Rosehip – scientific name Rosa canensis – contains a substance that might make muscles stronger, prevent muscle breakdown, stimulate the growth of cartilage in joints and rejuvenate the skin. The substance is called tiliroside. According to researchers at the Medical University of Bialystok in Poland, tiliroside boosts the effect of the anabolic hormone IGF-1.
You’ll find a few other posts on rosehips on this website. Extracts of rosehip taken in remarkably small quantities stimulate fat loss, according to a Japanese animal study, while human studies have shown that the dried powder has a rejuvenating effect on the skin and improves the functioning of worn joints.
The glycosidic flavonoid tiliroside is one of the interesting substances found in rosehips. In the animal study mentioned above, tiliroside stimulates fat burning, but the Polish study reveals another potential effect of tiliroside.
The Poles exposed collagen-producing cells in test tubes to t-butyl hydroperoxide for an hour a day, for a period of 1, 3 or 5 consecutive days. Researchers use t-butyl hydroperoxide when they want to imitate the effects of oxidative stress on cells.
The researchers then repeated their experiments, but used increasing concentrations of tiliroside in the test tubes as well as t-butyl hydroperoxide.
The figure below shows that the oxidative stress inhibited the uptake of marked thymidine in the DNA of the cells. This means that oxidative stress inhibits cell division, and as a result, also cell growth and vitality. Tiliroside protected the cells, however.
Oxidative stress also inhibited the uptake of marked proline in collagen structures in the cells. That means that oxidative stress inhibited the synthesis of collagen â€“ and probably also other proteins. But, as the figure above shows, tiliroside also reduced the amount of inhibition.
The figure below shows how tiliroside maintained the cells’ vitality, according to the Poles. The bigger the clot, the more IGF-1 receptors the cells synthesise.
1: no t-butyl hydroperoxide 2: 5 consecutive days, one hour exposure to 30 micromol t-butyl hydroperoxide 3: exposure to t-butyl hydroperoxide plus 50 micromol tiliroside.
The Potential Mechanism of Tiliroside-Dependent Inhibition of t-Butylhydroperoxide-Induced Oxidative Stress in Endometrial Carcinoma Cells
The effects of oxidative stress on collagen and DNA biosynthesis, ?-galactosidase activity, the expression of the ?-integrin receptor, FAK, the insulin-like growth factor-I receptor (IGF?IR), the hypoxia-inducible factor-1 (HIF-1), and the mitogen-activated protein kinases (MAP/ERK1, ERK2) were evaluated in human endometrial carcinoma cells. Subconfluent cells were subjected to oxidative stress with 30?µM t-butylhydroperoxide (t-BHP) for 1?h per day over the course of 5 days. It was found that oxidative stress contributed to an increase in the ?-galactosidase activity as well as to the inhibition of collagen and DNA biosynthesis. The mechanism of the process was found at the level of IGF?IR and HIF-1?. An increase in the expression of HIF-1? and a decrease in the expression of IGF?IR were observed in the cells subjected to oxidative stress. The role of IGF?IR signalling in the process was confirmed by an experiment showing downregulation of MAP kinases ERK1 and ERK2 expression in the studied cells. This phenomenon is probably responsible for the drastic inhibition of protein (up to 40?% of control) and DNA biosynthesis (up to 65?% of control) in the cells. An addition of tiliroside to the cells medium restored all parameters to the control level, including IGF?IR and HIF-1? expressions. The data suggest that the antioxidative activity of tiliroside isolated from Potentilla argentea may originate at the level of IGF?IR and HIF-1? signalling.