Objective: Myocardial infarction (MI) occurs when blood supply to a part of the heart is reduced, causing ischemia and cell death. Paradoxically, therapeutic reperfusion can damage heart tissue through the production of reactive oxygen species (ROS), leading to oxidative stress. LL is a potent medicinal plant recognized for its antioxidant, anti-inflammatory, anti-apoptotic, and anti-diabetic properties. Aims: This study aimed to investigate the effects and underlying mechanisms of LL on myocardial ischemia-reperfusion (IR) injury models in rats. Design and method: Healthy adult male albino Wistar rats (n=40) were randomly assigned to five groups: sham (n=8), IR-control (n=8), LL-100+IR (n=8), LL-200+IR (n=8), and LL 200 per se (n=8). LL was administered orally daily for 28 days. On 29th day rats were anaesthetized using pentobarbitone sodium (60 mg/kg i.p) and ischemia was developed on 29th day by the occlusion of LAD coronary artery for 60 mins followed by reperfusion for 60 mins and simultaneously hemodynamic parameters were recorded. The rats were then sacrificed, heart was excised and further biochemical, inflammatory, morphological, and molecular studies were done. One-way ANOVA with Tukey–Kramer post hoc analysis was used. Results: Pretreatment with LL at a dose of 200 mg/kg improved cardiac function, including ventricular performance, as evidenced by +LV dp/dt (1377.57 ± 32.10 vs. 1566.76 ± 16.65 mm Hg/sec),- LV dp/dt (1208.81 ± 21.68 vs. 1172.49 ± 16.58 mm Hg/sec), and LVEDP. It also prevented the release of cardiac injury markers, namely CK-MB (672.28 ± 36.99 vs. 515.00 ± 17.32 U/L) and LDH (722.69 ± 41.79 vs. 534.06 ± 20.35 U/L), in serum compared with the IR control group. Antioxidant activity was evident from increased levels of GSH and SOD along with reduced MDA levels. Histopathological evaluation revealed preservation of myocardial morphological integrity. The TUNEL assay demonstrated an anti-apoptotic effect with reduced DNA fragmentation. In addition, inhibition of MAP kinase signaling and enhancement of the Nrf-2/HO-1 pathway were observed. Conclusions: LL shows protective effects against ischemia-reperfusion injury by modulating MAPK/Nrf-2/HO-1, and MAPKNFBp65TNF pathways, exhibiting anti-inflammatory, antioxidant, and anti-apoptotic properties, suggesting potential as a therapeutic agent for myocardial ischemia-reperfusion injury.
Sahu et al. (2026) studied this question.