Poplar tree leaf bud extract could fight skin aging

Antioxidants are popular anti-aging ingredients in skin creams, and now scientists are reporting a new source of these healthful substances — leaf buds of poplar trees. Their study appears in the ACS' Journal of Agricultural and Food Chemistry.

Xavier Vitrac and colleagues note that there's a long history of using poplar buds to treat various health problems, such as colds, sinusitis, sunburn and arthritis. A substance found in beehives that is made from poplar buds (called propolis) also appears to have similar disease-fighting benefits. Propolis' effects seem to be due to poplar bud compounds, but very little is known about these substances. To see whether poplar buds are a good source of antioxidants for skin creams, the researchers decided to test an extract from the buds.

The group found that poplar bud extract had moderate antioxidant activity, and it demonstrated anti-aging effects on cells in the laboratory. "The collective antioxidant properties and transcriptional effect of this extract suggest potential anti-aging properties which could be utilized in cosmetic and nutraceutical formulations," the scientists say.

More information: “Phenolic Composition and Antioxidant Properties of Poplar Bud (Populus nigra) Extract: Individual Antioxidant Contribution of Phenolics and Transcriptional Effect on Skin Aging” J. Agric. Food Chem., 2011, 59 (9), pp 4527–4536 DOI: 10.1021/jf104791t

Abstract
The Populus species possess great potential for therapeutical applications, especially for their known anti-inflammatory properties. The antioxidant properties of propolis, a hive product collected by honey bees mainly from poplar bud exudates, suggest that poplar buds also possess antioxidant properties. Here is reported the characterization of the antioxidant properties of an aqueous poplar bud (Populus nigra) extract. It presented a high total phenolic content, and moderate antioxidant properties as determined by ORAC assay. The main phenolic compounds identified were phenolic acids and flavonoid aglycons. These phenolic compounds were analyzed by ORAC assay for their individual antioxidant activity, in order to determine the major contributors to the total antioxidant activity of the extract. Thanks to their high antioxidant activity, caffeic and p-coumaric acids were identified as the major antioxidant components. Representing only 3.5% of its dry weight, these compounds represented together about 50% of the total antioxidant activity of the extract. The antioxidant properties of poplar bud extract and the phenolic compounds identified were also analyzed by cellular antioxidant activity assay (CAA), which was weakly correlated with ORAC assay. The transcriptional effect of poplar bud extract on skin aging was evaluated in vitro on a replicative senescence model of normal human dermal fibroblasts, using a customized DNA macroarray specifically designed to investigate skin aging markers. Among the detected genes, poplar bud extract significantly regulated genes involved in antioxidant defenses, inflammatory response and cell renewal. The collective antioxidant properties and transcriptional effect of this extract suggest potential antiaging properties which could be utilized in cosmetic and nutraceutical formulations.

Provided by American Chemical Society (news : web)

Molecular researchers discover novel gene linked to aging hearts

Researchers at the University of Ottawa Heart Institute (UOHI) have identified a novel gene in the nucleus of muscle and brain cells that affects heart development and the aging process. Their investigation brings the promise of new treatments for an old, failing heart.

"We know that aging is the greatest predictor of cardiovascular disease and heart failure. So we have been working backward in time, looking at the fetal heart to understand changes in the process as it ages, grows frail and fails," said molecular biologist Patrick Burgon, PhD.

A research team led by Burgon discovered the gene in the cell's nucleus – the site where hereditary information or DNA is housed – suggesting that it may control the behavior of other genes important in heart development.

The researchers, who focus on the fetal heart as it grows into an adult heart, named the gene MLIP for Muscle enriched A-type Lamin Interacting Protein. Mutations in the Lamin gene family are associated with muscular dystrophy and other degenerative heart muscle diseases.

Their findings have been reported electronically in the Journal of Biological Chemistry and are scheduled for formal publication in June. Researchers now will investigate how animal models respond when the MLIP gene is removed to gain greater knowledge into its function.

"Greater knowledge of this gene and how it works will help us understand loss of cardiac function. Our research opens up new avenues relevant to the characteristics of cardiac development," said Burgon.

At the Heart Institute, studies to identify complex cardiovascular mechanisms are part of a world-wide effort among a core of leading scientific organizations. The Heart Institute collaborates with an international consortium that has already discovered 13 new genes that increase the risk of coronary artery disease (CAD).

Heart Institute researchers previously identified gene 9p21 – the first genetic risk factor recognized for heart disease and the first major new cardiovascular risk factor since the discovery of cholesterol. The Institute has also located a variety of other genes influencing diseases such as atrial fibrillation and biological processes such as obesity.

More information: http://www.jbc.org/content/early/2011/04/15/jbc.M110.165548.abstract

Provided by University of Ottawa Heart Institute

Computer modeling used to study protein involved with cancer, aging and chronic disease

A new biophysical and biochemical study may lead to better understanding of how structural flexibility controls the interaction of a protein that is closely involved with cancer, aging and other chronic diseases -- thereby facilitating future development of better therapeutic strategies, according to a Kansas State University biochemist.

Jianhan Chen, an assistant professor of biochemistry, was one of the researchers on a collaborative project that took a combined computational and experimental approach to understand how protein p21 functions as a versatile regulator of cell division. Their latest findings, "Intrinsic disorder mediates the diverse regulatory functions of the Cdk inhibitor p21," were published in a recent edition of Nature Chemical Biology.

The study used computer simulation to rationalize results from biochemical and biophysical experiments, and provided further insights that would guide future investigations, Chen said. In this case, the focus is human protein p21 and its ability to function as an inhibitor of normal cell growth.

The protein has been shown to be an intrinsically disordered protein. This means it lacks a well-defined three-dimensional structure, characteristics that, until roughly a decade ago, were thought to be necessary for the protein to function.

"For a long time it was believed that proteins must fold to function and it was hard to imagine how an unfolded protein could play a role in crucial cellular areas," Chen said. "What researchers before me found was that by lacking a stable structure, this actually turned out to be really, really important to how these proteins function."

Along with being an intrinsically disordered protein, p21 is a versatile cyclin-dependent kinase, or Cdk, inhibitor -- meaning it adapts to and inhibits a range of Cdk-cyclin complexes that regulate eukaryote cell division. It also has been connected to cancer and aging. For example, Chen said p21 is a principal trans-activation target of the p53 tumor suppressor protein and contributes to p53-dependent tumor suppression.

"This protein is extremely challenging to study. It's highly dynamic and it's heterogeneous," Chen said. Because of this, mechanistic studies of intrinsically disordered proteins like p21 have been limited. Experiment alone is not sufficient and computer modeling is necessary to provide important missing details, he said. A tight integration of both could lead to a precise understanding of how structural flexibility influences function of p21 and other intrinsically disordered proteins.

"For me this is one of the most interesting IDPs," Chen said. "I'm a theorist and I want to use this system to understand the principles of how this type of proteins can perform their functions. Even though they are disordered, they are not random; there is no chaos. They still have some type of residual structures and certain features which allow function to be controlled in a precise way, and I want to understand the underlying mechanism of how this occurs."

Chen is continuing work with p21 and other small proteins that regulate cell cycles.

Provided by Kansas State University (news : web)

New aging cause revealed by test tube

Chemists from The Australian National University have discovered a new way that ageing-related diseases can progress, opening up new preventative and treatment possibilities for conditions such as heart disease and Alzheimer’s disease.

Led by Professor Chris Easton and Dr. Dannon Stigers from the ARC Centre of Excellence for Free Radical Chemistry and Biotechnology at ANU, the researchers have used the test tube to simulate the living body, and revealed a new process through which ageing related diseases may develop. Their work has been published in a recent edition of The Royal Society Chemistry journal, Chemistry Communications.

“Remarkably the good old test tube has given us a fantastic window from which to look into the basic processes necessary for life and it has changed the way we think about how ageing related diseases develop,” said Dr. Stigers.

It had been assumed that lifestyle choices such as diet, exercise, and smoking caused some people to develop ageing related illnesses more rapidly than others. Poor lifestyle decisions increase exposure to free radicals which can damage proteins in the body leading to their accumulation and eventual disease. However, in this study the researchers were able to observe proteins being made with their building blocks already damaged, indicating there are two possible pathways to age-related disease development that can be exploited for future treatments.

“We are not saying that a healthy lifestyle is not important to prevent early onset of age-related disease, but we now need to acknowledge that it may not be enough to advise people to eat the right foods and exercise regularly,” said Dr. Stigers.

In their test tube of life, the researchers added all the necessary machinery to make proteins, including both damaged and healthy protein building blocks, and a type of biological proof-reader that ensures proteins are made with only the healthy building blocks. They then looked to see if any of the damaged building blocks made it into the finished protein.

“We were surprised to find that the damaged building blocks were able to effectively compete for incorporation into the final protein even when our proof-reader was present,” said Professor Chris Easton.

“It may seem subtle but from a treatment perspective the difference between preventing a protein from being damaged and dealing with one that is made from damaged goods is vast. This is a significant break through and one which we hope will prove revolutionary in terms of tackling age-related diseases,” he added.

Provided by Australian National University