Abstract
Phikud Navakot (PN) is nine major herbs in a famous traditional Thai recipe namely “Yahom Navakot” used to treat cardiovascular disorders. This study investigated the cardioprotective effects of PN formula on isoproterenol-induced myocardial infarction (IMI) in Sprague-Dawley rats. Forty-five rats were randomly divided into nine groups (n = 5 per group): the control, the IMI, the IMI + propranolol, the control or the IMI + PN formula (PN ethanolic extract at doses of 64, 127, or 255 mg/kg) by oroesophageal gavage for 28 days. The ST segment and serum troponin T levels were significantly increased in IMI rats. PN did not eliminate tissue necrosis, infiltration of inflammatory cells, or interstitial edema in IMI rats. All doses of PN decreased (p < 0.001) serum TNF-α and IL-6 levels. PN (127 and 255 mg/kg) up-regulated (p < 0.05) heme oxygenase (HO)-1 expression, whereas PN (255 mg/kg) significantly increased superoxide dismutase (SOD) 1 and 2 expression, compared with IMI rats. Nuclear factor erythroid 2-related factor 2 (Nrf2) and HO-1 expression significantly increased in IMI rats and IMI rats that received PN. PN formula possesses potential anti-inflammatory and antioxidant properties by modulating the levels of TNF-α, IL-6 and antioxidant enzymes. Our study reveals a novel cardioprotective effect of PN in IMI rats through the Nrf2/HO-1 signaling.
Highlights
Myocardial infarction (MI) is a major cause of death worldwide and puts surviving patients at risk of developing other vascular diseases
Phikud Navakot (PN) and some of its components, such as T. chebula, P. kurrooa, A. pallen, and N. jatamansi, were shown to possess free radical scavenging activities against superoxide anions and hydroxyl radicals in an in vitro study [8]. Due to this finding and the fact that oxidative stress and inflammation are the major causes of cardiac injury in MI [9, 10], this study evaluated the cardioprotective effects of PN in ISO-induced MI (IMI) in rats using various techniques. ese techniques included an assessment of the degree of histopathological changes, measurements of levels of nitric oxide (NO), and the proinflammatory cytokines tumor necrosis factor-α (TNF-α) and IL-6, and the evaluation of the protein expression of the antioxidant enzymes glutathione peroxidase (GPx), superoxide dismutase (SOD), catalase, nuclear factor erythroid 2-related factor 2 (Nrf2), and heme oxygenase (HO)-1
Effect of PN Formula on the Electrocardiogram. e control group and the normal rats that received orally administered PN (64, 127, or 255 mg/kg) showed normal ECG readings (Figure 1(a)), whereas rats injected with ISO showed a significant increase in the ST segment, an indicator of MI, when compared with the controls. e administration of Pro (30 mg/kg) was able to statistically significantly dampen ISO-induced ST elevations when compared with the induced myocardial infarction (IMI) rats (Figure 1(b)). ough PN formula treatment could not completely suppress the ISO-induced elevation of the ST segment, a significant decrease in the ST segment was observed in PNtreated rats compared with the IMI rats (Figure 1(b))
Summary
Myocardial infarction (MI) is a major cause of death worldwide and puts surviving patients at risk of developing other vascular diseases. ISO administration causes an elevation in the ST segment in ECG readings. It caused an increase in the levels of cardiac injury biomarkers, including troponin I, troponin T, creatine kinase-MB, lactate dehydrogenase, alkaline phosphatase, serum glutamic oxaloacetic transaminase, aspartate transaminase, and alanine transaminase [1,2,3,4]. The ISO-induced myocardial changes were the result of an increase in oxidative stress through reductions of the components of the Evidence-Based Complementary and Alternative Medicine myocardial antioxidant system, including glutathione, glutathione reductase, glutathione-S-transferase, glutathione peroxidase (GPx), superoxide dismutase (SOD), and catalase, in rat hearts [3, 5]. Other compounds associated with MI are nitric oxide (NO) and its metabolites, which have been reported to protect the heart from ischemia/reperfusion (IR) injury and decrease MI in general [7]
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