Cardioprotective role of phyllanthin against myocardial ischemia-reperfusion injury by alleviating oxidative stress and inflammation with increased adenosine triphosphate levels in the mice model.

BACKGROUND

Ischemic heart disease is an imperative cause of high morbidity and mortality globally. The cardiac ischemia/reperfusion damage occur in both reperfusion and ischemia.

OBJECTIVE

In this exploration, we have planned to examine the cardio-protective action of phyllanthin against the myocardial ischemic-reperfusion injury in mice.

MATERIALS AND METHODS

The myocardial ischemic reperfusion injury (MI-RI) stimulated via coronary artery occlusion, followed by the 10 mg/kg of phyllanthin treatment. The serum cardiac markers and pro-inflammatory markers level was investigated by using the assay kits. The expressions of oxidative stress and inflammatory markers level were investigated by immunohistochemical analysis. Lipid peroxidation, antioxidant enzymes, and ATPase levels level was examined by standard methods. The expression of oxidative stress markers were inspected by the reverse transcription polymerase chain reaction technique. The heart histology was investigated microscopically.

RESULTS

The phyllanthin treatment increased the body weight, and heart weight also diminished the infarct size in the MI/RI mice. Cardiac markers status was diminished and the blood pressure markers were augmented by the phyllanthin. Histological analysis revealed the protective role of phyllanthin. Suppressed lipid peroxidation and enhanced antioxidant enzymes were noted in the phyllanthin treated mice MI-RI mice. Phyllanthin appreciably suppressed the pro-inflammatory regulators that is, NF-αB p65, IL-6, IL-1β, and TNF-α and enhanced the antioxidant marker expressions. ATPase levels were improved by the phyllanthin in the MI-RI mice.

CONCLUSION

These novel findings were confirmed the therapeutic role of phyllanthin against the MI-RI in mice. Hence, it can be a promising agent to treat the MI-RI induced cardiac dysfunction.