Evaluating the Antioxidant Potential of Naringin in Combating Sodium Nitrite-Induced Heart dysfunction in male rats
DOI:
https://doi.org/10.64252/eywn8e46Keywords:
sodium nitrite, naringen, troponin I, lactate dehydrogenase ,Glutathione, melanodehydeAbstract
Sodium nitrite is extensively utilized as a food preservative; nevertheless, excessive exposure has been associated with oxidative stress. Citrus fruits naturally contain naringen, a flavonoid with strong anti-inflammatory and antioxidant qualities. In a rat model, this study sought to assess naringen ability to prevent sodium nitrite-induced heart oxidative dysfunction. Forty adult male rats were randomly divided into four groups: Rats in the control group (C) were given only food and water for the course of the investigation. Sodium Nitrite Group (G1): Rats were given oral sodium nitrite at a dose of 5 mg/kg/BW and, after three weeks, were given oral naringin at a dose of 25 mg/kg/BW. Rats in the naringin + sodium nitrite Group (G2) were given an oral dose of 25 mg/kg/Bw of naringin along with 5 mg/kg/Bw of sodium nitrite. Naringin Group (G3): During the trial, rats were given naringin orally at a dose of 25 mg/kg/BW. The results showed that oral intubation of Sodium nitrite for 45days induce oxidative heart stress, by a substantial elevated (P≤0.05) in troponin I, ck-mb , LDH , malondialdehyde MDA and decrease in GSH, whereas naringen was given orally showed a considerable decrease (P≤0.05) in cardiac markers and MDA with inceased in GSH. Histological examination revealed myocardial changes . Co-treatment with naringenin markedly attenuated these changes, restoring antioxidant levels and preserving cardiac damage tissue . The outcome of this study indicate that by improving the antioxidant defense system and maintaining myocardial structure, naringen significantly minimizes the harmful impact of sodium nitrite on heart tissue.