaline phosphatase levels: (I) model group, (II) silymarin 25 mg/kg group, (III) RA 2.5 mg/kg group, (IV) RA 5 mg/kg group and (V) RA 10 mg/kg group. After 4 weeks of daily treatment the RA groups (especially over 10 mg/kg) were found to have lower scores of hepatic fibrosis grade and decreased serum alanine amino transferase and glutamate pyruvate transferase. This indicates less fibrosis and improved liver function compared with the untreated rats.

The results of the study overall suggested that RA could prevent hepatic fibrosis due to chronic liver damage and thus delay cirrhosis development. While the results are promising, the authors do caution that long term suppression of TGF-[beta] may be detrimental to the organism as it is a cytokine with a number of roles in the body. It modulates the immune system, inhibiting inflammatory responses and plays antiangiogenic and antitumour roles against certain types of cancer. Other experiments have shown long term TGF-[beta] suppressed mice to have excessive inflammation leading to tissue necrosis in certain organs. Inhibiting CTGF, which is a downstream mediator of this cytokine, and suitable inhibition of TGF-[beta] may be a better option.

In the study, the RA effects were also compared with that of silymarin, a known antifibrotic agent. Results showed that RA exhibited significantly higher potency in inhibiting TGF-[beta] and CTGF expression in fibrotic liver tissue and reducing the severity of decrease in liver function. In summary RA seems to be a promising candidate for ameliorating liver fibrosis.

Tessa Finney-Brown MNHAA
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