Since the olden days herbal therapy has always been popular in India. Before such modern techniques came into prominence, almost all the Indians depended on them for curing diseases. And now, an Indian scientist has put forward the advantages of herbal therapy in averting hypertrophy in a new study.
Mahesh Gupta, who is the director of the Cardiac Cell Biology Research Program at the University of Chicago and author of the research, along with his research team performed a test on mice that proved to cure hypertrophy – a thickening of cardiac muscle a lot due to chronic blood pressure that causes the heart to enlarge and can direct to heart failure as a consequence.
Photo Credit: Kuebi
The research team obtained a natural compound namely “honokiol (hoh-NOH’-kee-ohl)” from the bark of magnolia tree and introduced it into the mice. They observed that “honokiol” decreased the extra growth of separate cardiac muscle cells, decreased ventricular wall thickness and averted the gathering of interstitial fibrosis – hardening of cardiac muscle cells, which cuts their capability to contract. Not only this, it protected cardiac muscle cells from the harm that oxidative stress produced, which can destroy DNA.
The research team, based at the University of Chicago, also discovered that “honokiol” stimulates SIRT3 – a defensive protein, related to late ageing, stress resistance and metabolic regulation.
Gupta said that by increasing the SIRT3 levels, honokiol “effectively blocked both the induction and progression of cardiac hypertrophy in mice.” He added that the compound even alleviated already “pre-existing hypertrophy,” showing potentiality to play an important part in averting and treating heart failure.
SIRT3 that belongs to the family of “sirtuin” proteins is chiefly active in mitochondria from where the cells derive their main source of energy. In mitochondria SIRT3 plays the lead part in energy metabolism and in thwarting acetylation – a procedure that can modify the operation of proteins altogether. If SIRT3 is missing in the mitochondrial proteins then the latter becomes hyperacetylated that can damage its operation.
The research stated that human studies reflect that inactive patients whose age is over 60 years have almost 40 percent less SIRT3 levels in them. In case of mice, the ones that lack the gene for SIRT3 have 40 percent lower levels of ATP, which is a chief source of energy as compared to the ones who have the gene.
As part of their research, the team examined several compounds in quest of one, which could stimulate SIRT3 levels. They discovered that “honokiol” decreased acetylation in mitochondrial proteins and when introduced in the cardiac muscle cells in mice, within 24 hours only a little amount of it triggered almost two-fold increase in the SIRT3 levels.
Other than reducing or preventing hypertrophy increase in cardiac muscle cells and even decreasing pre-existing hypertrophy in mice, honokiol also impeded the manufacture of fibroblasts, which are the cells that meddle with cardiac muscle functioning.
It also diminished the manufacture of myofibroblasts, which are cells that pace up wound healing, but at the cost of possible harm to heart function. The research team didn’t discover any considerable toxicity.
To authenticate the procedure, the research team conducted the same examinations on mice that had no SIRT3 present in their genes and saw that honokiol had no effect on them.
They also established that honokiol directly attaches with SIRT3 and the grouping appeared to provoke SIRT3’s activity.
The researchers wrote that these results that advocate pharmacological activation of SIRT3 by honokiol could be a “potential therapeutic strategy” to thwart harmful “cardiac remodeling” and other illnesses related with “abnormal cellular growth and organ fibrosis.”
The study was published in the journal Nature Communications.
According to the Cleveland Clinic, around 600,000 to 1.5 million Americans , which is one in 500 people are affected by hypertrophy. WHO report on 2008 tables shows that 17,327,000 people suffer from cardiovascular diseases altogether across the globe.