Jasminum sambac: A Potential Candidate for Drug Development to Cure Cardiovascular Ailments

Abstract

Jasminum sambac (L.) is a South Asian folkloric medicinal plant that has traditionally been used to treat cardiovascular problems. The current investigation was meticulously organized to explore the pharmacological foundation for the medicinal uses of J. sambac pertaining to cardiovascular ailments and to investigate the core mechanisms. Mechanistic investigation revealed that crude leaf extract of J. sambac produced ex-vivo vasorelaxant effects in endotheliumintact aorta ring preparation and hypotensive effect was recorded via pressure and force transducers coupled to the Power Lab Data Acquisition System. Moreover; J. sambac showed cardioprotective effects against adrenaline -induced left ventricular hypertrophy in rabbits observed hemodynamic. CK-MB, LDH, troponin, CRP, ALT, AST, ALP levels were shown to be lower in the myocardial infarction model, as were necrosis, oedema, and inflammatory cell recruitment in comparison to control. J. sambac has shown good antioxidant potential as well as prolonged the noradrenaline induced platelet adhesion. The vasorelaxant and cardioprotective effects in both in vivo and ex vivo experiments, which are enabled by activation of muscarinic receptor and/or releasing the nitric oxide and by reducing the adrenaline, induced oxidative stress, justifying its usage in cardiovascular disorders.

Keywords: ALT; AST; CK-MB; CRP; adrenaline; cardioprotective.

Figure 1

HPLC chromatogram of hydroalcoholic leaf extract of J. samabac showing rutin (A) and isoquercetin (B) similar to standard.

Figure 2

Antioxidant potential of hydroalcoholic leaf extract of J. sambac by DPPH assay.

Figure 3

Cardioprotective effect of different doses of J. sambac extracts on the cardiac biomarkers, LDH (a), troponin (b) and CK-MB (c) against ADR-induced myocardial infarction in rabbits. One-way ANOVA was performed for the statistical analysis, comparisons among different groups was carried out by Dunnett’s multiple comparison test; ** p < 0.005 and *** p < 0.0001 (n = 5).

Figure 4

Cardioprotective effect of different doses of J. sambac extracts on the cardiac biomarkers, ALP (a), AST (b), ALT (c) and CRP (d) against ADR-induced myocardial infarction in rabbits. One-way ANOVA was performed for the statistical analysis, comparisons among different groups was carried out by Dunnett’s multiple comparison test; ** p < 0.005 and *** p < 0.0001 (n = 5).

Figure 5

Cardioprotective effect ofdifferent doses of J. sambac on (a) cardiac weight to body weight ratio and (b) cardiac weight to tail length ratio in ADR-induced cardiac hypertrophied rabbits. One-way ANOVA was performed for the statistical analysis, comparisons among different groups was carried out by Dunnett’s multiple comparison test; ** p < 0.005 and *** p < 0.0001 (n = 5).

Figure 6

Photomicrographs of rabbit ventricle section from ADR-induced group (a) shows images from ventricle sections received J. sambac 100 mg/kg + ADR (b) shows images from ventricle sections received J. sambac 200 mg/kg (c) Shows ventricle sections received J. sambac 300 mg/kg + ADR (d). Fewer cardiomyocytes deterioration, fibrosis and less inflammatory cells were observed in dose dependent fashion in comparison with ADR intoxicated group.

Figure 7

Effect of hydroalcoholic extract J. sambac against PE (1 μM) induced contraction on endothelium intact and denuded aorta (a), noradrenaline (10 µM) induced contraction (b), effect against PE (1 μM) induced contraction pretreated with L-NA (c) (1 × 10⁻⁴ M) and (d) atropine (1 × 10⁻⁶ M). All the values (n = 5) are depicted as mean ± SEM.

Figure 7

Effect of hydroalcoholic extract J. sambac against PE (1 μM) induced contraction on endothelium intact and denuded aorta (a), noradrenaline (10 µM) induced contraction (b), effect against PE (1 μM) induced contraction pretreated with L-NA (c) (1 × 10⁻⁴ M) and (d) atropine (1 × 10⁻⁶ M). All the values (n = 5) are depicted as mean ± SEM.

Figure 8

Effect of hydroalcoholic extract of J. sambac on the aggregation of platelet against ADR induced aggregation.