Pharmacological Justification for the Medicinal Use of Plumeria rubra Linn. in Cardiovascular Disorders.
Imran Ahmad KhanMusaddique HussainShahzada Khurram SyedMalik SaadullahAli Musfer AlqahtaniTaha AlqahtaniAfaf A AldahishSaeed AsiriLing-Hui ZengPublished in: Molecules (Basel, Switzerland) (2021)
Plumeria rubra (L.) is a traditional folkloric medicinal herb used to treat cardiovascular disorders. The present investigation was methodically planned to investigate the pharmacological foundations for the therapeutic effectiveness of P. rubra in cardiovascular illnesses and its underlying mechanisms. Ex vivo vaso-relaxant effects of crude leaf extract of P. rubra were observed in rabbit aorta ring preparations. Hypotensive effects were measured using pressure and force transducers connected to the Power Lab data acquisition system. Furthermore, P. rubra displayed cardioprotective properties in rabbits when they were exposed to adrenaline-induced myocardial infarction. In comparison to the intoxicated group, the myocardial infarction model showed decreased troponin levels, CK-MB, LDH, ALT, ALP, AST, and CRP, as well as necrosis, apoptosis, oedema, and inflammatory cell enrollment. P. rubra has revealed good antioxidant properties and prolonged the noradrenaline intoxicated platelet adhesion. Its anticoagulant, vasorelaxant, and cardioprotective effects in both in vivo and ex vivo investigations are enabled by blocking L-type calcium channels, lowering adrenaline, induced oxidative stress, and tissue tear, justifying its therapeutic utility in cardiovascular disorders.
Keyphrases
- oxidative stress
- heart failure
- single cell
- randomized controlled trial
- left ventricular
- systematic review
- hydrogen peroxide
- pulmonary artery
- cell death
- endoplasmic reticulum stress
- venous thromboembolism
- nitric oxide
- electronic health record
- coronary artery
- pulmonary hypertension
- cell proliferation
- staphylococcus aureus
- stem cells
- high glucose
- single molecule
- cystic fibrosis
- mesenchymal stem cells
- cell cycle arrest