||Naringin exhibits antioxidant, anti-atherogenic, antiulcer, anti-hypocholesterolemic, anti-lipoperoxidative, and anti-hyperglycemia effects. Naringin reduces Ara-C-induced oxidative stress through both an inhibition of the generation of ROS production and an increase in antioxidant enzyme activities, it blocks apoptosis caused by Ara-C-induced oxidative stress, resulting in the inhibition of the cytotoxicity of Ara-C. Naringin attenuates epidermal growth factor (EGF)-induced MUC5AC secretion in A549 cells by suppressing the cooperative activities of MAPKs-AP-1 and IKKs-IκB-NF-κB signaling pathways. |
|J Pharm Bioallied Sci. 2015 Apr-Jun;7(2):121-7. |
|Effect of naringin on hemodynamic changes and left ventricular function in renal artery occluded renovascular hypertension in rats.[Pubmed: 25883516]|
|Renal artery occlusion (RAO) induced hypertension is a major health problem associated with structural and functional variations of the renal and cardiac vasculature. Naringin a flavanone glycoside derived possesses metal-chelating, antioxidant and free radical scavenging properties. The objective of this study was to investigate the antihypertensive activity of Naringin in RAO induced hypertension in rats. |
METHODS AND RESULTS:
Male Wistar rats (180-200 g) were divided into five groups Sham, RAO, Naringin (20, 40 and 80 mg/kg). Animals were pretreated with Naringin (20, 40 and 80 mg/kg p.o) for 4 weeks. On the last day of the experiment, left renal artery was occluded with renal bulldog clamp for 4 h. After assessment of hemodynamic and left ventricular function various biochemical (superoxide dismutase [SOD], glutathione [GSH] and malondialdehyde [MDA]) and histological parameters were determined in the kidney. RESULTS: RAO group significantly (P < 0.001) increased hemodynamic parameters at 15, 30 and 45 min of clamp removal. Naringin (40 and 80 mg/kg) treated groups showed a significant decrease in hemodynamic parameters at 15 min. after clamp removal that remained sustained for 60 min. Naringin (40 and 80 mg/kg) treated groups showed significant improvement in left ventricular function at 15, 30 and 45 min after clamp removal. Alteration in level of SOD, GSH and MDA was significantly restored by Naringin (40 and 80 mg/kg) treatment. It also reduced histological aberration induced in kidney by RAO.
It is concluded that the antihypertensive activity of Naringin may result through inhibition of oxidative stress.
|Life Sci. 2010 Jun 19;86(25-26):928-35. |
|Nitric oxide mechanism in the protective effect of naringin against post-stroke depression (PSD) in mice.[Pubmed: 20433854 ]|
|The present study has been designed to explore the nitric oxide mechanism in the protective effect of Naringin against I/R induced neurobehavioral alterations, oxidative damage and mitochondrial dysfunction in mice.
METHODS AND RESULTS:
Laca mice (25-30 g) were subjected twice to BCCAO occlusion (5 min) at the interval of 10 min, followed by 96 h reperfusion. Naringin (50 and 100 mg/kg) was administered for 10 days, starting 7 days before the animals were subjected to I/R injury. On day 10, various neurobehavioral parameters followed by biochemical parameters and mitochondrial enzyme complex activities were assessed.
Ischemia reperfusion injury caused significant (increased immobility period, neurological score and decreased locomotor activity) oxidative damage (increased lipid peroxidation and nitrite concentration and depleted reduced glutathione, glutathione-S-transferase, superoxide dismutase and catalase) and altered mitochondrial enzyme complex activities (complex I to IV) as compared to sham treatment. Naringin (50 and 100 mg/kg) treatment significantly attenuated neurobehavioral alterations, oxidative damage and restored mitochondrial enzyme complex activities as compared to control (ischemia reperfusion) group. Further, protective effect of Naringin (50 mg/kg) was attenuated by l-arginine (100 mg/kg) or sildenafil (5 mg/kg) pretreatment. Further, L-NAME (10 mg/kg) or 7-NI (10 mg/kg) pretreatment with Naringin (50 mg/kg) significantly potentiated their protective effect as compared to their treatment alone.
The present study suggests the involvement of nitric oxide mechanism in the protective effect of Naringin against post-stroke depression induced neurobehavioral, biochemical and cellular alterations in mice.
|Toxicology. 2007 Feb 12;230(2-3):178-88. |
|Preventive effect of naringin on cardiac markers, electrocardiographic patterns and lysosomal hydrolases in normal and isoproterenol-induced myocardial infarction in Wistar rats.[Pubmed: 17188415 ]|
|Diets rich in natural antioxidants are associated with reduced risk of heart diseases. |
METHODS AND RESULTS:
This study was aimed to evaluate the preventive role of Naringin on cardiac troponin T (cTnT), lactate dehydrogenase (LDH)-isoenzyme, cardiac marker enzymes, electrocardiographic (ECG)-patterns and lysosomal enzymes in isoproterenol (ISO)-induced myocardial infarction (MI) in male Wistar rats. Rats subcutaneously injected with ISO (85mg/kg) at an interval of 24h for 2 days showed a significant increase in the levels of cTnT, intensity of the bands of LDH-isoenzyme (LDH1 and LDH2) and the activities of cardiac marker enzymes such as creatine kinase-MB (CK-MB), creatine kinase (CK), LDH, aspartate transaminase (AST) and alanine transaminase (ALT) in serum with subsequent decrease in the activities of CK, LDH, AST and ALT in the heart and alterations in ECG-patterns. The activities of lysosomal enzymes (beta-glucuronidase, beta-N-acetyl glucosaminidase, beta-galactosidase, cathepsin-B and cathepsin-D) were increased significantly in serum and the heart of ISO-induced rats, but the activities of beta-glucuronidase and cathepsin-D were decreased significantly in the lysosomal fraction of the heart. Pretreatment with Naringin (10, 20 or 40mg/kg) daily for a period of 56 days positively altered the levels of cTnT, intensity of the bands of the LDH1 and LDH2-isoenzyme and the activities of cardiac marker enzymes, ECG-patterns and lysosomal hydrolases in ISO-induced rats.
Thus, Naringin possess cardioprotective effect in ISO-induced MI in rats.
|Pharmacology. 1994 Sep;49(3):144-50. |
|Antiulcer effect of naringin on gastric lesions induced by ethanol in rats.[Pubmed: 7972328]|
|This study was designed to determine the gastroprotective properties of Naringin on and the involvement of endogenous prostaglandins in mucosal injury produced by absolute ethanol. |
METHODS AND RESULTS:
Oral pretreatment with the highest dose of Naringin (400 mg/kg), 60 min before absolute ethanol was the most effective antiulcer treatment. Subcutaneous administration of indomethacin (10 mg/kg) to the animals treated with Naringin (400 mg/kg) partially inhibited gastric protection, but the prostaglandin E2 determination did not show any increase in prostanoid levels. The contents of gastric mucus and total proteins were not significantly modified. Naringin-treated rats showed a marked increase in hexosamine levels, but this increase was less in animals pretreated with indomethacin.
These results show that Naringin has a 'cytoprotective' effect against ethanol injury in the rat, but this property appears to be mediated by non-prostaglandin-dependent mechanisms.