Toxicology Reports (Jan 2021)

The cardio and renoprotective role of ginseng against epinephrine-induced myocardial infarction in rats: Involvement of angiotensin II type 1 receptor/protein kinase C

  • Abeer Salama,
  • Dina Mansour,
  • Rehab Hegazy

Journal volume & issue
Vol. 8
pp. 908 – 919

Abstract

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The expression of angiotensin II type 1 receptor (AT1 receptor)/protein kinase C (PKC) in heart tissues has a vital role in myocardial infarction (MI). The current work aimed to clarify the renal complication enhanced by MI following epinephrine injection via AT1 receptor/ PKC expression; in addition, the impact of ginseng extract on epinephrine-induced MI and its renal complication was assessed. Adult male albino Wistar rats were pretreated orally with ginseng extract (200 & 400 mg/kg/day) for 14 days, then two successive doses of epinephrine injection (100 mg/kg, i.p.). Epinephrine evoked electrocardiographic (ECG) and renal changes accompanied with a significant increase in heart and kidney contents of malodialdehyde (MDA), nitric oxide (NO), protein kinase C (PKC), heart contents of nuclear factor-kabba B (NF-κB) and angiotensin 1receptor (AT1R), as well as a decrease in heart and kidney reduced glutathione (GSH) and nuclear factor-erythroid-related factor 2 (Nrf2) contents. In histopathological investigations epinephrine exhibited deleterious heart changes in the form of acute MI with the presence of necrosis of cardiomyocytes with iNOS expression and produced glomerulus and renal tubules degeneration. Pretreatment of rats with ginseng extract in both doses significantly corrected epinephrine-induced heart and renal changes. The current work revealed that epinephrine-induced MI associated with aggravated renal complication and ginseng extract has cardio and reno protective role against this as it reduces infarct size, preserves cardiac and renal tissues and functions through activating Nrf2 and down-regulating NF-κB, PKC, AT1R and iNOS.

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