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Herbal Munziq Ameliorates Myocardial Ischemia-Reperfusion Injury by Inhibiting Inflammation
Published on: January 10, 2025
Curcuma oil reduces endothelial cell-mediated inflammation in postmyocardial ischemia/reperfusion in rats
Amit Manhas1, Vivek Khanna, Prem Prakash
1*Department of Pharmacology, CSIR-Central Drug Research Institute, Lucknow, India; †Department of Internal Medicine, University of Iowa Health care, Iowa City, IA; ‡Department of Pharmaceutics, CSIR-Central Drug Research Institute, Lucknow, India.
Insights
Curcuma oil (C.oil) effectively protects against myocardial ischemia/reperfusion (MI/RP) injury by reducing inflammation in endothelial cells and improving heart function. This herbal treatment offers a potential therapeutic strategy for post-heart attack complications.
Area of Science:
- Cardiovascular Biology
- Pharmacology
- Cellular Biology
Background:
- Post-myocardial infarction inflammation involving endothelial cells can lead to severe complications.
- Curcuma oil (C.oil), derived from Curcuma longa, is known for neuroprotection but its role in myocardial ischemia/reperfusion (MI/RP) and endothelial function is unclear.
Purpose of the Study:
- To investigate the protective effects of Curcuma oil on myocardial ischemia/reperfusion (MI/RP) injury and endothelial cell-mediated inflammation.
- To elucidate the mechanisms by which C.oil modulates endothelial cell responses in the context of MI/RP.
Main Methods:
- In vivo studies using a rat MI/RP injury model.
- In vitro assays with EA.hy926 endothelial cells.
- Enzyme-linked immunosorbent assay (ELISA), real-time polymerase chain reaction (RT-PCR), and myography were employed.
- Assessment of inflammatory gene and adhesion factor expression, and inflammatory cell adhesion to endothelial cells.
Main Results:
- C.oil treatment (250 mg/kg) before and after MI/RP surgery significantly protected rats, reducing left ventricular ischemic area and inflammation.
- C.oil decreased the expression of proinflammatory genes and adhesion factors (E-selectin, ICAM-1) on endothelial cells.
- Reduced adhesion of THP-1 monocytes to endothelial cells was observed, indicating decreased inflammatory cell recruitment.
- C.oil demonstrated efficacy in both in vivo and in vitro models, confirming its anti-inflammatory effects on endothelial cells.
Conclusions:
- Curcuma oil exerts a protective effect against MI/RP injury by mitigating endothelial cell-mediated inflammation, particularly in the ischemic region.
- Pretreatment and posttreatment with C.oil can reduce MI/RP-induced damage, highlighting its therapeutic potential.
- The findings suggest C.oil is a promising agent for managing post-myocardial infarction inflammation and improving endothelial function.
Abstract:
Endothelial cells initiated inflammation persisting in postmyocardial infarction needs to be controlled and moderated for avoiding fatal complications. Curcuma oil (C.oil, Herbal Medicament), a standardized hexane soluble fraction of Curcuma longa has possessed neuroprotective effect. However, its effect on myocardial ischemia/reperfusion (MI/RP) and endothelial cells remains incompletely defined. Here, using in vivo rat MI/RP injury model and in vitro cellular approaches using EA.hy926 endothelial cells, enzyme-linked immunosorbent assay, real-time polymerase chain reaction, and myograph, we provide evidence that with effective regimen and preconditioning of rats with C.oil (250 mg/kg, PO), before and after MI/RP surgery protects rats from MI/RP-induced injury. C.oil treatment reduces left ventricular ischemic area and endothelial cell-induced inflammation, specifically in the ischemic region (*P < 0.0001) and improved endothelial function by reducing the expression of proinflammatory genes and adhesion factors on endothelial cells both in vitro and in vivo. Furthermore, mechanistic studies have revealed that C.oil reduced the expression of adhesion factors like E-selectin (#P = 0.0016) and ICAM-1 ($P = 0.0069) in initiating endothelial cells-induced inflammation. In line to the real-time polymerase chain reaction expression data, C.oil reduced the adhesion of inflammatory cells to endothelial cells as assessed by the interaction of THP-1 monocytes with the endothelial cells using flow-based adhesion and under inflammatory conditions. These studies provide evidence that salutary effect of C.oil on MI/RP could be achieved with pretreatment and posttreatment of rats, C.oil reduced MI/RP-induced injury by reducing the endothelial cell-mediated inflammation, specifically in the ischemic zone of MI/RP rat heart.

