The ethanolic extract of Kaempferia parviflora reduces ischaemic injury in rat isolated hearts

Aims of the study

The ethanolic extract of Kaempferia parviflora (KPE) has been reported to contain a range of flavonoids and to enhance endothelial synthesis of NO. We investigated the vascular relaxant, antioxidant and cardioprotective activities of KPE.

Materials and methods

Vascular function was assessed in rat aortic rings and superoxide generation determined using lucigenin enhanced chemiluminescence. Ischaemia and reperfusion were induced in rat isolated, perfused hearts.

Results

KPE caused vasorelaxation (R_max 102 ± 2%), which was partly inhibited by removal of the endothelium (R_max 91 ± 1%) or by N^G-nitro-l-arginine (L-NNA, R_max 83 ± 3%) or 1H-1,2,4] oxadiazolo4,3-a]quinoxaline-1-one (ODQ, R_max 80 ± 2%). In addition KPE caused concentration-dependent inhibition of the contractile response to exogenous Ca²⁺. KPE (10⁻³ M) also significantly inhibited superoxide radical generation induced by of xanthine/xanthine oxidase (2.3 ± 0.4% of control) to a similar extent to the xanthine oxidase inhibitor allopurinol (10⁻⁴ M, 1.6 ± 0.5%) or by rat isolated aorta in the presence of NADPH (30.0 ± 6.3% of control) similarly to the NADPH oxidase inhibitor diphenyliodonium (5 × 10⁻⁶ M, 23.1 ± 5.6%). In the presence of oxidant stress generated by pyrogallol endothelium-dependent relaxation of rat aortic rings was impaired (ACh R_max control 99 ± 1%; pyrogallol 44 ± 5%), an effect that was significantly reduced by KPE (10⁻⁴ M, ACh R_max 82 ± 4%). In addition, KPE was found to attenuate the ventricular dysfunction caused by 20 min global ischaemia and 30 min reperfusion (I/R) in rat isolated hearts (dP/dt IR 1016 ± 242, IR + KPE 2238 ± 233 mmHg/s).

Conclusion

KPE is an effective vasodilator and antioxidant that is able to prevent myocardial ischaemia-reperfusion injury. We suggest that KPE may be useful as an adjunct to thrombolytic therapy in the management of reperfusion injury.