Abstract
Mitochondrial dysfunction plays a critical role in the development of cardiac hypertrophy and heart failure. So mitochondria are emerging as one of the important druggable targets in the management of cardiac hypertrophy and other associated complications. In the present study, effects of ethanolic extract of Boerhaavia diffusa (BDE), a green leafy vegetable against mitochondrial dysfunction in angiotensin II (Ang II) induced hypertrophy in H9c2 cardiomyoblasts was evaluated. H9c2 cells challenged with Ang II exhibited pathological hypertrophic responses and mitochondrial dysfunction which was evident from increment in cell volume (49.09±1.13%), protein content (55.17±1.19%), LDH leakage (58.74±1.87%), increased intracellular ROS production (26.25±0.91%), mitochondrial superoxide generation (65.06±2.27%), alteration in mitochondrial transmembrane potential (ΔΨm), opening of mitochondrial permeability transition pore (mPTP) and mitochondrial swelling. In addition, activities of mitochondrial respiratory chain complexes (I-IV), aconitase, NADPH oxidase, thioredoxin reductase, oxygen consumption rate and calcium homeostasis were evaluated. Treatment with BDE significantly prevented the generation of intracellular ROS and mitochondrial superoxide radicals and protected the mitochondria by preventing dissipation of ΔΨm, opening of mPTP, mitochondrial swelling and enhanced the activities of respiratory chain complexes and oxygen consumption rate in H9c2 cells. Activities of aconitase and thioredoxin reductase which was lowered (33.77±0.68% & 45.81±0.71% respectively) due to hypertrophy, were increased in BDE treated cells (P≤0.05). Moreover, BDE also reduced the intracellular calcium overload in Ang II treated cells. Overall results revealed the protective effects of B. diffusa against mitochondrial dysfunction in hypertrophy in H9c2 cells and the present findings may shed new light on the therapeutic potential of B. diffusa in addition to its nutraceutical potentials.
Highlights
Heart diseases are one of the leading causes of death worldwide [1]
Alteration in mitochondrial function plays a key role in the pathogenesis of cardiac hypertrophy that may leads to heart failure [6]
Over 90% of energy consumption of the heart is from mitochondria and it plays key role in many cellular functions including energy production, calcium homeostasis and cell signalling [34]
Summary
Hypertension accounts a major risk for the development of cardiac diseases through induction of left ventricular hypertrophy and this leads to congestive heart failure and death [2]. It has been shown that angiotensin II stimulate mitochondrial dysfunction in cardiac cells and subsequently produce excessive amounts of ROS such as superoxide, hydrogen peroxide, and peroxynitrite. This overproduction of mitochondrial ROS has been implicated in heart failure [8]. Since mitochondrial dysfunction plays a critical role in the development of cardiac hypertrophy and heart failure, the mitochondria is emerging as one of the important druggable targets in the management of cardiac hypertrophy and other associated complications
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