Beneficial Effect of Silymarin in Pressure Overload Induced Experimental Cardiac Hypertrophy.
Basant SharmaUdit ChaubeBhoomika M PatelPublished in: Cardiovascular toxicology (2019)
The present investigation was undertaken to study the effect of silymarin on cardiac hypertrophy induced by partial abdominal aortic constriction (PAAC) in Wistar rats. Silymarin was administered for 9 weeks at the end of which we evaluated hypertrophic, hemodynamic, non-specific cardiac markers, oxidative stress parameters, and determined mitochondrial DNA concentration. Hypertrophic control animals exhibited cardiac hypertrophy, altered hemodynamics, oxidative stress, and decreased mitochondrial DNA (mtDNA) concentration. Treatment with silymarin prevented cardiac hypertrophy, improved hemodynamic functions, prevented oxidative stress and increased mitochondrial DNA concentration. Docking studies revealed that silymarin produces maximum docking score with mitogen-activated protein kinases (MAPK) p38 as compared to other relevant proteins docked. Moreover, PAAC-control rats exhibited significantly increased expression of MAPK p38β mRNA levels which were significantly decreased by the treatment of silymarin. Our data suggest that silymarin produces beneficial effects on cardiac hypertrophy which are likely to be mediated through inhibition of MAPK p38β.
Keyphrases
- mitochondrial dna
- oxidative stress
- copy number
- diabetic rats
- signaling pathway
- dna damage
- induced apoptosis
- ischemia reperfusion injury
- molecular dynamics
- abdominal aortic
- heart failure
- molecular dynamics simulations
- protein protein
- pi k akt
- genome wide
- machine learning
- spinal cord injury
- electronic health record
- combination therapy
- dna methylation
- small molecule
- heat shock
- long non coding rna
- binding protein
- endoplasmic reticulum stress
- heat shock protein
- preterm birth
- neuropathic pain
- cell proliferation
- spinal cord
- drug induced
- case control
- stress induced
- data analysis