Beneficial Effects Of Hesperidin Research Articles

Beneficial effects of hesperidin following cis-diamminedichloroplatinum-induced damage in heart of rats.

Increased oxidative stress and histopathological damage have been implicated in the cardiotoxicity that limits the clinical therapy of cisplatin (CP) as an anti-cancer drug. This study aimed to investigate the protective effect of hesperidin (HP) against CP-induced cardiotoxicity in rats. Rats were divided into four groups (n = 7/group), and the first group served as the control group. Animals in Group CP and Group CP + HP received a single dose of CP (CP - 7 mg/kg); animals in Group HP and Group CP + HP received 50 mg/kg/day HP with gavage for 14 days. At the end of day 14, cardiac tissue samples were histologically and biochemically examined. In this experimental study, thiobarbituric acid reactive substances levels in the cardiac tissue were significantly higher in the CP group, whereas glutathione (GSH), superoxide dismutase (SOD), and CAT levels were significantly lower in this group. On the other hand, GSH and SOD levels in the CP + HP group were similar to the control group. There was no significant difference in cardiac CAT levels between Group CP and Group CP + HP. Hesperetin treatment leads to a decrease in oxidative stress, and associated histological damage. The findings of the current study suggest that HP has a protective effect against CP-induced cardiotoxicity.

Beneficial Effects of Hesperidin against Cisplatin-Induced Nephrotoxicity and Oxidative Stress in Rats

Cisplatin has been frequently used for treatment of wide variety of tumors. The use of cisplatin is associated with severe cytotoxicity such as nephrotoxicity, hepatotoxicity and spermiotoxicity which radically limits its clinical use. The present study aimed to investigate the possible protective effects of multiple doses of hesperidin against cisplatin-induced nephrotoxicity induced by single i.p injection of cisplatin (7.5 mg/kg). Hesperidin was given to rats at two different doses (100 and 200 mg/kg p.o) for 7 days starting one day before cisplatin injection. Blood samples were collected for determination of serum creatinine and Blood Urea Nitrogen (BUN) levels. Kidneys were used for the determination of Malondialdehyde (MDA), Glutathione (GSH) and total nitrate and nitrite contents. Liver samples were also used for histopathological examination. Results showed that hesperidin significantly reduced cisplatin-induced elevations in serum creatinine and BUN levels. It also significantly reduced kidney MDA and NO content and elevated GSH content. In conclusion, hesperidin greatly protected kidney against cisplatin-induced toxicity in a dose-dependent manner.

Hesperidin, a Citrus Flavonoid, Has the Ameliorative Effects Against Experimental Autoimmune Encephalomyelitis (EAE) in a C57BL/J6 Mouse Model.

The aim of this study was determined the effects of Hesperidin (HP) on neuronal damage in brain tissue caused by Experimental allergic encephalomyelitis (EAE), an established model of multiple sclerosis in C57BL/J6 mice. To explore 40 mice were equally divided into four groups: (1) Control, (2) EAE, (3) HP, and (4) HP + EAE. 14 days after induction of EAE with MOG35-55 and pertussis toxin, the mice treated with HP at the doses of 50 mg/kg/day for 7 days subcutaneously. To our results HP treatment prevents the oxidative stress caused by EAE via a decrease in lipid peroxidations and increase in elements of the antioxidant defense systems in brain tissue. Also, EAE elevate the IL-17, express the pro-inflammatory cytokines, and caspase-3-like immunreactivity, show apoptosis, staining in EAE mice brain and increased the incidence of histopathological damage. However, immonohistochemical and histological changes were reversed with HP. Moreover, elevated TNF-α and IL-1β levels, a result of EAE, were decreased in serum and neurological deficits as clinical signs were reversed with HP treatment in EAE mice, given HP. In conclusion, HP treatment effectively prevents oxidative, immunological and histological damage in the brain caused by EAE. It was thought that the beneficial effects of HP are likely a result of its strong antioxidant and anti-inflammatory properties.

Toxic effects of systemic cisplatin on rat eyes and the protective effect of hesperidin against this toxicity

Context: In the present study, cisplatin (CP) induced eye toxicity and the beneficial effect of hesperidin (HP) was investigated.Methods: Twenty-eight rats were equally divided into four groups; the first group was kept as control. In the second and third group, CP and HP were given at the doses of 7 mg/kg and 50 mg/kg/d, respectively. In the fourth group, CP and HP were given together at the same doses. Tissue samples were collected on day 14 of CP treatment.Results: The results demonstrated that CP caused a significant increase in thiobarbituric acid reactive substances (TBARS) levels and decrease of glutathione levels and antioxidant enzyme activity (catalase, superoxide dismutase and glutathione peroxidase) in eye tissues compared to other groups, HP prevented these effects of CP. Besides, CP led to histopathological damage in the retina and cornea. On the other hand, HP treatment prevented histopathological effects of CP.Conclusion: CP had severe dose-limiting toxic effects and HP treatment can be beneficial against the toxic ocular effects of CP. Thus, it appears that co-administration of HP with CP may be a useful approach to attenuate the negative effects of CP on the eye.

Effect of Supplementation of Hesperidin on Growth Performance, Immune Response and Antioxidant Activity in Pigs

Three experiments were conducted to investigate the effects of hesperidin supplementation on growth performance, immune function, and antioxidant activity of growing pigs (56 d old; average BW 20.4±0.6kg). In Exp. 1, 24 pigs with an initial BW of 19.53 kg were randomly allotted to three treatments, and fed for 9-wk either on a basal diet (CON), alone or with 0.01% (Hes-1), and 0.02% hesperidin (Hes2). Initial and final BW, ADG or average daily feed intake were not different among the treatments. Hes-1 or Hes-2 groups, on the other hand, had a higher (P<0.05) gain: feed ratio compared to CON group. Antioxidant activity in terms of serum superoxide dismutase activity was increased (P<0.05) in Hes-2 compared to CON group. To confirm this beneficial effect of hesperidin as an antioxidant reagent, in vitro antioxidant activities of hesperidin were ascertained vis-a-vis butylated hydroxytoluence (BHT) in Exp. 2 by using the 1, 1-diphenyl-2-picrylhydrazyl (DPPH)-radical scavenging activity. Hesperidin showed lower (P<0.05) IC50(concentration for scavenging 50% of DPPH radicals) than BHT. In Exp.3, 12 barrows (13.8±0.9 kg BW) fed 0 (CON), 0.02% (Hes-0.02) or 0.04% (Hes-0.04) of hesperidin for 4-wk were challenged with lipopolysaccharide (LPS; 50 μg/kg BW). Blood samples were obtained at 0, 3, 6, 12 and 24 h to determine immune response. There was no effect of hesperidin on levels of immuneglobulins (IgM, IgG and IgA). Taken together, administration of hesperidin has beneficial effects on feed efficiency and antioxidant activity suggesting that hesperidin can be used as a feed additive in growing pigs.

Hesperidin attenuates oxidative and neuronal damage caused by global cerebral ischemia/reperfusion in a C57BL/J6 mouse model

The aim of this study was to determine the effects of hesperidin (HP) on neuronal damage in brain tissue caused by global cerebral ischemia/reperfusion (I/R) in C57BL/J6 mice. For this purpose, a total of 40 mice were divided equally into four groups: (1) sham-operated (SH), (2) global cerebral I/R, (3) HP, and (4) HP+I/R. The SH group was used as a control. In the I/R group, the bilateral carotid arteries were clipped for 15 min, and the mice were treated with vehicle for 10 days. In the HP group, mice were administered HP (100 mg/kg) for 10 days without carotid occlusion. In the HP+I/R group, the I/R model was applied to the mice exactly as in the I/R group, and they were then treated with 100 mg/kg HP for 10 days. Cerebral I/R significantly induced oxidative stress via an increase in lipid peroxidation and a decrease in the components of the antioxidant defense system. Furthermore, cerebral I/R increased the incidence of histopathological damage and apoptosis in brain tissue. HP treatment significantly reversed the oxidative effects of I/R and inhibited the development of neurodegenerative histopathology. Therefore, the current study demonstrates that HP treatment effectively prevents oxidative and histological damage in the brain caused by global I/R. In this context, the beneficial effects of HP are likely a result of its strong antioxidant and free radical-scavenging properties. HP may be an useful treatment to attenuate the negative effects of global cerebral I/R.

Hesperidin protects brain and sciatic nerve tissues against cisplatin-induced oxidative, histological and electromyographical side effects in rats

In the present study, the beneficial effect of hesperidin (HP), a citrus flavonoid, on cisplatin (CP)-induced neurotoxicity was investigated. A total of 28 rats were equally divided into four groups; the first group was kept as control. In the second and third groups, CP and HP were given at the doses of 7 and 50 mg/kg/day, respectively. In the fourth group, CP and HP were given together at the same doses. The results indicated that although CP caused significant induction of lipid peroxidations and reduction in the antioxidant defense system potency in the brain and sciatic nerve, HP prevented these effects of CP. Besides, CP led to histopathological damage, mainly apoptosis, as well as electromyographical (EMG) changes in sciatic nerve. On the other hand, HP treatment reversed histopathological and EMG effects of CP. In conclusion, CP had severe dose-limiting neurotoxic effects and these effects of CP can be prevented by HP treatment. Thus, it appears that coadministration of HP with CP may be a useful approach to attenuate the negative effects of CP on the nervous system.

Beneficial effect of hesperidin on lipopolysaccharide-induced hepatotoxicity

Hesperidin (HDN) is a flavanone glycoside abundantly found in citrus fruits. HDN has been reported to possess significant activities against allergy, heammorrhoids, hormonal disorders and ulcers. Other reported activities include anti-inflammatory, analgesic, antibacterial, antifungal, antiviral, antioxidant and free radical scavenger activity. A potentially important effect of endotoxin is the increased production of reactive oxygen intermediates as O 2 −, peroxides and nitric oxide. The study reported here show a beneficial effect of HDN in amelioration of endotoxin-induced hepatic dysfunction and oxidative stress in the liver of rats. Hepatotoxicity was induced by administering lipopolysaccharide (LPS), in a single dose of 1 mg/kg intraperitoneally to the rats. A marked hepatic dysfunction evident by rise in serum levels of liver enzymes (ALT, AST, ALP) and total bilirubin ( p < 0.05) was observed. Serum and tissue nitrite levels were also increased. LPS challenge further increased thiobarbituric acid reactive substances (TBARS) levels, whereas glutathione (GSH) content and superoxide dismutase (SOD) activity were decreased in the liver homogenates of the rats showing a marked oxidative stress. HDN administration successfully and dose dependently attenuated these effects of LPS. In conclusion, these findings suggest that HDN attenuates LPS-induced hepatotoxicity possibly by preventing cytotoxic effects of NO and oxygen free radicals.